A case is described of overwhelming pneumonia in a patient with a history of coughing since three months. Because of hypoxia and hypercapnia that could not be managed by optimal mechanical ventilation, the patient required urgent extracorporeal lung assistance (ECLA, also known as ECMO). Afterwards the diagnosis of full blown AIDS was made. Appropriate antiviral, antibiotic and antimycotic therapy was successfully established. The patient was weaned from ECLA 4 days later, and discharged from hospital after two months.
Malignant pleural effusion (MPE) is a common and challenging problem. Patients affected by MPE have a poor prognosis and suffer from breathlessness and impaired quality of life. The management of MPE has barely changed for many decades; however, recent research has driven new paradigms in the diagnosis and treatment of MPE and stimulated novel concepts that are being evaluated in many ongoing studies. This review provides an overview of recent advances in the diagnosis of MPE, including new cytopathology and imaging techniques, and the landmark studies that provide a solid evidence base to support the use of indwelling pleural catheters as first-line treatment in MPE. Lingering management dilemmas, including optimal chest drainage tube and role of surgery in MPE, and key knowledge gaps that are the focus of ongoing research are also highlighted.
The objective of the study was to examine associations between family history of premature cardiovascular disease (CVD), knowledge of CVD risk and protective factors, and health behaviours. The design was via administration of a questionnaire to 307 participants from four general practice centre waiting rooms in the Sydney West area. The most recognised CVD risk factor was smoking (97.7%) and the most recognised CVD protective factor was omega-3 fatty acids (78.5%). After adjustment for age, sex, education attainment and personal history of CVD, a strong family history of premature CVD was associated with being more likely to interpret a blood pressure of 130/85 as a CVD risk factor (OR 2.77, 95% CI 1.07-7.14), but less likely to identify being an ex-smoker (compared with never having smoked before) as a risk factor (OR 0.32, 95% CI 0.12-0.90). Those with a strong family history of premature CVD, on average, had smoked 0.82 pack years more than those with an average family history of premature CVD (s.e. 4.22, P=0.04). In conclusion, there continues to be both strengths and deficits in the community's overall knowledge of CVD risk and protective factors, and a strong family history of premature CVD appears to be an independent risk factor for smoking.
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