Intra-parenchymally sited electrodes can be used to consistently identify depolarization events in humans. This technique greatly extends the capability of monitoring for spreading depolarization events in injured patients, as electrodes can be sited without the need for craniotomy. The method provides a new investigative tool for the evaluation of the contribution of these events to secondary brain injury in human patients.
Data collected on adult cystic fibrosis (CF) patients and entered onto the CF database in the south and west regions of England were analysed for the year 2001. FEV1 was taken as a marker of lung disease severity. Data on 371 patients (158 female) mean age 24.7 years (range 16.0-48.9) were assessed. FEV1 was reduced in CF patients infected with Pseudomonas aeruginosa (Pa) (mean 62.6% predicted) compared with those without (mean FEV1 77.8%, P < 0.00001). The reduction was noted irrespective of age group. FEV1 progressively reduced with the increasing need for high-intensity treatment (P < 0.00001) and with the diagnosis of diabetes mellitus (P = 0.03). FEV1 correlated with body mass index (BMI) (r = + 0.42, P < 0.0001). Genetic profile and poverty and deprivation score did not affect the value of FEV1. Chronic infection with Pa mainly in young adults, treatment intensity, diabetes mellitus and reduced body mass index are associated with reduced FEV1 in adult patients with cystic fibrosis in the south and west regions of England. In this relatively affluent area, scores of poverty and deprivation were not associated with the decline in lung function tests.
Although sedative use is near-ubiquitous in the acute management of moderate to severe traumatic brain injury (m-sTBI), the evidence base for these agents is undefined. This review summarizes the evidence for analgosedative agent use in the intensive care unit management of m-sTBI. Clinical studies of sedative and analgosedative agents currently utilized in adult m-sTBI management (propofol, ketamine, benzodiazepines, opioids, and alpha-2 agonists) were identified and assessed for relevance and methodological quality. The primary outcome was the effect of the analgosedative agent on intracranial pressure (ICP). Secondary outcomes included intracranial hemodynamic and metabolic parameters, systemic hemodynamic parameters, measures of therapeutic intensity, and clinical outcomes. Of 594 articles identified, 61 met methodological review criteria, and 40 were included in the qualitative summary; of these, 33 were prospective studies, 18 were randomized controlled trials, and 8 were blinded. There was consistent evidence for the efficacy of sedative agents in the management of m-sTBI and raised ICP, but the overall quality of the evidence was poor, consisting of small studies (median sample size, 23.5) of variable methodological quality. Propofol and midazolam achieve the goals of sedation without notable differences in efficacy or safety, although high-dose propofol may disrupt cerebral autoregulation. Dexmedetomidine and propofol/ dexmedetomidine combination may cause clinically significant hypotension. Dexmedetomidine was effective to achieve a target sedation score. De novo opioid boluses were associated with increased ICP and reduced cerebral perfusion pressure. Ketamine bolus and infusions were not associated with increased ICP and may reduce the incidence of cortical spreading depolarization events. In conclusion, there is a paucity of high-quality evidence to inform the optimal use of analgosedative agents in the management of m-sTBI, inferring significant scope for further research.
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