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be assumed that in some the saturation of the brain by ammonia impairs the oxidative metabolism of cerebral neurons, and when blood levels of ammonium increase (from protein ingestion, constipation, etc), episodic coma or a more chronic impairment of cerebral functions occurs as it does in adults with cirrhosis of the liver and portal-systemic encephalopathy In the acutely fatal cases the brain is swollen and edematous and the astrocytes are diffusely increased in number and enlarged The neurons are normal Astrocytic swelling has been attributed to the accumulation of glutamate secondary to a suppression of glutamate synthetase These changes have been reproduced in animals by the injection of ammonium chloride When the hyperammonemia is abrupt in onset and severe, the resulting combination of encephalopathy, brain swelling, and respiratory alkalosis simulates the postinfectious Reye syndrome (page 969) As in all forms of liver disease, valproic acid and other hepatic toxins may cause hepatic coma by further impairing the urea cycle enzymes Notable are a few cases of inherited hyperammonemia that come to light in childhod or adulthood only after the administration of one of these drugs Ornithine Transcarbamylase De ciency and Argininosuccinic Aciduria These are episodic diseases in which hyperammonemia develops usually later in childhood, but they may become manifest in the neonatal period The main clinical features are episodic stupor, ataxia, and seizures Their other features have been mentioned above Treatment of the Hyperammonemic Syndromes The treatment of acute hyperammonemic syndromes is directed to the lowering of ammonia levels by hemodialysis, exchange transfusions, and administration of arginine and certain organic acids With subsidence of the acute symptoms, a systematic form of management should be undertaken, as outlined by Brusilow et al and by Msall et al Sodium benzoate should be given in doses up to 250 mg/day, supplemented by sodium phenylacetate or sodium phenylbutyrate, which on theoretical grounds should divert nitrogen from the ureagenesis cycle Arginine (50 to 150 mg/kg) should be added to the diet, since a de ciency of this substance may be responsible for the mental retardation and skin rashes In more chronic cases, treatment consists of decreasing the ammonium load by the use of dietary protein restriction and by administration of oral antibiotics and lactulose In infants with inborn errors of ureagenesis, there is a constant danger of recurrent episodes of hyperammonemia and coma, particularly in response to infections In a few instances, careful management of the metabolic error has resulted in normal psychomotor development Liver transplantation may prove to be a therapeutic option Branched-Chain Aminoacidopathies (Maple Syrup Urine Disease) These conditions are caused by a de ciency of -keto acid dehydrogenase, resulting in the accumulation of the branchedchain amino acids leucine, isoleucine, and valine and the corresponding branched-chain -keto acids Maple syrup urine disease may be taken as the prototype The pattern of inheritance is autosomal recessive With the most severe neonatal type, the infant appears normal at birth, but toward the end of the rst week, poor feeding, intermittent hypertonicity, opisthotonos, and respiratory irregularities appear These are followed by diminished neonatal automatisms, convulsions, severe ketoacidosis, and often coma and death toward the end of the second to fourth week This disease is one of the causes of the malignant epileptic syndrome of early infancy (Brett) Four milder forms of the disease have been de-.

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Device Manager The Device Manager is one of the key programs that you will need to troubleshoot problems on a system Device Manager allows you to remove, refresh, and install drivers You can access it by right-clicking My Computer and selecting Properties Click the Hardware tab to see a window similar to the one in Figure 10-6, which shows you the options on a Windows XP system Select Device Manager to view all of the devices on the system, as shown in Figure 10-7 To perform maintenance on a device driver, you can select the options shown in Figure 10-8 You can install a driver, update, or roll back a driver to a previous version As you can see, Device Manager is a central tool in correcting system problems WinMSD WinMSD is a system information and diagnostic program that can provide you with a wealth of information about your system You can display and save information for submission to either Microsoft or another vendor for troubleshooting This program has been around for several years and ships with all Microsoft operating systems The system information screen of this system shows you the BIOS date and other information that will be helpful in troubleshooting

scribed In these more chronic forms, feeding dif culties begin somewhat later in the early infantile period They are manifest as recurrent infections, episodic acidosis, coma, and retarded growth and psychomotor development Some of these patients, toward the end of the rst year, may become quadriparetic or ataxic; or there may be only a nonspeci c mental retardation The disease derives its name from the maple syrup odor of the child s urine which tests positively for 2,4-dinitrophenylhydrazine (DNPH) Other important laboratory ndings are increased plasma and urine concentrations of leucine, isoleucine, valine, and keto acids Secondary accumulation of a derivative of -hydroxybutyric acid probably accounts for the maple syrup odor The neuropathologic ndings are uncertain In the rst acute case described, only interstitial edema was observed; but in more chronic cases, pallor and loss of myelin and gliosis of parts of the cerebral white matter that myelinate after birth may be found This can be visualized in CT and MRI scans Treatment by restriction of foods containing branched-chain amino acids (leucine, isoleucine, and valine) allows reasonably normal mental development, but only if such restriction is begun in the neonatal period and maintained lifelong A thiamine-responsive variant with a slightly different pattern of keto acids described by Prensky and Moser responds variably to 30 to 300 mg of thiamine The acute episodes, which threaten life, may require peritoneal dialysis to remove the putative toxic metabolites; they respond to the administration of glucose amino acid mixtures that are free of branched-chain keto acids Other Organic Acidemias In addition to maple syrup urine disease, there are a number of other metabolic disturbances, some of them of mitochondrial origin, that appear in the neonatal period or later and are marked by an organic acidemia If they are severe, the infant develops a metabolic (lactic) acidosis soon after birth, with lethargy, feeding problems, rapid respirations, and vomiting Or there may be irritability, jerky limb movements, and hypertonia Later presentations take the form of feeding dif culties, repeated vomiting, hypotonia, and failure to thrive With the passage of time, psychomotor retardation and drug-resistant seizures become evident Metabolic stress eg, intercurrent infection or surgical procedures may precipitate an episode of lactic or ketoacidosis Biochemical studies may disclose a biotinidase de ciency, methylmalonic aciduria, glutaric acidemia, methylglutaconic acidemia, or any number of other organic acid abnormalities The precise abnormality is determined by measuring enzyme activity in white blood cells or cultured skin broblasts As remarked above, some of these enzymes act in conjunction with a speci c vitamin cofactor, so that exact diagnosis is imperative The biotinidase de ciency may respond to 10 mg of biotin per day; the methylmalonic acidemia to 1 to 2 mg of vitamin B12 per day; maple syrup urine disease to 10 to 20 mg of thiamine per day; and glutaric acidemia types I and II to 300 mg of ribo avin per day The administration of carnitine may increase the elimination of toxic metabolites The care of these patients during an acute illness is of extreme importance See Lyon and colleagues for a more complete description Sul te Oxidase De ciency with or without Molybdenum Cofactor De ciency (See also page 804) These are extremely rare autosomal recessive disorders of sulfur metabolism, manifest clinically during the neonatal period by seizures, axial hypotonia, re-.

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