Reye'S Syndrome: Mrs. Smitha.M Associate Professor Vijaya College of Nursing Kottarakkara

REYE’S SYNDROME
Mrs. Smitha.M
Associate Professor
Vijaya college of Nursing
Kottarakkara
REYE’S SYNDROME
I Introduction:
The syndrome was first described in 1963 in Australia by RDK Reye and described a few
months later in the United States by GM Johnson.
 Reye’s syndrome typically occurs after a viral illness, particularly an upper

respiratory tract infection, influenza, varicella, or gastroenteritis, and is associated
with the use of aspirin during the illness.
 Reye’s syndrome is characterized by acute noninflammatory encephalopathy and fatty
degenerative liver failure.
 A dramatic decrease in the use of aspirin among children, in combination with the
identification of medication reactions, toxins, and inborn errors of
metabolism (IEMs) that present with Reye’s syndrome–like manifestations, have
made the diagnosis of Reye’s syndrome exceedingly rare.
II Pathophysiology:
The pathophysiology of Reye’s syndrome appears as follows:
 The pathogenesis of Reye’s syndrome, while not precisely elucidated, appears to

involve mitochondrial injury resulting in dysfunction that inhibits oxidative
phosphorylation and fatty-acid beta-oxidation in a virus-infected, sensitized host.
 The host has usually been exposed to mitochondrial toxins, most
commonly salicylates.
 Histologic changes include cytoplasmic fatty vacuolization in hepatocytes, astrocyte
edema and loss of neurons in the brain, and edema and fatty degeneration of the
proximal lobules in the kidneys.
 All cells have pleomorphic, swollen mitochondria that are reduced in number, along
with glycogen depletion and minimal tissue inflammation.
 Hepatic mitochondrial dysfunction results in hyperammonemia, which is thought to
induce astrocyte edema, resulting in cerebral edema and increased intracranial
pressure (ICP).
III Causes
The causes of Reye’s syndrome include the following:
 Pathogens. Influenza virus types A and B and varicella-zoster virus are the pathogens
most commonly associated with Reye’s syndrome.
 Salicylates. Less than 0.1% of children who took aspirin developed Reye’s syndrome,
but more than 80% of patients diagnosed with Reye’s syndrome had taken aspirin in
the past 3 weeks.
 Inborn errors of metabolism. IEMs that produce Reye-like syndromes include fatty-
acid oxidation defects, particularly medium-chain acyl dehydrogenase (MCAD) and
long-chain acyl dehydrogenase deficiency (LCAD) inherited and acquired forms,
urea-cycle defects, amino and organic acidopathies, primary carnitine deficiency,
and disorders of carbohydrate metabolism.
IV Clinical Manifestations
Signs and symptoms of Reye’s syndrome include:
 Vomiting. Protracted vomiting is seen in patients with or without clinically

significant dehydration.
 Hepatomegaly. There is enlargement of the liver and development in fatty acids
which occur in 50% of patients.
 Lethargy. There is unusual sleepiness or lethargy progressing to encephalopathy.
The CDC uses the Hurwitz classification but adds stage 6.
V Classification
The stages used in the CDC classification of Reye’s syndrome are as follows:
 Stage 0. Alert, abnormal history and laboratory findings consistent with Reye’s
syndrome, and no clinical manifestations.
 Stage 1. Vomiting, sleepiness, and lethargy.
 Stage 2. Restlessness, irritability, combativeness, disorientation, delirium,
tachycardia, hyperventilation, dilated pupils with sluggish response, hyperreflexia,
positive Babinski sign, and appropriate response to noxious stimuli.
 Stage 3. Obtunded, comatose, decorticate rigidity, and inappropriate response to
noxious stimuli.
 Stage 4. Deep coma, decerebrate rigidity, fixed and dilated pupils, loss of
oculovestibular reflexes, and dysconjugate gaze with caloric stimulation.
 Stage 5. Seizures, flaccid paralysis, absent deep tendon reflexes (DTRs), no pupillary
response, and respiratory arrest.
 Stage 6. Patients who cannot be classified because they have been treated with curare
or another medication that alters the level of consciousness.
VI Assessment and Diagnostic Findings

Workup to exclude inborn errors of metabolism (IEMs) must be performed and should
include evaluation for defects of fatty-acid oxidation, amino and organic acidurias, urea-cycle
defects, and disorders of carbohydrate metabolism.
 Ammonia levels. An ammonia level as high as 1.5 times normal 24-48 hours after the
onset of mental status changes is the most frequent laboratory abnormality.
 ALT and AST levels. Levels of alanine aminotransferase (ALT) and aspartate
aminotransferase (AST) increase to 3 times normal but may return to normal by
stages 4 or 5.
 Bilirubin levels. Bilirubin levels are higher than 2 mg/dL (but usually lower than 3
mg/dL) in 10-15% of patients; if the direct bilirubin level is more than 15% of total
or if the total bilirubin level exceeds 3 mg/dL, consider other diagnoses.
 PT and aPTT levels. Prothrombin time (PT) and activated partial thromboplastin
time (aPTT) are prolonged more than 1.5-fold in more than 50% of patients.
 Glucose levels. Glucose, while usually normal, may be low, particularly during stage
5 and in children younger than 1 year.
 Lumbar puncture. If the patient is hemodynamically stable and shows no signs of
increased intracranial pressure (ICP); opening pressure may or may not be
increased; the white blood cell (WBC) count in the cerebrospinal fluid (CSF) is
8/µL or fewer.
VII Medical Management

No specific treatment exists for Reye syndrome; supportive care is based on the stage of the
syndrome.
 Stage 0-1. Keep the patient quiet; frequently monitor vital signs and laboratory
values; correct fluid and electrolyte abnormalities, hypoglycemia, and acidosis;
maintain electrolytes, serum pH, albumin, serum osmolality, glucose,
and urine output in normal ranges; consider restricting fluids to two thirds of
maintenance; overhydration may precipitate cerebral edema use colloids (eg,
albumin) as necessary to maintain intravascular volume.
 Stage 2. The standard of care consists of continuous cardiorespiratory monitoring,
placement of central venous lines or arterial lines to monitor hemodynamic status,
urine catheters to monitor urine output, ECG to monitor cardiac function, and EEG
to monitor seizure activity; prevent increased ICP; elevate the head to 30°, keep the
head in a midline orientation, use isotonic rather than hypotonic fluids, and avoid
overhydration.
 Stage 3-5. Continuously monitor ICP, central venous pressure, arterial pressure, or
end-tidal carbon dioxide; perform endotracheal intubation if the patient is not
already intubated.
VII Pharmacologic Management
No specific treatment is available for Reye syndrome.
 Urea cycle disorder treatment agents. Ammonia detoxicants are used for treatment
of hyperammonemia; they enhance elimination of nitrogen; sodium phenylacetate–
sodium benzoate is approved by the US Food and Drug Administration (FDA) for
treatment of hyperammonemia due to urea-cycle defects and is available only from
a specialty wholesaler, Ucyclyd Pharma, Inc.
 Antiemetic agents. Antiemetic agents such as ondansetron are administered to
decrease vomiting and during the initiation of sodium phenylacetate–sodium
benzoate therapy.
VIII Nursing Management

Nursing management for the patient with Reye’s syndrome include:
Nursing Assessment
Assessment findings for Reye’s syndrome:
 Stage 1. Lethargy, vomiting and hepatic dysfunction.

 Stage 2. Hyperventilation, hyperactive reflexes, delirium and hepatic dysfunction.
 Stage 3. Coma, decorticate rigidity, hyperventilation and hepatic dysfunction.
 Stage 4. Deepening coma, large fixed pupils, decerebrate rigidity and minimal hepatic
dysfunction
 Stage 5. Seizures, flaccidity, loss of deep tendon reflexes and respiratory arrest (death
is usually a result of cerebral edema or cardiac arrest).
Nursing Diagnosis
Based on the assessment data, the major nursing diagnoses are:
 Deficient fluid volume related to failure of regulatory mechanism.

 Ineffective cerebral tissue perfusion related to diminished arterial or venous blood
flow and hypovolemia.
 Risk for trauma related to generalized weakness, reduced coordination, and
cognitive deficits.
 Reduced breathing pattern related to decreased energy and fatigue, cognitive
impairment, tracheobronchial obstruction, and inflammatory process.
Nursing Care Planning and Goals
The major goals for the patient are:
 The patient will maintain adequate ventilation.

 The patient will maintain a normal respiratory status, as evidenced by normal
respiratory rate.
 The patient will maintain orientation to environment without evidence of deficit.
 The patient will maintain skin integrity.
 The patient will maintain joint mobility and range of motion.
Nursing Interventions
Nursing interventions for the patient are:
 Check oxygenation status. Monitor vital signs and pulse oximetry to determine

oxygenation status.
 Monitor ICP. Monitor ICP with a subarachnoid screw or other invasive device to
closely assess for increased ICP.
 Keep track of the blood glucose levels. Monitor blood glucose levels to
detect hyperglycemia or hypoglycemia and to prevent complications.
 Assess I&O. Monitor fluid intake and output to prevent fluid overload.
 Assess overall patient’s status. Assess cardiac, respiratory and neurologic status to
evaluate the effectiveness of interventions and monitor for complications such as
seizures.
 Check cardiopulmonary status. Assess pulmonary artery catheter pressures to
assess cardiopulmonary status.
 Position the patient appropriately. Keep the head of the bed at a 30 degree angle to
decrease ICP and promotes venous return.
 Observe seizure precaution. Maintain seizures precautions to prevent injury.
 Establish oxygen therapy. Maintain oxygen therapy, which may include intubation
and mechanical ventilation, to promote oxygenation and maintain thermoregulation.
 Provide medications. Administer medications as ordered and monitor for adverse
effects to detect complications.
 Transfuse blood products. Administer blood products as ordered to increase
oxygen-carrying of blood and to prevent hypovolemia.
 Check for neuro problems. Check for loss of reflexes and signs of flaccidity to
determine degree of neurologic involvement.
 Monitor patient’s temperature. Provide a hypothermia blanket as needed and
monitor the client’s temperature every 15 to 30 minute while the blanket is in use to
prevent injury and maintain thermoregulation.
 Provide postoperative care. Provide postoperative craniotomy care if necessary to
promote wound healing and to prevent complications.
 Prevent impaired skin integrity. Provide good skin and mouth care and perform
ROM exercise to prevent alteration in skin integrity and to promote joint motility.
 Support the patient and the family. Be supportive of the family and keep them
informed of the patient status to decrease anxiety.
Evaluation
The goals are met as evidenced by:
 The patient maintained adequate ventilation.

 The patient maintained a normal respiratory status, as evidenced by normal
respiratory rate.
 The patient maintained orientation to environment without evidence of deficit.
 The patient maintained skin integrity.
 The patient maintained joint mobility and range of motion.
Documentation Guidelines
Documentation for the patient include:
 Assessment findings, including degree of deficit and current sources of fluid intake.
 I&O, fluid balance, changes in weight, presence of edema, urine specific gravity, and
vital signs.
 Results of diagnostic studies.
 Past and recent history of injuries, awareness of safety needs.
 Use of safety equipment or procedures.
 Plan of care.
 Teaching plan.
 Client’s responses to interventions, teaching, and actions performed.
 Attainment or progress toward desired outcomes.
 Modifications to plan of care.

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REYE’S SYNDROME

 Reye’s syndrome typically occurs after a viral illness, particularly an upper

 The pathogenesis of Reye’s syndrome, while not precisely elucidated, appears to

 Vomiting. Protracted vomiting is seen in patients with or without clinically

VI Assessment and Diagnostic Findings

VII Medical Management

VIII Nursing Management

 Stage 1. Lethargy, vomiting and hepatic dysfunction.

 Deficient fluid volume related to failure of regulatory mechanism.

 The patient will maintain adequate ventilation.

 Check oxygenation status. Monitor vital signs and pulse oximetry to determine

 The patient maintained adequate ventilation.

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