DOCSLIB.ORG

Reye's Syndrome Difficult Its 32A, 381

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Reye's Syndrome Difficult Its 32A, 381 662 BRITISH MEDICAL JOURNAL 20 SEPTEMBER 1975 5 Dwyer, A. F., Newton, N. C., and Sherwood, A. A., Clinical Orthopaedics amino-acid pattern.7 Confirmation of the diagnosis requires and Related Research, 1969, 62, 192. Br Med J: first published as 10.1136/bmj.3.5985.662 on 20 September 1975. Downloaded from 6 Dewald, R. L., and Ray, R. D., Journal of Bone and Joint Surgery, 1970, liver biopsy, but this is frequently ruled out by the prolonged 52A, 233. prothrombin time. There is variable but often intense fatty 7O'Brien, J. P., et al.,Journal of Bone and Joint Sturgery, 1971, 53B, 217. infiltration of the liver, with diffuse vacuolation of the hepa- 8 MacEwen, G. D., Bunnell, W. P., and Sriram, K., Jrournal of Bonie and Joint Suirgery, 1975, 57A, 404. tocytes without nuclear displacement and no hepatocellular 9 Ransford, A. O., and Manning, C. W. S. F.,3Journal of Bone andJoint Sur- necrosis.8 gery, 1975, 57B, 131. Since the diagnosis of is 1 Ponseti, I. V., and Friedman, B.,Jrournal of Bone andJoint Surgery, 1950, Reye's syndrome difficult its 32A, 381. incidence may be higher than is generally realized. About I James, J. I. P.,3Journal of Bone and Joint Surgery, 1951, 33B, 399. 400/,, of children diagnosed in life die.9 Features associated 12 James, J. I. P., Scoliosis. E. &. S. Livingstone, Edinburgh & London, 1967. 13 Nachemson, A., Acta Orthopaedica Scandinavica, 1968, 39, 466. with poor prognosis include a blood ammonia level higher 14 Nilsonne, U., and Lundgren, K-D., Acta Orthopaedica Scandinavica, than 200 tmol 1, a rapid progression to deep coma, a pro- 1968, 39, 456. thrombin time prolonged more than twice normal, increased intracranial pressure,'0 and electroencephalographic ab- normalities." The aetiology and pathophysiology remain poorly under- stood. Some evidence links a variety of this syndrome in Reye's Syndrome Thailand with aflatoxin ingestion.12 A viral aetiology has been suggested owing to the recovery of viruses from the naso- A clinician presented with a child, previously well, who has pharynx and faeces in individual cases and on epidemiological developed convulsions or disturbances of consciousness or grounds,13 but there is no direct viral invasion of liver or both proceeding rapidly to coma is faced with a bewildering brain. The apparent concentration of 13 cases in one part of range of differential diagnoses. Head injuries, vascular acci- Canada which had been sprayed heavily with insecticide was dents, intracranial space-occupying lesions, and direct infec- followed by an experimental study in mice, in which path- tion of the central nervous system must be excluded on the ological features similar to those in Reye's syndrome were basis of the clinical features and by appropriate investigations. produced by a virus in those previously exposed to insecti- Exogenous toxins may need to be looked for as well as meta- cides. Neither the insecticides individually or in combina- bolic disorders such as hypernatraemia, hypoglycaemia, tion nor the virus caused similar pathological features.'4 diabetic acidosis, hypocalcaemia, hypomagnesaemia, uraemia, Even the cause of the encephalopathy remains undetermined. water intoxication, and acute porphyria. Hypertensive ence- For the time being the treatment of Reye's syndrome phalopathy occurring early in glomerulonephritis before a remains supportive and empirical-namely, the correction of renal lesion is suspected may also cause confusion. Also to be hypoglycaemia, electrolyte abnormalities, acidosis, and hy- considered is acute toxic encephalopathy, a poorly understood poxia. Artificial ventilation may be required. A reduced fluid condition in which convulsions and coma with fever and intake-10% dextrose with maintenance electrolytes-is vomiting develop during such illness as upper respiratory tract advised initially to minimize the risk of cerebral oedema, but infections, gastroenteritis, dysentery, pneumonia, or one ofthe this may have to be modified if the patient is dehydrated or exanthemata. Only supportive and symptomatic treatment is if inappropriate release of antidiuretic hormone occurs. available for this condition. Neomycin by nasogastric tube and laxatives and enemata to http://www.bmj.com/ With such a range of differential diagnoses, it is disappoint- minimize ammonia reabsorption from the gut seem rational ing but understandable that another well-recognized cause of treatment, but they are not of proved value,"7 nor is dexa- coma and convulsions in this age group, Reye's syndrome or methasone or mannitol, the usual treatment for increased encephalopathy with fatty degeneration of the viscera, is often intracranial pressure.'0 The bleeding diathesis may require not recognized in life' 12 years after Reye, Morgan, and correction with fresh frozen plasma or whole blood. The Baral2 first drew attention to it. Classically there may be a apparent beneficial effects ofperitoneal dialysisl8 and exchange history of a mild prodromal illness from which the child is transfusion'7 have not been confirmed in some subsequent on 26 September 2021 by guest. Protected copyright. apparently recovering.35 Vomiting, which may be severe, studies.'0 19 Potentially hazardous recommendations that have may precede central nervous system symptoms by 3-72 hours, been associated with recovery include glucose and insulin,20 but it does not occur in all cases. The common course is rapid L-citrulline," 16 21 and nicotinic acid.22 All must be considered progressive deterioration of consciousness, with convulsions of unproved value. No data are available on optimum calorie proceeding to coma and decerebrate posturing, death often intake nor on how they should be provided. following in 24-48 hours. There are no focal central nervous The acute nature of this syndrome, its sporadic occurrence, system signs, nor meningismus. Papilloedema is unusual early and its variable severity caused difficulties in assessing the in the course. Hyperpnoea or irregular respiration should value of therapeutic regimens as well as in sorting out the arouse diagnostic suspicion. Mild to moderate hepatomegaly pathophysiology, a necessary requisite for rational therapy. may indicate visceral lesions, but it is absent in more than Co-operative studies may resolve these difficulties, but they half of cases. Jaundice is unusual. will be successful only if Reye's syndrome is considered during Only by doing liver function tests is the diagnosis likely to life in all children with acute encephalopathy of unknown be suspected in life. If two ofthe following criteria are satisfied cause. without any other obvious explanation for the clinical and biochemical features, Reye's syndrome is a probable diagnosis: I Kearney, P. J., Deasy, P. F., and O'Donohoe, N. V., J'ournal of the Ir'sh aspartate aminotransferase level more than two and a half Medical Association, 1975, 68, 169. times normal, a prothrombin activity of less than 600% of 2 Reye, R. D. K., Morgan, G., and Baral, J., Lancet, 1963, 2, 749. a 3 British Medical_Journal, 1973, 3, 308. normal, and a blood sugar of less than 3 mmol or C.S.F. 4Lancet, 1974, 2, 445. glucose of less than 2 mmol 1. A blood ammonia level higher 5 Mowat, A. P., Archives of Disease in Childhood, 1973, 48, 411. than 0-1 further supports the diagnosis,6 but hyper- 6 Glasgow, A. M., Cotton, R. B., and Dhiensiri, K., American J'ournal of Vmol/l Diseases of Children, 1972, 124, 827. ammonaemia may be transient. Raised serum levels of alanine, Hilty, M. D., Romshe, C., and Delamater, P. V., J7ournal of Pediatrics, lysine, and glutamine and a low citrulline are the typical 1974, 84, 362. BRITISH MEDICAL JOURNAL 20 SEPTEMBER 1975 663 8 Partin, J. C., Schubert, W. K., and Partin, J. S., New England 3ournal of sarily prove infection, since it is also observed in equal or Medicine, 1971, 285, 1339. Br Med J: first published as 10.1136/bmj.3.5985.662 on 20 September 1975. Downloaded from 9 Morbidity and Mortality, Weekly Report, 1974, 23, 115. greater frequency after transfusion both in patients who sub- 10 Lovejoy, F. H., et al., American Jfournal of Diseases ofChildren, 1974,128,36. sequently develop typical HB,Ag-positive hepatitis due to the " Aoki, Y., and Lombrosa, C. T., Neurology, Minneapolis, 1973, 23, 333. B virus and in those who never contract acute hepatitis.4 8 '' Bourgeois, C., et al., American Journal of Clinical Pathology, 1971, 56, 558. 13 Linnemann, C. C., et al., Lancet, 1974, 2, 179. Secondly, it is still uncertain in the cases that show serocon- 14 Crocker, J. F. S., et al., Lancet, 1974, 2, 22. version whether the disease is transmitted de novo or reflects 15 Delong, G. R., Glick, T. H., and Shannon, D. C., New England Journal a of of Medicine, 1974, 290, 1488. merely reactivation pre-existing infection-though the 16 Oetgen, W. J., et al., New England Jouirnal of Medicine, 1974, 291, 421. observation that the frequency of seroconversion increases 71 Huttenlocher, P. R., Journal of Pediatrics, 1972, 80, 845. with the number of units transfused and that the antibody is 18 Samaha, F. J., Blau, E., and Berardinelli, J. L., Pediatrics, 1974, 53, 336. 19 Samaha, F. J., Quoted by Nadler, H., Pediatrics, 1974, 54, 265. often of IgM class favours a primary infection.8 Finally, the 2(1 Brown, R. E., and Madge, C. E., Pediatrics, 1971, 48, 162. incubation period ofcytomegalovirus is about 2-4 weeks, much 2I Glasgow, A. M., and Chase, H. P., Nezw, England Journal of Medicine, shorter than that observed in most cases of hepatitis after 1974, 291, 421. 22 Powell, H. C., and Rosenberg,
Load more

Recommended publications
  • Raised Intracranial Pressure and Hydrocephalus
    Raised Intracranial Pressure and Hydrocephalus Sept 2014 Raised Intracranial Pressure 500ml/day CSF made to replenish volume of 150ml. ICP = MAP-CPP. Normal ~10mmHg. Raised = >20mmHg sustained for >15min. ICP monitoring if severe HI & coma, intracerebral haemorrhage, Reye’s, hydrocephalus Causes of raised intracranial pressure Localised mass lesions: traumatic haematomas (extradural, subdural, intracerebral) Neoplasms: glioma, meningioma, metastasis Abscess Focal oedema secondary to trauma, infarction, tumour Disturbance of CSF circulation: obstructive hydrocephalus, communicating hydrocephalus Obstruction to venous sinuses: depressed fractures overlying venous sinuses, cerebral venous thrombosis Diffuse brain oedema or swelling: encephalitis, meningitis, diffuse head injury, SAH, Reye's syndrome, lead encephalopathy, water intoxication, near drowning Idiopathic intracranial hypertension Presentation Headache: nocturnal, on waking, worse on coughing/moving head ↓LOC: lethargy, irritability, slow decision making, abnormal behaviour → stupor, coma and death Vomiting Eye changes: irregularity or dilatation in one eye. Unilateral ptosis or III and VI nerve palsies. In later stages, ophthalmoplegia and loss of vestibulo-ocular reflexes. Papilloedema: blurring of disc margins, loss of venous pulsations, disc hyperaemia, flame haemorrhages. Later, obscured disc margins and retinal haemorrhages. Cushing reflex: ( ↑BP, widened pulse pressure and ↓HR). Other: Late hemiparesis Investigations CT/MRI Check and monitor ABG, blood glucose, renal function,
    [Show full text]
  • Annual Summary of Communicable Disease Reported to MDH, 2003
    MINNESOTA DEPARTMENT OF HEALTH DISEASE CONTROL N EWSLETTER Volume 32, Number 4 (pages 33-52) July/August 2004 Annual Summary of Communicable Diseases Reported to the Minnesota Department of Health, 2003 Introduction Minnesota Government Data Practices do not appear in Table 2 because the Assessment is a core public health Act (Section 13.38). Provisions of the influenza surveillance system is based function. Surveillance for communi- Health Insurance Portability and on reported outbreaks rather than on cable diseases is one type of ongoing Accountability Act (HIPAA) allow for individual cases. assessment activity. Epidemiologic routine communicable disease report- surveillance is the systematic collec- ing without patient authorization. Incidence rates in this report were tion, analysis, and dissemination of calculated using disease-specific health data for the planning, implemen- Since April 1995, MDH has participated numerator data collected by MDH and a tation, and evaluation of public health as one of the Emerging Infections standardized set of denominator data programs. The Minnesota Department Program (EIP) sites funded by the derived from U.S. Census data. of Health (MDH) collects disease Centers for Disease Control and Disease incidence may be categorized surveillance information on certain Prevention (CDC) and, through this as occurring within the seven-county communicable diseases for the program, has implemented active Twin Cities metropolitan area (Twin purposes of determining disease hospital- and laboratory-based surveil- Cities metropolitan area) or outside of it impact, assessing trends in disease lance for several conditions, including (Greater Minnesota). occurrence, characterizing affected selected invasive bacterial diseases populations, prioritizing disease control and food-borne diseases. Anaplasmosis efforts, and evaluating disease preven- Human anaplasmosis (HA) is the new tion strategies.
    [Show full text]
  • Atypical Reye Syndrome
    Acta Biomed 2021; Vol. 92, Supplement 1: e2021110 DOI: 10.23750/abm.v92iS1.10205 © Mattioli 1885 Case report Atypical Reye syndrome: three cases of a problem that pediatricians should consider and remember Serena Ferretti1, Antonio Gatto2, Antonietta Curatola1, Valeria Pansini2, Benedetta Graglia1, Antonio Chiaretti1,2 1 Department of Woman and Child Health and Public Health, Università Cattolica del Sacro Cuore, Rome, Italy; 2 Department of Woman and Child Health and Public Health, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy Abstract. Introduction: Reye syndrome is a rare acquired metabolic disorder appearing almost always dur- ing childhood. Its etiopathogenesis, although controversial, is partially understood. The classical disease is typically anticipated by a viral infection with 3-5 days of well-being before the onset of symptoms, while the biochemical explanation of the clinical picture is a mitochondrial metabolism disorder, which leads to a metabolic failure of different tissues, especially the liver. Hypothetically, an atypical response to the preceding viral infection may cause the syndrome and host genetic factors and different exogenous agents, such as toxic substances and drugs, may play a critical role in this process. Reye syndrome occurs with vomiting, liver dys- function and acute encephalopathy, characterized by lack of inflammatory signs, but associated with increase of intracranial pressure and brain swelling. Moreover, renal, and cardiac dysfunction can occur. Metabolic acidosis is always detected, but diagnostic criteria are not specific. Therapeutic strategies are predominantly symptomatic, to manage the clinical and metabolic dysfunctions. Case reports: We describe three cases of chil- dren affected by Reye syndrome with some atypical features, characterized by no intake of potentially trigger substances, transient hematological changes and dissociation between hepatic metabolic impairment, severe electroencephalographic slowdown and slightly altered neurological examination.
    [Show full text]
  • Raised Drug in Patient Recovered Completely Etiology Or Reye
    upwards fixed gaze. The liver was enlarged and hypoglycemia and raised transaminases were noted. The encephalopathy and dystonic reactions were considered secondary to the anti-emetic drug in combination with liver disease most probably due to viral infection. Neurological examination was normal after 36 hours and the patient recovered completely after 10 days. The author stresses the need to consider drugs other than salicylates in the etiology or Reye syndrome and particularly the use anti-emetics (Casteels- VanDaele M. Reye syndrome or side effects of anti-emetics? Eur J Pediatr May 1991; 150:456-4591. COMMENT. In the 1960's several cases of toxic encephalopathy resembling Reye syndrome were reported in patients who had received the anti-emetic Tigan for vomiting. Dr. John Pepper, the Director of Toxicological Studies at Hoffman Laroche Company investigated these reports with customary thoroughness and with the aid of many consultants. No specific correlation between the use of Tigan and the toxic encephalopathy was determined. The lack of association of Reye syndrome with aspirin use has been reported from Australia (Orlowski J P et al. A catch in the Reye Pediatrics 1987; 80:638. See Ped Neur Briefs Nov 1987). HEADACHE CHOCOLATE IS A MIGRAINE-PROVOKING AGENT Patients with migraine who believe that chocolate could provoke their attacks were challenged with either chocolate or a closely matching placebo in a double-blind parallel group study at the Princess Margaret Migraine Clinic, Charing Cross Hospital, London, England. The placebo contained no cocoa butter or cocoa powder and the carob powder used in the placebo was also added to the chocolate and successfully disguised by the use of a peppermint- masking flavor.
    [Show full text]
  • Influenza a Virus and Reye's Syndrome in Adults
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.43.6.516 on 1 June 1980. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry, 1980, 43, 516-521 Influenza A virus and Reye's syndrome in adults LARRY E DAVIS AND MARIO KORNFELD From the Neurology Service, Veterans Administration Medical Center and Department of Neurology and Pathology, University of New Mexico School of Medicine, Albuquerque, New Mexico S U M M A R Y We report fatal Reye's syndrome in two adults following proven influenza A viral infections. Reye's syndrome is, therefore, not confined to children but may also occur in adults. Many reported cases of postinfluenza A encephalopathy have clinical and pathological features of Reye's syndrome suggesting that they are not due to postinfectious perivenous demyelination. In 1963, Reye, Morgan, and Baral described 21 died. No one in his family had ever had illnesses children who, following a prodromal illness, suggesting abnormalities of the urea cycle. developed vomiting, seizures, coma and death.' Laboratory tests included a normal brain com- Noninflammatory cerebral oedema and fatty meta- puterised tomogram (CT), blood count, and serum morphosis of the liver was found at necropsy. An electrolytes. A traumatic lumbar puncture done Protected by copyright. increasing number of similar cases have since on admission had a normal opening pressure. The been reported worldwide. Reye's syndrome is gen- cerebrospinal fluid (CSF) contained 900 fresh red erally thought to occur only in children. The blood cells per mm3, 5 lymphocytes per mm3, 250 aetiology is unknown, but the syndrome has been mg per dl protein, 150 mg per dl glucose, and associated with epidemics of influenza B virus2 sterile bacterial and fungal cultures.
    [Show full text]
  • Reye Syndrome
    Number 84 January 2019 Reye Syndrome What is Reye Syndrome? Diarrhea and rapid breathing in infants and Reye Syndrome is a rare disease that mainly toddlers affects children and teenagers when they have, Persistent vomiting in children and teenagers or recently had, a viral infection such as Changes in personality or behaviour such as chickenpox or influenza. Reye Syndrome confusion, irritability or aggression. Reye causes swelling of the liver and brain, and it Syndrome may also cause strange behavior can also cause death. such as staring and slurred speech How can I prevent Reye Syndrome? Seizures and comas The use of acetylsalicylic acid (ASA or Loss of consciousness Aspirin®) has been strongly linked to Reye Syndrome. Do not give ASA or Aspirin® to Reye Syndrome occurs 3 to 7 days after the anyone under 18 years of age to manage beginning of an infection or illness caused by a symptoms such as fever, headache and muscle virus, or during recovery from the infection or aches. illness. Reye Syndrome can be misdiagnosed as swelling of the brain, also known as Instead, use acetaminophen for anyone under encephalitis or swelling of the lining of the 18 years of age. Examples of medications with brain (meningitis), diabetes, drug overdose, acetaminophen are Tylenol®, Tempra® and poisoning, sudden infant death syndrome Atasol®. (SIDS) or a psychiatric illness. You can also use ibuprofen for relief of What is the treatment? symptoms in children under 18 years of age. Early diagnosis and treatment in a hospital can Examples of ibuprofen include Advil® and save your child’s life.
    [Show full text]
  • Reye's Syndrome in an Adult Patient
    .A Ar'N zo following complex commands. Speech was sparse, garbled, Reye's Syndrome in inappropriate and only semi-intelligible. On serial cranial an Adult Patient nerve testing, the discs were slightly hyperemic but she had no overt papilledema, no focal cranial nerve dysfunction and DOUGLAS B. KIRKPATRICK, MD no focal deficits. She did not blink to visual threat. Motor COLLEEN OTTOSON testing showed no significant focal paresis or incoordination, LYNN L. BATEMAN, MD although the patient was somewhat diffusely dyspraxic and Provo, Utah disorganized in her motor movement. Symmetrically in- creased tone was noted. In addition, the patient occasionally REYE'S SYNDROME is a relatively recently recognized clinical swiped at her face with her right hand, as though halluci- syndrome of rapid and sometimes catastrophic neurologic de- nating. Bilateral spontaneous extensor posturing was periodi- terioration in pediatric patients, with associated hepatic dys- cally observed. Sensation was intact to noxious stimuli only, function, elevated plasma ammonia and amino acid levels and as the patient could not cooperate for more definitive testing. a preexisting viral syndrome. In rare cases, this syndrome can Reflexes were normoactive and symmetric, but a bilaterally occur in adults. We describe such a case in the oldest patient positive Babinski's response was noted. reported. Physicians treating older patients need to be aware The patient's family history was unremarkable. Review of of the possibility of the Reye's syndrome in this age group her personal history showed that a probable early childhood because prompt recognition and treatment are vital. Vigorous case of polio resulted in a slight but permanent right hemipa- clinical support, reduction of increased intracranial pressure resis, most prominent in the lower limb.
    [Show full text]
  • Reye's Syndrome
    118 TIlE NATIONAL MEDICAL JOURNAL OF INDIA VOL. 4, NO.3 production of insulin-like growth factor I (IGF I) mRNA in administration of corticoids: A new and peculiar stimulus of growth hypophysectomized rats and reduces IGF 1 mRNA abundance in hormone secretion in man. J c/in Endocrinol Metab 1990;70:234-7. intact rats. Endocrinology 1989;125:165-71. 22 Freidman M. Strang LB. Effect of long-term corticosteroids and 13 Gourmelen M. Girard F. Binoux M. Serum somatomedin/insulin- corticotrophin on the growth of children. Lancet 1966;1:568-72. like growth factor (IGF) and IGF carrier levels in patients with 23 Norman AP. Sanders S. Effect of corticotrophin on skeletal matura- Cushing's syndrome or receiving glucocorticoid therapy. J C/in tion and linear growth in six patients with severe asthma. Lancet Endocrinol Metab 1982;54:885-92. 1969;1:287-9. 14 Unterman TG. Phillips LS. Glucocorticoid effects on somatomedins 24 Brown DCP. Savacool AM. Letizia CM. A retrospective review of and somatomedin inhibitors. J Clin Endocrinol Metab 1985; the effects of one year of triamcinolone acetonide aerosol treatment 61:618-26. on the growth patterns of asthmatic children. Ann Allergy 1989; 15 Hyams JS. Carey DE. Corticosteroids and growth. J Pediatr 63:47-51. 1988;113:249-54. 25 Littlewood JM. Johnson AW. Edwards PA. Littlewood AE. 16 Hyams JS. Carey DE. Leichtner AM, Goldberg BD. Type I pro- Growth retardation in asthmatic children treated with inhaled collagen as a biochemical marker of growth in children with beclomethasone dipropionate. Lancet 1988;1:115-16.
    [Show full text]
  • Encephalopathy and Fatty Degeneration of Viscera Reye's Syndrome
    Arch Dis Child: first published as 10.1136/adc.48.6.411 on 1 June 1973. Downloaded from Annotation Archives of Disease in Childhood, 1973, 48, 411. Encephalopathy and fatty degeneration of viscera Reye's syndrome Encephalopathy and fatty degeneration of the relatively bloodless, greasy, and firm. In liver viscera were reported as early as 1929 (Brain, biopsy specimens fatty infiltration is seen as diffuse Hunter, and Turnbull), but it is only in the past 10 small vacuoles most prominent in the periportal years that the clinical and pathological features have areas, but there is massive fatty infiltration in been clearly defined (Mann et al., 1962; Reye, necropsy material. Liver glycogen is decreased. Morgan, and Baral, 1963; Lancet, 1969; Evans et The nuclei of the hepatocytes may contain 1 to 4 al., 1970; Guillete, Berlin, and Finkelstein, 1971). irregular enlarged nucleoli but hepatocellular Considerable problems still exist regarding many necrosis is not seen except in necropsy material. aspects of the disorder. The aetiology remains The portal tracts are normal. Electron micro- unknown and the pathogenesis is poorly understood. scopical examination of liver biopsy material The lack of striking clinical features of hepatic (Partin, Schubert, and Partin, 1971) early in the involvement may cause the disorder to be over- course of the encephalopathy shows the hepatocytes looked in life, but even if the diagnosis is made, to be universally affected by a process which results there are considerable problems in management. in swollen pleomorphic mitochondria, as well as copyright. The assessment of the relative efficacy of different small droplet triglyceride accumulation.
    [Show full text]
  • Reye's Syndrome: Children and Teenagers Who Have Or Are Recovering from Chickenpox Or Flu- Like Symptoms Should Not Use This Product
    Reye's Syndrome: Children and teenagers who have or are recovering from chickenpox or flu- like symptoms should not use this product. When using this product, if changes in behavior with nausea and vomiting occur, consult a doctor because these symptoms could be an early sign of Reye's syndrome, a rare but serious illness. Allergy alert: Aspirin may cause a severe allergic reaction, which may include: • Hives • Facial swelling • Shock • Asthma (wheezing) Stomach bleeding warning: This product contains an NSAID, which may cause severe stomach bleeding. The chance is higher if you: • Are age 60 or older • Have had stomach ulcers or bleeding problems • Take a blood-thinning (anticoagulant) or steroid drug • Take other drugs containing prescription or nonprescription NSAIDs (aspirin, ibuprofen, naproxen, or others) • Have 3 or more alcoholic drinks every day while using this product • Take more or for a longer time than directed Caffeine Warning: This product contains caffeine. Limit the use of caffeine- containing medications, foods, or beverages while taking this product because too much caffeine may cause nervousness, irritability, sleeplessness, and, occasionally, rapid heart beat. Do not use if you have ever had an allergic reaction to aspirin or any other pain reliever/fever reducer. Ask a doctor before use if: • Stomach bleeding warning applies to you • You have a history of stomach problems, such as heartburn • You have high blood pressure, heart disease, liver cirrhosis, or kidney disease • You are taking a diuretic • You have asthma Ask a doctor or pharmacist before use if you are taking a prescription drug for: • Gout • Diabetes • Arthritis Stop use and ask a doctor if: • An allergic reaction occurs.
    [Show full text]
  • Review of Aspirin / Reye's Syndrome Warning Statement
    Medicines Evaluation Committee Review of Aspirin / Reye’s syndrome warning statement April 2004 Medicines Evaluation Committee Review of Aspirin / Reye’s syndrome warning statement Prepared for the TGA by Dr Susan James April 2004 REVIEW OF ASPIRIN/REYE’S SYNDROME WARNING STATEMENT REVIEW OF ASPIRIN/REYE’S SYNDROME WARNING STATEMENT REVIEW OF ASPIRIN/REYE’S SYNDROME WARNING STATEMENT..............1 ACKNOWLEDGEMENTS ......................................................................................................2 ABBREVIATIONS ................................................................................................................3 INTRODUCTION..............................................................................................................4 BACKGROUND....................................................................................................................4 TERMS OF REFERENCE .......................................................................................................4 HISTORY OF APPENDIX F WARNING STATEMENT ...............................................................4 RECENT OVERSEAS REGULATORY ACTION.........................................................................5 WHAT IS REYE’S SYNDROME? ..................................................................................6 THE ASSOCIATION BETWEEN ASPIRIN AND REYE’S SYNDROME................7 EPIDEMIOLOGY STUDIES ....................................................................................................7 THE AUSTRALIAN SITUATION
    [Show full text]
  • Prescribing Informationcompro
    COMPRO- prochlorperazine suppository Padagis US LLC ---------- PRESCRIBING INFORMATION COMPRO® PROCHLORPERAZINE SUPPOSITORIES USP, 25 mg Rx only ANTIEMETIC - TRANQUILIZER WARNING Increased Mortality in Elderly Patients with Dementia-Related Psychosis Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. Analyses of seventeen placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients. Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality. The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear. Compro® Prochlorperazine Suppositories USP is not approved for the treatment of patients with dementia-related psychosis (see WARNINGS). DESCRIPTION Prochlorperazine, a phenothiazine derivative, is designated chemically as 2-Chloro -10- [3-(4-methyl-1-piperazinyl)propyl]phenothiazine with the following structural formula: Each suppository, for rectal administration, contains 25 mg of prochlorperazine; with glycerin, glyceryl monopalmitate, glyceryl monostearate, hydrogenated coconut oil fatty acids and hydrogenated palm kernel oil fatty acids.
    [Show full text]