Pediatric clinics of North America
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The morbidity and mortality that are associated with child abuse is a serious concern for the practicing pediatrician. If abuse is to be prevented, physicians must become skilled in recognizing factors that place a child at risk for abuse. Early and minor signs of abuse and neglect must be recognized and reported to assure services if more serious abuse and neglect are to be prevented. ⋯ This is best accomplished by careful examination and documentation of each injury. If the injury is not in keeping with the history given or the child's level of development, abuse must be considered as a cause. A suspicion of abuse should result in a report.
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Pediatr. Clin. North Am. · Apr 1990
ReviewConcepts of fluid therapy in diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma.
Despite many advances in the overall treatment of type I diabetes mellitus during the last few years, no major advance has been made in decreasing the mortality rate of diabetic ketoacidosis or hyperosmolar hyperglycemic nonketotic coma. A major concern in both of these disease states is the development of cerebral edema during treatment. The guiding principles of therapy in both disease states are rehydration, electrolyte replacement, insulin therapy, and treatment of any underlying illnesses. ⋯ Fluid and electrolyte deficits should be calculated and replaced during 48 hours. Low-dose insulin therapy is employed for treatment of hyperglycemia. Neurologic function should be carefully monitored and mannitol administered if a change in neurologic function occurs.
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Pediatr. Clin. North Am. · Apr 1990
Review Case ReportsEstimation of parenteral fluid requirements.
This article reviews the normal physiologic losses of water and electrolytes from the body, the source of the loss, and the increased body loss of water associated with fever. The three different methods for estimating replacement of water and electrolyte losses are described in this review.
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Congenital heart disease occurs in approximately 1 per cent of liveborn children, but in a much higher percentage of those aborted spontaneously or stillborn. To detect as many as possible with CHD, including those with mild lesions, very intensive studies are needed. Studies that are not so intensive, especially those done before modern diagnostic techniques were in general use, considerably underestimated the incidence of CHD in liveborn children. ⋯ The popular explanation for their inheritance has been the interaction of polygenic effects and the environment, but recent studies of the recurrence and transmission risks of various forms of CHD do not fit this model well. The alternative model is a single gene defect modulated by random events. The recurrence risks for future siblings are 2 to 6 per cent, and for offspring are 1 to 10 per cent, but in a few families the recurrence and transmission risks may be much higher.