Paediatric drugs
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Nosocomial pneumonia is a common hospital-acquired infection in children, and is often fatal. Risk factors for nosocomial pneumonia include admission to an intensive care unit, intubation, burns, surgery, and underlying chronic illness. Viruses, predominantly respiratory syncytial virus (RSV), are the most common cause of pediatric nosocomial respiratory tract infections. ⋯ Therapy should be modified when a specific pathogen and its antimicrobial susceptibility are identified. Effective prevention of nosocomial pneumonia requires infection control measures that affect the environment, personnel, and patients. Of these, hand hygiene, appropriate infection control policies, and judicious use of antibacterials are essential.
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Review
Should beta-blockers be used for the treatment of pediatric patients with chronic heart failure?
In multiple clinical trials, beta-blockers have been shown to significantly improve morbidity and mortality in adults with chronic congestive heart failure, but there is little reported experience with their use in children. Heart failure involves activation of the adrenergic nervous system and other neurohumoral systems in order to maintain cardiovascular homeostasis. These compensatory mechanisms have been shown to cause myocardial damage with chronic activation, which has been hypothesized to be a major contributing factor to the clinical deterioration of adults with heart failure. ⋯ Adverse effects were common and many patients in these studies had adverse outcomes (death and/or need for transplantation). One study has noted differences in pharmacokinetics in children compared with adults. However, a multicenter, randomized controlled trial to evaluate carvedilol in pediatric heart failure from systolic ventricular dysfunction is currently ongoing and should help to clarify the efficacy and tolerability of carvedilol in children.
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The newest treatment strategies for pediatric myocarditis have evolved from an understanding of the pathophysiology of myocyte damage. Although the initial stages of viral myocarditis apparently result from the direct cytopathic effects on the atrial and ventricular myocardium, later stages of progressive decompensation result from immune-mediated myocyte destruction common to many forms of myocarditis. Despite advances in the understanding of the role of genetics, immunologic mechanisms, and infectious causes of myocarditis, supportive therapy continues to remain the cornerstone of treatment. ⋯ Clinical studies have yet to provide convincing evidence that the use of immunosuppressants and gamma-globulin favorably alters the outcome for pediatric patients with acute myocarditis. Ventricular assist devices and heart transplantation remain as treatment options for all pediatric patients with severe myocarditis resistant to all other therapies. Although this review will focus on viral myocarditis, the supportive strategies and surgical treatment options apply to most forms of cardiomyopathy.
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Regional anesthesia has become a routine part of the practice of anesthesiology in infants and children. Local anesthetic toxicity is extremely rare in infants and children; however, seizures, dysrhythmias, cardiovascular collapse, and transient neuropathic symptoms have been reported. Infants and children may be at increased risk from local anesthetics compared with adults. ⋯ Two new enantiomerically pure local anesthetics, ropivacaine and levobupivacaine, offer clinical profiles comparable to that of bupivacaine but without its lower toxic threshold. The extreme rarity of major toxicity from local anesthetics suggests that widespread replacement of bupivacaine with ropivacaine or levobupivacaine is probably not necessary. However, there are clinical situations, including prolonged local anesthetic infusions, use in neonates, impaired hepatic metabolic function, and anesthetic techniques requiring a large mass of local anesthetic, where replacement of bupivacaine with ropivacaine, levobupivacaine or (for continuous techniques) chloroprocaine appears prudent.
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In diabetes insipidus, the amount of water ingested and the quantity and concentration of urine produced needs to be carefully regulated if fluid volume and osmolality are to be maintained within the normal range. One of the principal mechanisms controlling urine output is vasopressin which is released from the posterior pituitary gland and enhances water reabsorption from the renal collecting duct. In diabetes insipidus, the excessive production of dilute urine, and the causes of this clinical picture can be divided into three main groups: the first is primary polydipsia where the amount of fluid ingested is inappropriately large; the second group is cranial diabetes insipidus where the production of vasopressin is abnormally low; and, the third group is nephrogenic diabetes insipidus where the kidney response to vasopressin is impaired. ⋯ The treatment of these patients is difficult and typically involves therapy with a diuretic such as chlorothiazide, as well as indomethacin. These agents enhance urine osmolality by their effect on circulating volume and renal solute and water handling. The fluid intake of most young children with primary polydipsia can be safely reduced to a more appropriate level.