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Lead Poisoning in Children In the United States, this disease has been identi ed most often in 1- to 3-year-old children who inhabit urban slum areas where old, deteriorated housing prevails (Lead paint was used in most houses built before 1940 and in many built before 1960) The chewing of leaded paint is promoted by compulsive ingestion (pica) from windowsills and painted plaster walls The development of an acute encephalopathy is the most serious complication, resulting in death in 5 to 20 percent of cases and in permanent neurologic and mental de cits in more than 25 percent of survivors Clinical Manifestations These develop over a period of 3 to 6 weeks The child becomes anorectic, less playful and less alert, and more irritable These symptoms may be misinterpreted as a behavior disorder or a manifestation of mental retardation Intermittent vomiting, vague abdominal pain, clumsiness, and ataxia may be added If these early signs of intoxication are not recognized and the child continues to ingest lead, more agrant signs of acute encephalopathy may develop most frequently in the summer months, for reasons that are not understood Vomiting becomes more persistent, apathy progresses to drowsiness and stupor interspersed with periods of hyperirritability, and nally, seizures and coma supervene This syndrome may evolve in a period of a week or less, most rapidly in children under 2 years of age; in older children, it is more likely to develop in recurrent and less severe episodes This clinical syndrome must be distinguished from tuberculous meningitis, viral meningoencephalitis, and the various conditions causing acute increased intracranial pressure Usually, in lead encephalopathy, the CSF is under increased pressure with manifest papilledema, and there may be a slight lymphocytic pleocytosis and elevated protein, but normal glucose values It follows that lumbar puncture should be done with caution and only if it is essential for diagnosis Diagnosis Since the symptoms of plumbism are nonspeci c, the diagnosis depends on an appreciation of the causative factors, a high index of suspicion, and the results of certain laboratory tests The presence of lead lines at the metaphyses of long bones and basophilic stippling of red cells are too inconstant to be relied on, but basophilic stippling of bone marrow normoblasts is uniformly increased Impairment of heme synthesis, which is exquisitely sensitive to the toxic effects of lead, results in the increased excretion of urinary coproporphyrin (UCP) and of -aminolevulinic acid (ALA) These urinary indices and the lead concentrations in the serum bear an imperfect relationship to the clinical manifestations In the test for UCP, which is readily performed in the clinic and emergency department, a few milliliters of urine are acidi ed with acetic acid and shaken with an equal volume of ether; if coproporphyrin is present, the ether layer will reveal a reddish uorescence under a Wood s lamp This test is strongly positive when the whole blood concentration of lead exceeds 80 mg/dL The diagnosis can be con rmed by promoting lead excretion with calcium disodium edetate (CaNa2 EDTA), given in three doses (25 mg/kg) at 8-h intervals Excretion of over 500 mg in 24 h is indicative of plumbism The measurement of zinc protoporphyrin (ZPP) in the blood is another reliable means of determining the presence and degree of lead exposure The binding of erythrocyte protoporphyrin to zinc occurs when lead impairs the normal binding of erythrocyte protoporphyrin to iron Elevated ZPP can also be induced when access to iron is limited by other conditions, such as iron de ciency anemia Pathology In children who die of acute lead encephalopathy, the brain is massively swollen, with herniation of the temporal lobes. convert mvc view to pdf using itextsharp Generate pdf in Asp.Net Mvc using ITextSharp library - Syncbite.com
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NET MVC applications to convert HTML pages and websites to PDF documents preserving all the ... You can use the EVO HTML to PDF Converter Library for . and cerebellum, multiple microscopic ischemic foci in the cerebrum and cerebellum, and endothelial damage and deposition of proteinaceous material and mononuclear in ammatory cells around many of the small blood vessels There are also hyperplastic changes in arteries and arterioles, and in some places, perivascular in ltrates of lymphocytes and mononuclear cells In the territories of some of these vessels there are foci of ischemic necrosis with surrounding glial reaction appropriate for the age of the lesion Similar changes are present in the kidney At blood lead concentrations of 70 mg/dL symptoms may be minimal, but acute encephalopathy may occur abruptly and unpredictably, for which reason the child should be hospitalized for chelation therapy Some children with a blood lead level of 50 mg/dL may have symptoms of severe encephalopathy, whereas others may be asymptomatic In the latter case, an attempt should be made to discover and remove the source of lead intoxication and the child should be reexamined at frequent intervals The seriousness of lead encephalopathy is indicated by the fact that most of the children who become stuporous or comatose remain mentally retarded despite treatment The physician s aim, therefore, is to institute treatment before the severe symptoms of encephalopathy have become manifest Treatment The plan of therapy includes the following: 1 Establishment of urinary ow, following which intravenous uid therapy is restricted to basal water and electrolyte requirements In cases of acute encephalopathy, combined chelation therapy with 2,3-dimercaptopropanol (BAL, 12 to 24 mg/kg) and CaNa2 EDTA (05 to 15 g/m2 body surface area) for 5 to 7 days This is followed by a course of oral penicillamine (40 mg/kg, not exceeding 1 g/day) In acute cases the goal is to reduce the serum lead levels below 40 mg/dL Once the absorption of lead has ceased, chelating agents remove lead only from soft tissues and not from bone, where most of the lead is stored Any intercurrent illness may result in a further mobilization of lead from bones and soft tissues and an exacerbation of symptoms of lead intoxication Repeated doses of mannitol for relief of cerebral edema Microcytic hypochromic anemia is treated with iron once the chelating agents have been discontinued Seizures are best controlled with intravenous diazepam or midazolam. embed pdf in mvc view AtoZSourceCode: How to open pdf file in new tab in MVC using c#
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