Acute necrotizing gastritis.

A 17-year-old man presented with signs of peritonitis. Laparotomy revealed gangrene of the stomach without obvious cause. The patient underwent total gastrectomy with esophago-jejunal anastomosis with formation of jejunal pouch. Bacterial culture of the peritoneal fluid grew Strept. pyogenes and E. coli. The patient was discharged on day 21 after a stormy postoperative course.     

Comparison of asthma treatment given in addition to inhaled corticosteroids on airway inflammation and responsiveness.

There is increasing evidence that the assessment of eosinophilic airway inflammation using induced sputum and measurement of airway hyperresponsiveness provides additional, clinically important information concerning asthma control. The aim of this study was to directly compare the effects of different treatments on these markers in patients with asthma and persistent symptoms, despite the use of low-dose inhaled corticosteroids. A double-blind four-way crossover study was performed, which compared a 1-month treatment with budesonide 400 mug b.i.d., additional formoterol, additional montelukast and placebo in 49 patients with uncontrolled asthma despite budesonide 100 mug b.i.d., with each treatment separated by a 4-week washout period. The change in sputum eosinophil count with formoterol (2.4 to 3.8% change, 0.6-fold reduction, 95% confidence interval (CI) 0.5-0.9) differed significantly from placebo (2.8 to 2.5% change, 1.1-fold reduction, 95% CI 0.7-1.6) and high-dose budesonide (2.7 to 1.6% change, 1.6-fold reduction, 95% CI 1.2-2.2). The effects of montelukast did not differ from placebo. The changes in methacholine airway responsiveness were small and did not differ between treatments. High-dose budesonide had the broadest range of beneficial effects on other outcomes, including symptom scores, morning peak expiratory flow and forced expiratory volume in one second. In conclusion, treatment given in addition to low-dose inhaled corticosteroids results in modest benefits. Formoterol and high-dose budesonide have contrasting effects on eosinophilic airway inflammation.     

Melioidosis: an important cause of pneumonia in residents of and travellers returned from endemic regions.

Melioidosis is endemic in South East Asia, Asia and northern Australia. Infection usually follows percutaneous inoculation or inhalation of the causative bacterium, Burkholderia pseudomallei, which is present in soil and surface water in the endemic region. While 20-36% of melioidosis cases have no evident predisposing risk factor, the vast majority of fatal cases have an identified risk factor, the most important of which are diabetes, alcoholism and chronic renal disease. Half of all cases present with pneumonia, but there is great clinical diversity, from localised skin ulcers or abscesses without systemic illness to fulminant septic shock with multiple abscesses in the lungs, liver, spleen and kidneys. At least 10% of cases present with a chronic respiratory illness (sick > 2 months) mimicking tuberculosis and often with upper lobe infiltrates and/or cavities on chest radiography. As with tuberculosis, latency with reactivation decades after infection can also occur, although this is rare. Confirmation of diagnosis is by culture of B. pseudomallei from blood, sputum, throat swab or other samples. Microbiology laboratories need to be informed of the possibility of melioidosis, as those not familiar with it can misidentify the organism. Antibiotic therapy is initial intensive therapy with i.v. ceftazidime or meropenem or imipenem +/- cotrimoxazole for > or = 10 days, followed by eradication therapy with cotrimoxazole +/- doxycycline +/- chloramphenicol (first 4 weeks only) for > or = 3 months. Melioidosis has been increasingly recognised in returning travellers in Europe and recently melioidosis and colonisation with B. pseudomallei have been documented in cystic fibrosis patients visiting or resident in endemic areas.     

Making clinical decisions for dental care: concepts to consider

Clinical decisions are often made with incomplete information, yet patient care decisions are made every day. Patients vary clinically, uncertainty exists in diagnostic and prognostic information, and many preventive and treatment alternatives have not been formally assessed for their effectiveness. Because scientific information will never answer all clinical questions, clinical decisions are partially based on probabilistic information.
This paper describes how to apply clinical decision making to diagnosing and managing dental caries and periodontal diseases. By using explicit information to quantify probabilities and outcomes, clinical decision making analyzes decisions made under uncertain conditions and the uncertain impact of clinical information.
Clinical decision making incorporates concepts for preventing, diagnosing and treating dental caries and periodontal diseases: risk assessment, evidence-based dentistry, and multiple oral health outcomes. This information can serve as a tool for clinicians to augment clinical judgment and expertise.