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: Mrs. Smitha.M Associate Professor Vijaya College of Nursing Kottarakkara
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.
II Pathophysiology:
The pathophysiology of Reye’s syndrome appears as follows:
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:
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.
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.
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.
Nursing Assessment
Assessment findings for Reye’s syndrome:
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.