Much of the research on RS focuses on answering fundamental questions about the disorder such as how problems in the body's metabolism may trigger the nervous system damage characteristic of RS and what role aspirin plays in this life-threatening disorder. The ultimate goal of this research is to improve scientific understanding, diagnosis and medical treatment of RS.
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Reye's Syndrome
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Definition
Reye's syndrome [RS] is primarily a children's disease, although it can occur at any age. It affects all organs of the body but is most harmful to the brain and the liver--causing an acute increase of pressure within the brain and, often, massive accumulations of fat in the liver and other organs. RS is defined as a two-phase illness because it generally occurs in conjunction with a previous viral infection, such as the flu or chicken pox. The disorder commonly occurs during recovery from a viral infection, although it can also develop 3 to 5 days after the onset of the viral illness. RS is often misdiagnosed as encephalitis, meningitis, diabetes, drug overdose, poisoning, sudden infant death syndrome, or psychiatric illness. Symptoms of RS include persistent or recurrent vomiting, listlessness, personality changes such as irritability or combativeness, disorientation or confusion, delirium, convulsions, and loss of consciousness. If these symptoms are present during or soon after a viral illness, medical attention should be sought immediately. The symptoms of RS in infants do not follow a typical pattern; for example, vomiting does not always occur. Epidemiologic evidence indicates that aspirin [salicylate] is the major preventable risk factor for Reye's syndrome. The mechanism by which aspirin and other salicylates trigger Reye's syndrome is not completely understood. A "Reye's-like" illness may occur in children with genetic metabolic disorders and other toxic disorders. A physician should be consulted before giving a child any aspirin or anti-nausea medicines during a viral illness, which can mask the symptoms of RS.
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Treatment
There is no cure for RS. Successful management, which depends on early diagnosis, is primarily aimed at protecting the brain against irreversible damage by reducing brain swelling, reversing the metabolic injury, preventing complications in the lungs, and anticipating cardiac arrest. It has been learned that several inborn errors of metabolism mimic RS in that the first manifestation of these errors may be an encephalopathy with liver dysfunction. These disorders must be considered in all suspected cases of RS. Some evidence suggests that treatment in the end stages of RS with hypertonic IV glucose solutions may prevent progression of the syndrome.
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Prognosis
Recovery from RS is directly related to the severity of the swelling of the brain. Some people recover completely, while others may sustain varying degrees of brain damage. Those cases in which the disorder progresses rapidly and the patient lapses into a coma have a poorer prognosis than those with a less severe course. Statistics indicate that when RS is diagnosed and treated in its early stages, chances of recovery are excellent. When diagnosis and treatment are delayed, the chances for successful recovery and survival are severely reduced. Unless RS is diagnosed and treated successfully, death is common, often within a few days.
1,2 Department of Anesthesia and Intensive Care, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
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Suma Rabab Ahmad
1,2 Department of Anesthesia and Intensive Care, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
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1,2 Department of Anesthesia and Intensive Care, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
Swagata Tripathy, Department of Anesthesia and Intensive Care, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India, Phone: 8763400534, e-mail: moc.liamg@atagawsyhtapirt
Copyright © 2019; Jaypee Brothers Medical Publishers [P] Ltd.
This work is licensed under a Creative Commons Attribution 4.0 Unported License. To view a copy of this license, visit //creativecommons.org/licenses/by/4.0/
ABSTRACT
Raised intracranial pressure [rICP] syndrome is seen in various pathologies. Appropriate and systematic management is important for favourable patient outcome. This review describes the stepwise approach to control the raised ICP in a tiered manner, with increasing aggressiveness. The role of ICP measurement in the assessment of cerebral autoregulation and individualised management is discussed. Although a large amount of research has been undertaken for the management of raised ICP, there still remain unanswered questions. This review tries to put together the best evidence in a succinct manner.
How to cite this article
Tripathy S, Ahmad SR. Raised Intracranial Pressure Syndrome: A Stepwise Approach. Indian J Crit Care Med 2019;23[Suppl 2]:S129–S135.
Keywords: Complications, Cerebrospinal fluid, Hypertonic saline, Intracranial pressure, Management, Steroids
INTRODUCTION
Raised intracranial pressure [rICP] syndrome is a constellation of clinical symptoms and signs associated with a rise in intracranial pressure. Various pathologies may lead to a rise in intracranial pressure [ICP]. The realm of management of raised ICP has progressed over time with the development of new monitoring technology and treatment modalities. There is more clarity now in the understanding of the management; however, there are still some gaps. Here we attempt to review the systematic approach to management of the rICP syndrome.
Pathophysiology of Raised ICP Syndrome
The Monro-Kellie doctrine originated from the first description of ICP by Scottish anatomist Alexander Monro in 1783.1He was supported by his colleague George Kellie some years later. Harvey Cushing, American neurosurgeon, in 1926, formulated the doctrine as we know it today.2 He stated that with an intact skull, the volume of the brain, blood, and cerebrospinal fluid [CSF] is constant. An increase in one component will cause a decrease in one or both of the other components. Thus, when there is a growing mass lesion of the brain parenchyma there will be decrease of the CSF or the blood [mainly venous] until the compensatory point is exceeded where we get an elevated ICP3 [Fig. 1]. Various causes enumerated in Table 1 lead to rICP by increase of either one or all of the three components namely brain, CSF or blood.4
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Fig. 1
Cerebral volume–pressure curve showing the relationship between ICP and an increase in the intracranial component volume
Table 1
Causes of raised intracranial pressure
PathophysiologyCausesFocal brain oedema [localized mass lesion]Traumatic hematomas [extradural, subdural, intracerebral] Neoplasms [gliomas, meningiomas, metastasis]
Ischemic or hemorrhagic stroke, abscessDiffuse brain oedemaEncephalitis, meningitis, diffuse head injury, seizures, encephalopathy [hepatic, toxic, uremic or septic], hypoxemic ischemic encephalopathy, water intoxication, Reye's syndromeDisturbance of CSF circulationObstructive hydrocephalus
Communicating hydrocephalus
Subarachnoid hemorrhageObstruction to major venous sinusesDepressed fractures overlying major venous sinuses.
Cerebral venous thrombosisVascular malformationsArteriovenous malformationIdiopathicBenign intracranial hypertension
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Normal ICP is defined as the pressure inside the lateral ventricles or lumbar subarachnoid space in supine position. It normally ranges from