Fever in children: diagnosis and management by nurses, medical students, doctors and parents.

Thirty-six nurses, 18 final year medical students, 24 doctors and 36 parents were questioned about their understanding and management of the symptom "fever". There was an obvious tendency to over-diagnose fever by the nursing and medical staff. Antipyretics and sponging were unnecessarily prescribed. Most parents do not have a thermometer and have minimal understanding of fever and its management, and 37% regard fever as a cause of brain damage. Their main sources of information on the subject derive from relatives and friends: only 9% mentioned nurses or doctors as their source of information. Medical students receive little teaching on fever. It is recommended that more time should be devoted to teaching nurses, medical students and junior doctors about fever and they in turn should educate parents on the subject.

Coagulation changes in sickle cell disease in early childhood.

Measurements of the coagulation system were carried out in children with sickle cell disease (SCD) in both steady state and on the 1st day of painful crisis and were compared to age- and sex-matched healthy controls. No significant differences were found in prothrombin time, partial thromboplastin time, thrombin time, reptilase time, plasma fibrinogen, antithrombin III, factor VIII:C, ristocetin-cofactor (Ri-Cof) and platelet aggregation responses to ADP, collagen and adrenaline. Abnormal aggregation responses to ristocetin were noted in all patients with SCD when compared to controls. Daily measurements during the first 4 days of painful crisis showed significant elevation of fibrinogen and Ri-Cof and enhancement of aggregation to ADP and adrenaline by the 3rd day of crisis. It was concluded that the changes noted, rather than being primarily responsible for the onset of crisis, can only be secondary changes arising from the aetiological factors of crisis, i.e. stasis and acute-phase proteins.

Acute reversible pulmonary ischemia. A cause of the acute chest syndrome in sickle cell disease.

A 6-year-old girl with sickle cell disease was admitted to the hospital with the diagnosis of the acute chest syndrome. The laboratory findings and the radionuclear lung scan supported a diagnosis of pulmonary infarction rather than pneumonia. She improved with intravenous fluids, oxygen, penicillin, and theophylline. The most likely explanation for the rapid resolution of the clinical syndrome, the chest x-ray, and lung scan abnormalities is that masses of sickled cells caused transient pulmonary vascular occlusion leading to perfusion defects and ischemia, and that the sickled cell thrombi were dislodged before the infarction occurred. To our knowledge, this phenomenon has not been described as a cause of the acute chest syndrome in sickle cell disease in children.