Physician's perceptions of fever in children. Facts and myths.

OBJECTIVE: To ascertain the knowledge and attitude of physicians, regarding fever in children. METHODS: A self-administered questionnaire was mailed to 600 randomly selected pediatricians, family practice physicians, emergency medicine physicians and general practitioners, who practice in Saudi Arabia. Appropriateness of responses to questions was determined on the basis of current medical literature. A rectal temperature of 38.0 degrees C is generally accepted as indicative of fever in children. RESULTS: Of the 600 physicians surveyed, 419 (70%) completed and returned the questionnaire; 17% of the physicians were consultants, 28% specialists and 55% general practitioners. Fifty-eight percent of the physicians had 10 years or more of experience. A rectal temperature of less than 38.0 degrees C was considered to indicate fever by 38% of physicians. Nearly 84% of physicians would initiate antipyretic therapy at a temperature of 38.5 degrees C or less and 56% cited a temperature of 40.0 degrees C or less to be dangerous. Only 5% believed that fever was not dangerous, while the remaining cited the principal danger of fever to be convulsions (69%), brain damage (35%), or death (8%). The responses to the main purpose of antipyretic treatment were to prevent convulsions (70%), to make the child comfortable (55%) and to prevent brain damage (29%). Approximately 53% of physicians reported that the most serious consequences of febrile convulsions were brain damage, learning disability, epilepsy, or death. Only 26% of physicians agreed that a sleeping child with fever should be left undisturbed. Approximately 25% advised inappropriate dosage or administration intervals of paracetamol. Almost all physicians recommended sponging or bathing to reduce fever. All respondents try to educate parents regarding fever and its management. CONCLUSION: A significant number of the surveyed physicians have demonstrated a serious lack of knowledge of the nature, dangers and management of an extremely common health problem. Physicians differ substantially in their knowledge of, and attitude toward fever in children, which is perhaps attributed to their different background in medical education and clinical training.

Clinical and brain 18fluoro-2-deoxyglucose positron emission tomographic findings in ethylmalonic aciduria, a progressive neurometabolic disease.

We report a 2-year-old boy with ethylmalonic aciduria and vasculopathy syndrome evaluated by 18fluoro-2-deoxyglucose positron emission tomographic (18FDG PET) brain scan, with intense uptake of 18FDG in the caudate nucleus and putamen bilaterally but with no morphological changes on magnetic resonance imaging (MRI). A repeat 18FDG PET brain scan 1 year later showed a significant bilateral decreased uptake of glucose in the putamen and the head of the caudate nucleus as well as a decreased uptake in the frontal lobes. On MRI, there was atrophy and watershed infarcts in the basal ganglia, explaining the loss of glucose uptake. These results reflect a selective vulnerability of the basal ganglia, their functional derangement, and ultimate degeneration.

18Fluoro-2-deoxyglucose (18FDG) PET scan of the brain in propionic acidemia: clinical and MRI correlations.

The clinical data and the imaging findings of the positron emission tomography (PET) and the magnetic resonance imaging (MRI) studies in five patients, previously diagnosed to have propionic acidemia, were retrospectively reviewed. The patients were all normal at birth. The first clinical signs, typically hypotonia and failure to thrive, appeared during the first 2 years of life. With progression of the disease, the neurological findings consisted of variable degrees of dementia and extrapyramidal symptoms, notably dystonia, choreoathetosis and rigidity of variable degrees. Initial cerebral PET and MRI studies were normal. Follow-up MRI examinations showed progressive basal ganglia degeneration, with evidence of atrophy and signal abnormalities within the caudate nuclei and the putamina. The thalamic structures were normal. The PET studies demonstrated increased uptake in the basal ganglia and thalami, followed by decreased uptake in the basal ganglia at a later stage of the disease. The structural (MRI) and the functional (PET) studies of the brain were found to be complementary in the evaluation of propionic acidemia, and were in good correlation with the clinical findings.

18Fluoro-2-deoxyglucose (18FDG) PET scan of the brain in type IV 3-methylglutaconic aciduria: clinical and MRI correlations.

The clinical, 18fluorodeoxyglucose positron emission tomography (18FDG PET) and the magnetic resonance imaging (MRI) brain scan characteristics of four patients diagnosed to have 3-methylglutaconic aciduria were reviewed retrospectively. The disease has a characteristic clinical pattern. The initial presentations were developmental delay, hypotonia, and severe failure to thrive. Later, progressive encephalopathy with rigidity and quadriparesis were observed, followed by severe dystonia and choreoathetosis. Finally, the patients became severely demented and bedridden. The 18FDG PET scans showed progressive disease, explaining the neurological status. It could be classified into three stages. Stage I: absent 18FDG uptake in the heads of the caudate, mild decreased thalamic and cerebellar metabolism. Stage II: absent uptake in the anterior half and posterior quarter of the putamina, mild-moderate decreased uptake in the cerebral cortex more prominently in the parieto-temporal lobes. Progressive decreased thalamic and cerebellar uptake. Stage III: absent uptake in the putamina and severe decreased cortical uptake consistent with brain atrophy and further decrease uptake in the cerebellum. The presence of both structural and functional changes in the brain, demonstrated by the combined use of MRI and 18FDG PET scan, with good clinical correlation, make the two techniques complementary in the imaging evaluation of 3-methylglutaconic aciduria.