In the probable cases of Reye syndrome , it is necessary to investigate about previous viral disease , which may lead from 1 to 6 sidereal day , and clinical symptom of vomiting and progressive neurological involvement until reaching acoma . There may be a adrenergic state increase with sweating , sometimes fever , tachycardia , tachypnea and pupillary dilation . increase hyperventilation is another central clinical fact . ictus do not commonly seem until the comatoseness is deep . It may take from 8 hours to 4 twenty-four hours from the first symptoms to the establishment of the coma .
How do They Test for Reye’s Syndrome?
Paraclinical Tests
There does not be a test to detect Reye syndrome . As an alternative , the psychoanalysis for the detection of the syndrome usually begins with stock tests and with an interrogatory to detect disorders of fatty acid oxidisation and other metabolic disorders .
Sometimes more invasive symptomatic tests are needed to check over other likely grounds . For model :
Lumbar Puncture : Useful for ruling out similar diseases , such as an transmission in the membrane lining the brain andspinal cord(meningitis ) or an fervor or infection in the brain ( encephalitis ) .
Liver Biopsy : A liver biopsy can help to identify or rule out other disease that may affect the liver .
Computed Tomography ( CT)orMagnetic Resonance Imaging ( MRI )
It can help the Dr. to identify or govern out other causes of change in behavior or decreased attention .
In blood , there are unremitting reflection of liver dysfunction , with elevation of transaminases , hyperammonemia ( particularly in the first minute ) , and hypoprothrombinemia ; other blood serum enzyme ( creatine phosphokinase , lactic dehydrogenase , amylase , lipase ) are also usually elevated .
The finding of hypoglycemia is mutual , in relation to the depletion of hepatic glycogen deposits , bilirubin seldom arise above 2 - 3 m% , atomic number 15 is usually lower and uric acid is elevated , and it is usual that there are modifications of the amino group acid figure .
Organic battery-acid ( lactic , pyruvic , isobutyric , propionic , isovaleric and caprylic ) are raise ; cholesterol , lipoproteins , coagulation factors and component of the complement system are depressed .
leucocytosis is frequent ( up to 40,000 - 50,000 / mm3 ) and the cerebrospinal fluid ordinarily shows increase pressure , with down in the mouth glucose ( relative to plasm ) , normal proteins , without pleocytosis .
In the histopathological studies it is evidenced , in liver , animal starch depletion , steatosis , proliferation of peroxisomes , contortion of mitochondria , these are also altered in brain and muscle .
All these finding are an saying of the decreased action of mitochondrial enzymes , which supports the idea that this syndrome represent the metabolous response to a mitochondrial aggression .
In the electroencephalogram , alterations in prognostic time value have been described , which correlate with the clinical stages .
The diagnosis of Reye syndrome can be made by tax the presence of
Clinical Criteria : History of previous viral infection , regurgitation , encephalopathy , comatoseness , convulsions , with other laboratory test : meridian of transaminases and ammonium hydroxide , lengthen of prothrombin time , cerebrospinal unstable normality ; next to it the absence seizure of other causes of encephalopathy or liver disease .
The differential diagnosis must be made with :
Acute Infections : Of the fundamental nervous system . The field of study of cerebrospinal fluid allows the distinction because it is normal in Reye syndrome ( it may show increased pressure and low grade of glucose in cerebrospinal fluid ) the uncovering of red blood cells or white cell , as well as the elevation of protein go against this syndrome and should suggest other possibility ( meningitis , encephalitis , as well as subarachnoid hemorrhages ) .
Fulminant Hepatitis : It produces a picture similar to the Reye syndrome , but this is characterise by the absence of thorniness ( variable in hepatitis ) and liver biopsy allow , in any case , the distinction between these mentioned two entities .
Acute Pancreatitis : It can give a like clinical picture and difficult eminence since pancreatic involvement is common in Reye syndrome .
Conclusion
symptomatic uncertainty in a first phase angle will be with any discriminating encephalopathy of nameless source , phrenitis , salicilic intoxication , drug overdose and needlelike hepatic failure .
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