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General principles of thermoregulation, the pathophysiology of fever, controversies concerning the use of antipyretic therapy, and nonpharmacologic and pharmacologic treatments commonly used for antipyresis in the pediatric population are reviewed. Several arguments can be made for not ameliorating the febrile response. Fever is an important diagnostic and prognostic clinical sign that may have beneficial effects for the host. In addition, body temperatures of < or = 41 degrees C (105.8 degrees F) are relatively harmless. Reasons for treating fever include patient discomfort, the potential for adverse sequelae, the possibility of seizures, and the possibility that fever could affect the pharmacokinetic profiles of drugs. Nonpharmacologic treatment for fever includes environmental measures to enhance dissipation of body heat and sponging. Aspirin and acetaminophen are the agents used most frequently for antipyresis in pediatric patients. However, aspirin use in children with a viral illness has been associated with development of Reye's syndrome. As a result, its use in children has declined in the United States. Acetaminophen is relatively free of adverse effects and is considered first-line pharmacologic antipyresis therapy. Ibuprofen suspension should be considered as second-line antipyretic therapy. Combination therapy with acetaminophen and aspirin may be considered if the patient fails to respond to other nonpharmacologic and pharmacologic therapies; however, combination therapy may result in increased risk of drug toxicity, increased probability of adverse reactions, and increased risk of intoxication. Aspirin, acetaminophen, and ibuprofen are equally effective for antipyresis in pediatric patients. However, because acetaminophen is the safest medication, it is currently the therapy of choice.

The effects of the Gemini PC-2 linear peristaltic infusion device on the integrity of packed red blood cells (RBC) and whole blood products are reported. Thirty-eight units of blood products were infused at rates of 999, 100, 50, and 5 mL/hr under simulated clinical conditions. To evaluate the effect of hematocrit on cell survival, fresh and stored packed RBCs preserved with adenine-saline 3 (AS-3) and fresh and stored packed RBCs and fresh and stored whole blood preserved with citrate-phosphate-dextrose-adenine 1 (CPDA-1) were used. No two units tested came from the same donor. Plasma potassium and plasma free hemoglobin concentrations were determined before and after simulated infusion for 80 experimental runs. Preinfusion plasma potassium and free hemoglobin concentrations varied significantly among the blood products. Stored products were associated with higher plasma potassium and free hemoglobin levels than fresh units, both before and after infusion. Concentrations also differed significantly between AS-3-preserved and CPDA-1-preserved fresh and stored packed RBCs. Infusion did not change plasma potassium values appreciably under any conditions. Plasma free hemoglobin increased in the fresh products only. Donor-specific differences were significant for potassium but not for free hemoglobin. There was no significant effect of infusion rate on either biochemical marker. In all the experimental runs, less than 0.01% of cells were lysed. The Gemini PC-2 linear peristaltic infusion device delivered a variety of blood products at a wide range of infusion rates without inducing a substantial degree of hemolysis.

Monitoring of inline intravenous pressure as a method for predicting or detecting infiltration of peripheral catheter sites in infants was evaluated. Inline intravenous pressure was measured every 30 minutes in infants less than 12 months of age who had standardized peripheral catheters through which they were receiving a continuous infusion. Pressure was measured by an inline pressure transducer, and the signal was recorded by a strip chart recorder. Physical activities or manipulations of the patients were recorded simultaneously with each pressure reading. The catheter site was inspected hourly for clinical signs of infiltration. There was no significant difference in baseline or final pressure measurements between patients whose catheter sites became infiltrated (n = 20) and patients whose catheter sites did not (n = 22). Likewise, changes in pressure from baseline did not differ between the infiltrated and noninfiltrated groups. At 12 hours before the final reading, pressures for the infiltrated group did not differ significantly from pressures for the noninfiltrated group, nor did these values differ from the respective baseline values. Over the final 12 hours of catheterization, mean slopes (changes in pressure over time) for the two groups did not differ significantly from 0 or from each other. Intrapatient specificity and sensitivity of the method and the false-alarm rate were clinically unacceptable. Monitoring of inline intravenous pressure is not useful for predicting or detecting infiltration of peripheral catheter sites in infants.

The epidemiology, pathogenesis, clinical features, and treatment of Rocky Mountain spotted fever are reviewed. Rocky Mountain spotted fever is a severe infection caused by Rickettsia rickettsii transmitted to man by various species of ticks. High-incidence areas exist in the southeast and south central United States. Only 60-70% of patients with the disease report a history of tick bite or exposure to tick-infested areas. The disease is initially characterized by fever, headache, gastrointestinal complaints, myalgia, and a generalized rash. In several days generalized vasculitis may lead to periorbital edema and nonpitting edema of the face and extremities. Central nervous system involvement is common. Because signs and symptoms associated with the disease are nonspecific, the diagnosis is often delayed or missed. Traditionally diagnostic confirmation relied on serologic testing, but an indirect fluorescent antibody assay will soon be commercially available. Rocky Mountain spotted fever is usually treated with the rickettsiostatic agents chloramphenicol or tetracycline, but few comparative data on these agents in patients with the disease are available. For patients who cannot tolerate oral medications, intravenous chloramphenicol sodium succinate is the preferred treatment; chloramphenicol is also the drug of choice for children less than eight years of age. Otherwise, oral tetracycline hydrochloride is the drug of choice. Antibiotic therapy should be continued for 7-10 days or until the patient is afebrile for two to five days. All cases of Rocky Mountain spotted fever must be reported to the Centers for Disease Control. The best ways to decrease the morbidity and mortality of the disease are to increase awareness of its signs and symptoms and to prevent exposure to ticks.

The metabolic alterations, nutritional and metabolic assessment, and nutritional requirements of critically ill patients are discussed, and parenteral nutrition support therapies are reviewed. Physiological alterations in the metabolism of the injured or septic patient are mediated through the interactions of neuroendocrine, cardiovascular, toxic, and starvation responses. These responses cause mobilization of nutritional substrates in an effort to maintain vital organ function and immune defenses. A patient's nutritional status can be determined from anthropometric measurements, creatinine excretion rate, and evaluations of protein stores and immune reserves and function; body weight is a poor indicator. Nitrogen-balance calculations are also useful for determining the adequacy of nutritional intake and the degree of metabolic stress. Early assessments of nutritional status may assist in identifying those patients for whom nutritional support interventions are needed. Nutritional requirements are altered by the metabolic responses to injury and sepsis. Studies suggest that use of nutrient solutions enriched for branched-chain amino acids may enhance nitrogen retention and that energy expenditures in injured or septic patients are only moderately elevated. Most nonprotein calories in parenteral nutrient solutions are provided as glucose, but lipids are an important source of energy in the critically ill patient who has high energy requirements or carbohydrate intolerance; however, clearance of lipids may be decreased. Fluid, electrolyte, and mineral status must be evaluated frequently. Critically ill patients have unique nutritional requirements, and parenteral nutrition support therapies for these patients are being investigated and refined.

Protein, calorie, fluid, fat, and micronutrient requirements of pediatric patients are reviewed, as are methods of nutritional assessment and complications associated with the use of parenteral nutrition in these patients. In general, preterm infants and neonates require greater per-kilogram amounts of protein, calories, fluid, and micronutrients than older children. In addition, preterm infants and neonates have deficiencies in enzymes that metabolize certain amino acids, making otherwise nonessential amino acids essential. These unique protein needs have been addressed in amino acid formulations designed specifically for this group of patients. Supplying the neonate with the calcium and phosphorus needed for bone growth can be difficult because of solubility limitations in parenteral nutrient solutions. The use of intravenous fat emulsion in infants with hyperbilirubinemia or pulmonary complications is controversial. However, only rarely does fat emulsion have to be completely withheld. Complications associated with parenteral nutrition in pediatric patients include infection, metabolic disorders (cholestasis, bone demineralization), and mechanical problems. Cholestasis induced by parenteral nutrition has been shown to be more common in low-birth-weight infants; however, the precise etiology is unknown and may be multifactorial. Basic requirements necessary to promote growth while pediatric patients are receiving parenteral nutrition have been determined. However, current studies are challenging what were thought to be standards of pediatric parenteral nutrition therapy.