When was reyes syndrome first discovered

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Medically reviewed by University of Illinois. But even if your child has not taken aspirin, Reye's syndrome needs to be ruled out.

The exact cause of Reye's syndrome is unknown, but it most commonly affects children and young adults recovering from a viral infection — for example a cold, flu or chickenpox. In most cases, aspirin has been used to treat their symptoms, so aspirin may trigger Reye's syndrome.

In Reye's syndrome, it's thought that tiny structures within the cells called mitochondria become damaged. Mitochondria provide cells with energy and they're particularly important for the healthy functioning of the liver. If the liver loses its energy supply, it begins to fail. This can cause a dangerous build-up of toxic chemicals in the blood, which can damage the entire body and can cause the brain to swell. As Reye's syndrome is so rare, other conditions that can cause similar symptoms need to be ruled out.

These include:. Blood tests and urine tests can help detect if there's a build-up of toxins or bacteria in the blood, and they can also be used to check if the liver is functioning normally. Tests may also be carried out to check for the presence or absence of certain chemicals that could indicate an inherited metabolic disorder.

If Reye's syndrome is diagnosed, your child will need to be immediately admitted to an intensive care unit. Treatment aims to minimise the symptoms and support the body's vital functions, such as breathing and blood circulation. It's also essential to protect the brain against permanent damage that can be caused by the brain swelling. A ventilator breathing machine may be used if your child needs help with breathing.

Vital body functions will also be monitored, including the heart rate and pulse, the air flow to their lungs, blood pressure and body temperature. Once the swelling in the brain has reduced, the other functions of the body should return to normal within a few days, although it may be several weeks before your child is well enough to leave hospital.

Reye described 21 children who presented with severe vomiting, tachypnea, hypoglycemia, and elevated liver enzymes.

Of these 21 children, 17 died within the first 3 days of admission. Prior to this syndrome, each of the patients had experienced malaise, usually associated with an upper respiratory infection.

In this report, Reye notes that the etiology may not be identical in all of these 21 cases. As early as , it was suggested that the syndrome could be caused by hypersensitivity to salicylates. From until , identified cases in the U. Because of efforts to educate the public regarding the potential danger of using aspirin in children and adolescents, aspirin use in this population has been largely abandoned, except for several clinical scenarios in which aspirin is significantly beneficial, such as Kawasaki disease.

An additional explanation that has been proposed to explain the changing rates is viral mutation over time. Bhutta et al reported on a 3-year-old boy in with recent history of fever and upper respiratory infection who presented with vomiting and mental status changes.

Chow and Cherry report a year-old girl presenting in with a recent history of sore throat and upper respiratory infection, for which she had taken aspirin. Once admitted, she became obtunded and apneic and was therefore intubated. After a few days, the patient was declared brain dead.

He had been treated with aspirin for this illness. Two days later, he was admitted with neurologic distress and gastrointestinal GI disease and hematemesis. He also had hypoglycemia and liver dysfunction. Soon after, he experienced confusion and drowsiness, and later cerebral edema. This patient died 2 days after admission. High concentrations of ammonia may accumulate due to the decrease in the activity of the mitochondria. On biopsy, the liver will appear fatty, and changes to the appearance of the mitochondria are often evident.

A brain biopsy will show similar findings, along with edema. One study found a dose-response effect as well. Skeptics of this link further highlight that these case studies are retrospective, and recall bias can be an issue with this type of study design. They also point out that at the time most of these case studies were done, parents may not have distinguished between acetaminophen and aspirin.

Viral agents include influenza A and B, varicella, parainfluenza, measles, adenoviruses, coxsackie viruses, cytomegalovirus, Epstein—Barr virus, HIV, hepatitis A and B, and rotavirus. A high index of suspicion must be present in a patient with vomiting and mental status changes.

These conditions include metabolic disorders such as defects in fatty acid oxidation including acyl-CoA dehydrogenase deficiencies , disorders of oxidative phosphorylation, urea-cycle defects, disorders of carbohydrate metabolism, other metabolic disorders and errors of inborn metabolism, CNS infection or meningitis, and drug or toxic ingestion. Disorders causing presentation with acute liver failure should also be ruled out.

It begins as a prodromal febrile illness that is likely viral in nature, such as an upper respiratory infection or varicella, or possibly rotavirus. Patients will often present with some degree of hepatomegaly and hepatic dysfunction due to fatty degeneration of the liver, but they will not be icteric. There also may be an elevation of intracranial pressure.