Rates of radiologically confirmed pneumonia as defined by the World Health Organization in Northern Territory Indigenous children.

OBJECTIVE: To determine the burden of hospitalised, radiologically confirmed pneumonia (World Health Organization protocol) in Northern Territory Indigenous children. DESIGN, SETTING AND PARTICIPANTS: Historical, observational study of all hospital admissions for any diagnosis of NT resident Indigenous children, aged between > or = 29 days and < 5 years, 1 April 1997 to 31 March 2005. INTERVENTION: All chest radiographs taken during these admissions, regardless of diagnosis, were assessed for pneumonia in accordance with the WHO protocol. MAIN OUTCOME MEASURE: The primary outcome was endpoint consolidation (dense fluffy consolidation [alveolar infiltrate] of a portion of a lobe or the entire lung) present on a chest radiograph within 3 days of hospitalisation. RESULTS: We analysed data on 24,115 hospitalised episodes of care for 9492 children and 13,683 chest radiographs. The average annual cumulative incidence of endpoint consolidation was 26.6 per 1000 population per year (95% CI, 25.3-27.9); 57.5 per 1000 per year in infants aged 1-11 months, 38.3 per 1000 per year in those aged 12-23 months, and 13.3 per 1000 per year in those aged 24-59 months. In all age groups, rates of endpoint consolidation in children in the arid southern region of NT were about twice that of children in the tropical northern region. CONCLUSION: The rates of severe pneumonia in hospitalised NT Indigenous children are among the highest reported in the world. Reducing this unacceptable burden of disease should be a national health priority.

Economic evaluation of a clinical protocol for diagnosing emergency patients with suspected pulmonary embolism.

BACKGROUND: The objective of this paper is to estimate the amount of cost-savings to the Australian health care system from implementing an evidence-based clinical protocol for diagnosing emergency patients with suspected pulmonary embolism (PE) at the Emergency department of a Victorian public hospital with 50,000 presentations in 2001-2002. METHODS: A cost-minimisation study used the data collected in a controlled clinical trial of a clinical protocol for diagnosing patients with suspected PE. The number and type of diagnostic tests in a historic cohort of 185 randomly selected patients, who presented to the emergency department with suspected PE during an eight month period prior to the clinical trial (January 2002-August 2002) were compared with the number and type of diagnostic tests in 745 patients, who presented to the emergency department with suspected PE from November 2002 to August 2003. Current Medicare fees per test were used as unit costs to calculate the mean aggregated cost of diagnostic investigation per patient in both study groups. A t-test was used to estimate the statistical significance of the difference in the cost of resources used for diagnosing PE in the control and in the intervention group. RESULTS: The trial demonstrated that diagnosing PE using an evidence-based clinical protocol was as effective as the existing clinical practice. The clinical protocol offers the advantage of reducing the use of diagnostic imaging, resulting in an average cost savings of at least $59.30 per patient. CONCLUSION: Extrapolating the observed cost-savings of $59.30 per patient to the whole of Australia could potentially result in annual savings between $3.1 million to $3.7 million.

Reducing the use of diagnostic imaging in patients with suspected pulmonary embolism: validation of a risk assessment strategy.

OBJECTIVES: The aims of this study were to measure the: (i) effects of implementation of a new risk assessment strategy for patients with suspected pulmonary embolism (PE) on the use of imaging and D-dimer assay; (ii) negative predictive value for PE of a combination of low risk and negative D-dimer assay; and (iii) compliance of ED clinicians with the strategy. METHODS: A non-randomized clinical trial was conducted in the ED of a 720-bed teaching hospital between November 2002 and August 2003. Study subjects with suspected PE were compared with 191 randomly selected historical controls. The risk assessment strategy of Kline et al. was disseminated and implemented. RESULTS: The negative predictive value for PE was 99% (95% confidence interval [CI] = 97-100%) in 114 patients with low risk and negative D-dimer. There was a 21% absolute reduction in the rate of imaging following the implementation of the risk assessment strategy (56% vs 77%, P < 0.001). CONCLUSION: Low risk combined with a negative D-dimer result may allow exclusion of PE without imaging.

Persistent renal cortical scintigram defects in children 2 years after urinary tract infection.

BACKGROUND: Renal cortical scintigraphic studies challenge the role of vesicoureteric reflux in renal scar development, emphasizing instead the part played by acute pyelonephritis. OBJECTIVE: To determine the prevalence of renal cortical defects in a child cohort 2 years after the child's first diagnosed urinary tract infection and to analyze the relationship of these defects with acute illness variables, primary vesicoureteric reflux and recurrent infections. MATERIALS AND METHODS: In a prospective cohort study, 193 children younger than 5 years with their first proven urinary tract infection underwent renal sonography, voiding cystourethrogram, and renal cortical scintigraphy within 15 days of diagnosis. Two years later, 150 of the 193 children, or 77.7%, had a further renal cortical scintigram, including 75, or 86.2%, of the 87 children who had acute scintigraphic defects. The relationship of cortical defects to age, gender, pre-treatment symptom duration, hospitalization, presence and grade of vesicoureteric reflux, and recurrent urinary tract infections was evaluated. RESULTS: Overall, 20 of the 150 (13.3%; 95% confidence interval (CI) 8.3, 19.8) children had persistent defects 2 years after infection. This included 20 of 75 (26.7%; 95% CI 17.1, 38.1) with initially abnormal scintigrams. No new defects were detected. Although acute defects were more common in the young, those with persistent defects were older (median ages 16.4 vs. 6.8 months, P=0.004) than those with transient abnormalities. After adjustment for age, persistent defects were no longer associated with gender and were not predicted by acute illness variables, primary vesicoureteric reflux or recurrent infections. CONCLUSIONS: Renal cortical scintigraphic defects persisted in approximately one-quarter of young children after their first proven urinary tract infection. The associated clinical features, however, failed to predict scar formation. It is possible that some of the scintigraphic defects preceded the infection by arising from either previously undiagnosed acute pyelonephritis or from underlying congenital dysplasia. The etiology of scars may be best addressed by determining whether prevention of urinary tract infections from birth avoids post-natal scar acquisition or extension.

Time course of transient cortical scintigraphic defects associated with acute pyelonephritis.

BACKGROUND: Acute pyelonephritis is distinguished from renal scarring using repeat cortical scintigraphy. The defects of acute pyelonephritis resolve, while those of scars persist. OBJECTIVE: To determine the duration of reversible cortical defects following acute pyelonephritis and the time interval required to differentiate infection from scars. MATERIALS AND METHODS: An observational prospective study of 193 children (386 kidneys) aged less than 5 years following their first proven urinary tract infection (UTI). Renal cortical scintigraphic defects were detected in 112 (29%) kidneys within 15 days of diagnosis. Of these, 95 underwent repeat renal cortical scans 2 years after the UTI, including 50 with additional scans performed within 2-6 months of infection. RESULTS: Of the 50 kidneys undergoing a second renal cortical scan within 2-6 months of the first UTI, 22 (44%) had persistent defects. A third scan was performed on 17 (77%) kidneys after 2 years, by which time defects had resolved in another 8 (47%) kidneys. The predictive value of defects detected within 2-6 months of UTI representing scars is 53% (95% CI 28, 77). Overall, nine (18%) kidneys with initial renal cortical abnormalities had permanent defects. In the 45 kidneys undergoing a second cortical scan more than 6 months after the UTI, 11 (24%) had persistent defects. None of the 95 kidneys undergoing serial scans developed new or larger defects. CONCLUSIONS: Renal scars may not be reliably diagnosed by cortical scintigraphy performed within 6 months of UTI because the inflammatory lesions may not have fully resolved.