The Role of Biofilm in Central Venous Catheter Related Bloodstream Infections: Evidence-based Nursing and Review of the Literature.

BACKGROUND: Biofilm is a fundamental component in the pathogenesis of infections related to the use of the central venous catheter (CVC,) which can represent an important health issue in everyday practice of nursing and medical staff. OBJECTIVE: The objective of the following review is to analyze the components of biofilm and their role in catheter-related infection determinism in an evidencebased nursing perspective in such a way as to give health professionals useful suggestions in the prevention and management of these complications. METHODS: The following databases were consulted for the bibliographic search: Medline, Scopus, Science Direct. Biofilm can be the cause of CVC extraction and can lead to serious haematogenic infectious complications that can increase the morbidity and mortality of affected patients. RESULTS: Updated pathophysiologic knowledge of biofilm formation and appropriate diagnostic methodology are pivotal in understanding and detecting CVC-related infections. Lock therapy appears to be a useful, preventive, and therapeutic aid in the management of CVCrelated infections. New therapies attempting to stop bacterial adhesion on the materials used could represent new frontiers for the prevention of CVC-related infections. CONCLUSION: The correct evidence-based nursing methods, based on the use of guidelines, provides the opportunity to minimize the risks of infection through the implementation of a series of preventive measures both during the CVC positioning phase and in the subsequent phase, for example, during device management which is performed by medical and nursing staff.

Effects of acetaminophen and ibuprofen in children with migraine receiving preventive treatment with magnesium.

AIM: The purpose of this study was to evaluate both the effects of ibuprofen and/or acetaminophen for the acute treatment of primary migraine in children in or out prophylactic treatment with magnesium. METHODS: Children ranging from the ages of 5 to 16 years with at least 4 attack/month of primary migraine were eligible for participation the study. A visual analog scale was used to evaluate pain intensity at the moment of admission to the study (start of the study) and every month up to 18 months later (end of the study). RESULTS: One hundred sixty children of both sexes aged 5-16 years were enrolled and assigned in 4 groups to receive a treatment with acetaminophen or ibuprofen without or with magnesium. Migraine pain endurance and monthly frequency were similar in the 4 groups. Both acetaminophen and ibuprofen induced a significant decrease in pain intensity (P < .01), without a time-dependent correlation, but did not modify its frequency. Magnesium pretreatment induced a significant decrease in pain intensity (P < .01) without a time-dependent correlation in both acetaminophen- and ibuprofen-treated children and also significantly reduced (P < .01) the pain relief timing during acetaminophen but not during ibuprofen treatment (P < .01). In both acetaminophen and ibuprofen groups, magnesium pretreatment significantly reduced the pain frequency (P < .01). CONCLUSIONS: Magnesium increased the efficacy of ibuprofen and acetaminophen with not age-related effects.

Effects of carbamazepine/oxycodone coadministration in the treatment of trigeminal neuralgia.

OBJECTIVE: To report on a patient with trigeminal neuralgia who responded positively to combined carbamazepine/oxycodone treatment. CASE SUMMARY: A 48-year-old woman with a 4-month history of left facial pain consisting of episodes lasting less than 5 minutes was brought to our institution for clinical evaluation. Clinical, laboratory, and neuroradiologic findings led to a diagnosis of idiopathic trigeminal neuralgia. Carbamazepine treatment was started at 200 mg every 12 hours and increased at discharge to 300 mg every 8 hours. Two weeks later the patient was readmitted with trigeminal neuralgia symptoms that had persisted since the previous admission, although they had decreased in intensity. Carbamazepine was reduced to 200 mg every 8 hours and oxycodone 5 mg every 12 hours was added to the treatment regimen, with a complete resolution of pain within 7 days. DISCUSSION: Pathophysiological mechanisms involved in both the genesis and the maintenance of trigeminal neuralgia have not yet been defined. Several hypotheses could explain this disorder, ranging from peripheral neural ectopic pacemaker to central disinhibition. Both the interruption of the sodium channel and the modulation of both κ- and µ-opioid receptors contributed to antinociceptive effects in trigeminal neuralgia. CONCLUSIONS: Treatment with a combination of carbamazepine, a sodium channel blocker, and oxycodone, a mixed κ- and µ-opioid receptor agonist, may be useful in alleviating symptoms of trigeminal neuralgia.