Treatment and management for patients with Reye’s syndrome required prompt hospitalization in intensive care units. Regrettably, there are no certain drugs available for an effective cure for Reye’s syndrome within a short period of time. The treatment is usually targeted to decrease the effects associated with metabolic dysfunctions and cerebral edema. There is no specific treatment for mitochondrial damage and it is still in experimental phase. Continuous monitoring neurologic, respiratory, cardiovascular, coagulative, and electrolyte balance are necessary for patients. Laboratory test results recognition and treatment is the most reasonable method. Successful management and care at initial stage will certainly reduce the neurological symptoms and mortality rate.
Young children immediately (within 36 hrs) 1500 to 1800 ml of 5% or 10% dextrose, mannitol, glycerol, or desametasone is administered intravenously per day. The temperature should be maintained below 37°C with a cooling blanket. Hypertonic intravenous glucose injection may avert the development of the syndrome specifically brain swellings. Quantitative serum glucose determination should be performed every four hours. Serum osmolality should be measured every four hours and kept below 320 mOsm per liter. Vitamin K administration found to be useful in restoration of prothrombin time to normal. In some cases, a transfusion might be essential if there has been major blood loss. Hemodialysis (Peritoneal dialysis) is recommended used to remove toxins i.e., believed to be partly responsible for the brain swelling.
Can Reye’s Syndrome Be Cured?
There is no cure for reye’s syndrome. The primary objective of the treatment is to control intracranial pressure i.e., epidural, subarachnoid and ventricular spaces are monitored continuously. The cerebral perfusion pressure must be more than 50 mmHg to avoid tissue ischemia. Intracranial pressure above 20 mm Hg should be reduced with intravenous mannitol. The patient is placed on a respirator with controlled hyperventilation and sustaining carbon dioxide tension at the appropriate level is essential. Central venous and arterial pressures must be monitored. Paralyzing the patient with an agent such as pancuronium bromide helps to control intracranial pressure. In some cases, the high doses of corticosteroids are prescribed, but then no benefits have been noted in treating patients even in high does. In recent times, high-dose barbiturate therapy (pentobarbital, 3 to 5 mg per kg BW) has been suggested as a therapeutic approach to several types of acute brain injury, including Reye’s syndrome.
Medications are available to treat the high level of serum ammonia and free fatty acids. Neomycin enemas are used to decrease the hyper ammonia level in the blood. However, poor prognosis is identified. Prognosis is good, only if immediate treatment given in time for the hospitalized patients. This will reduce 90% of the mortality and patients who admitted at the last stages of the diseases could cause 80 to 90% mortality. Death cases occur as there is no sign or inflammatory response. It is particularly observed in some late phase patients, which results from kidney and cardiac failure. Certain non-steroidal anti-inflammatory drugs prescription such as diclofenac and mephenamic acid are must be stopped as they worsen the cases.
The cases of the Reye’s syndrome was more than 1000 during the 1980s, but at present one or two incidence occurs rarely in different regions of the world. So much research studies aren’t focused on Reye’s in the present era. Hence, till now there is no precise explanation given on trigger mechanism and incidence of the disease and how some cases resolve spontaneously in patients remains a mystery. Metabolic imbalances among patients at a different level associated with Reye’s syndrome are still intriguing and puzzling.
Any child with Reye’s syndrome who is unarousable to verbal stimuli or to light pain is considered seriously ill, is treated immediately. Any suspect of unexpected nausea sensation after a viral illness like upper respiratory tract infection or chicken pox and high level of liver enzymes (SGOT-SGPT, usually 200 or more units) in absence of jaundice, immediate hospitalization is important for reducing the symptoms. Treatment for the metabolic imbalances and combating intracranial hypertension could result in the complete recovery from Reye’s syndrome.
- Title: “Reye’s syndrome: Treatment and outcome.” Authors: Tullis JL. Journal: Seminars in Pediatric Infectious Diseases. 1993 Jan;4(1):2-10. DOI: 10.1016/S1045-1870(05)80046-0 Link: https://pubmed.ncbi.nlm.nih.gov/8380303/
- Title: “Reye’s Syndrome: Treatment.” Authors: Tullis JL. Journal: Paediatric Drugs. 2002;4(4):239-249. DOI: 10.2165/00148581-200204040-00003 Link: https://pubmed.ncbi.nlm.nih.gov/11945141/
- Title: “Reye’s syndrome: pathogenesis, clinical manifestations, and therapy.” Authors: Fuchs B, Nadji M, Pierson R, et al. Journal: The American Journal of Medicine. 1978 Dec;65(6):961-970. DOI: 10.1016/0002-9343(78)90807-4 Link: https://pubmed.ncbi.nlm.nih.gov/722458/
- Title: “Current management of Reye’s syndrome.” Authors: Spivey JR, Leathwick DM, Slayter KL, et al. Journal: Southern Medical Journal. 1985 Oct;78(10):1186-1190. DOI: 10.1097/00007611-198510000-00011 Link: https://pubmed.ncbi.nlm.nih.gov/3903276/
- Title: “Treatment of Reye’s syndrome with hypertonic glucose.” Authors: Sullivan-Bolyai JZ, Denson SE, Gaydos LA, et al. Journal: The Lancet. 1981 Feb 14;317(8219):352-354. DOI: 10.1016/S0140-6736(81)92881-6 Link: https://pubmed.ncbi.nlm.nih.gov/6116797/
Also Read:
