Current Respiratory Medicine Reviews - Volume 7, Issue 4, 2011

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Severity assessment tools in patients with community-acquired pneumonia can serve multiple purposes. These include the identification of low risk patients who may be suitable for management at home, higher risk patients who should be managed in hospital and patients with more severe illness who may require admission to the intensive care unit (ICU). The best known are the PSI and CURB-65, which are based on patients' risk of dying within 30 days. While such tools are reasonably accurate at stratifying mortality risks, they are much less accurate in predicting which patients will be admitted to the ICU. This reflects the fact that there is often little overlap between the patients who die and those admitted to ICU. This begs the question of how useful it is to identify the higher mortality patients if they usually die because active medical treatment is withdrawn. Thus there is increasing interest in tools that predict which patients are more likely to need management in ICU. Examples include SMART-COP, REA-ICU, SCAP and the minor criteria of the IDSA/ATS rule. While all are at least moderately accurate for this purpose, limitations of previous studies, such as not recording ‘do not resuscitate’ status makes valid comparisons difficult.

The management of community-acquired pneumonia remains mainly driven by empiric antibiotic therapy because existing microbiological techniques are relatively insensitive and rarely deliver an answer within a useful time frame. Advances in the molecular detection of Streptococcus pneumoniae in whole blood have been published that suggest that a new era of diagnostics may be ready for routine clinical practice. As well as improved sensitivity over existing culture techniques and a very high specificity, the new assays quantitate the amount of bacteremia which appears to be an extremely useful prognostic marker. Here we review the recent studies and their implications in the setting of pneumococcoal pneumonia.

Community-acquired pneumonia (CAP) is not a homogeneous entity. S. pneumoniae is the most prevalent pathogen associated with severe CAP and is responsible for two-thirds of CAP-related deaths. Today, there is a need for effective strategies to develop and establish the optimum dosage regimen of new antimicrobial options. Morbidity and mortality in cases with severe CAP are determined by a complex interaction between host factors, features of the microorganism and the therapy administered. The major challenge that CAP presents is the early recognition of subsets requiring Intensive Care Unit (ICU) admission. Despite recent advances in antibiotic therapy, severe CAP remains associated with unacceptable levels of mortality. The present manuscript summarizes the current key points that should be taken into account in the strategies for severe CAP management.

Infection by Streptococcus pneumoniae (the pneumococcus) is associated with enormous morbidity and mortality worldwide and this bacterium remains the commonest cause of pneumonia, meningitis and otitis media. While immunity to pneumococcal disease has been widely accepted to depend mainly on the humoral arm of the immune system recent studies have shown a critical role for cellular immunity, specifically T lymphocytes (T cells), that is independent of antibody, in the prevention and clearance of pneumococcal infection. Here we review the evidence that supports the importance of T cells, specifically CD4+, CD8+ and regulatory T cells, in host responses to pneumococcal infection.

Community-acquired pneumonia (CAP) is a serious health problem worldwide with an annual incidence of 0.3%-0.5% in the adult population. Moreover, CAP continues to be the leading cause of death from infectious diseases. This justifies the interest in studying all clinical aspects relating to CAP. A new approach is to evaluate biological markers of infection and inflammation as an expression of the host's inflammatory response against the microorganism, in order to obtain diagnosis, aetiology, prognosis and treatment information. The most frequently studied biomarkers are C-reactive protein (CRP), procalcitonin (PCT) and cytokines; other biomarkers are currently obtaining promising results. Although not uniformly, most authors conclude that biomarkers can help in the diagnosis of CAP, few studies analyse the capacity of biomarkers to identify the potential causative agent and the best results have been established children. Linked with this, biomarkers (mainly PCT) have been successfully used to guide prescription of antibiotics in patients with suspected CAP. Treatment guided by serum PCT was a safe way to avoid antibiotics, although economic savings were overshadowed by PCT analysis costs. Approximately 10%-15% of patients hospitalized for CAP develop treatment failure and almost 6% may manifest rapidly progressive pneumonia; serum levels of biomarkers have been shown to identify patients at risk of treatment failure and may therefore guide treatment management. Clinical data scoring systems have been recognized as useful tools to assess the stability and outcome of patients with CAP. Analysis of systemic biomarkers in addition to clinical scores has been shown to improve both prediction of the absence of severe complications and 30- day mortality as predicted by the PSI or CURB65/CRB65 scales. Data from the literature appears to support the use of biomarkers in routine clinical practice when CAP is suspected.

Purpose of Review: Staphylococcus aureus and particularly MRSA has become an increasingly important etiology of pneumonia at the community settings. Associated with highest morbidity, mortality and costs in public health, it represents a major challenge for the management of this group of patients. Recent Findings: MRSA estimated incidence for community acquired pneumonia has risen in the past decades, and it's characterized for been particularly virulent and difficult to treat. There are some clinical and radiological features that suggest CA-MRSA pneumonia, like young age, previous flulike illness, acute impaired general status, and bilateral consolidation with tendency to cavitations. Although vancomycin at standard doses remains as the mainstay for its treatment, the increasing rate of treatment failure have prompted other strategies of use (more frequent administration, continuous infusion, combination therapy), and the use of newer antimicrobials, particularly linezolid, with pharmacokinetic and pharmacodinamics profiles that produced promisingly improving clinical results. Summary: Clinicians should be aware of CA-MRSA as a potential pathogen in any patient presenting with severe community-acquired pneumonia; if a risk assessment suggests the possibility of MRSA, initial empiric therapy directed against MRSA appears reasonable until this infection can be excluded microbiologically.

A delay in time between arrival to the hospital or emergency department and the time to first antibiotic dose (TFAD) in patients with community-acquired pneumonia has been found to correlate with an increased risk of mortality. This finding, in combination with increasing realization during the 1990s that there was an unnecessary delay in antibiotic treatment for many patients led regulatory bodies and payers in the United States to use TFAD as a measure for public reporting and/or pay for performance programs. The use of this measure has generated a great deal of controversy due to the lack of prospective, randomized data demonstrating improved outcomes in patients who receive earlier antibiotics. There is also evidence suggesting that efforts to deliver antibiotics earlier have resulted in increased numbers of patients getting unnecessary antibiotics, as many patients present in an atypical manner making it difficult to rapidly confirm a diagnosis of pneumonia. Nonetheless, intuitive, biologic and observational data support the importance of rapid delivery of antibiotics to patients with pneumonia. In the United States, 93% of patients presenting to the hospital with pneumonia now receive antibiotics within 6 hours. This suggests that there is limited opportunity for further improvement and that this measure may have outlived its usefulness.

Pulmonary arterial hypertension (PAH) is a progressive, debilitating, and potentially fatal disease. Symptoms of PAH are non-specific and may include dyspnea, fatigue, chest discomfort, pre-syncope/syncope, palpitations, lower extremity swelling, non-specific gastro-intestinal symptoms, weight loss, and cyanosis. Pulmonologists are increasingly involved in the care of these patients, whether at the initial presentation and diagnosis, medication titration, or for symptom relief and management of complications. The pulmonologist and intensivist also frequently care for patients that are at an increased risk of developing PAH, such as patients with cirrhosis, hypoxic lung disease, scleroderma, sickle cell disease, and HIV to name a few. An echocardiogram, although often inaccurate in estimating the right-sided heart pressures, is the best screening tool for PAH. A right heart catheterization is the gold standard for diagnosing PAH. Supplemental therapies may include oxygen, diuretics, and anticoagulation. In addition to the limited role of calciumchannel blockers, PAH-specific therapies fall into one of 3 families for now: Phospho-diesterase-5 inhibitors, endothelin receptor antagonists, and prostacyclins. The current estimated 2 year survival of PAH patients now exceeds 90%, compared to a historical median survival of 2-3 years.

Asthma is a respiratory syndrome occurring in individuals who have genetic susceptibility to develop exaggerated airway narrowing to environmental triggers. The symptoms are generally paroxysmal and typically reversible by the use of drugs relaxing airway smooth muscle (ASM). Despite considerable heterogeneity with respect to etiology, age of onset and severity, all affected individuals display some degree of airway hyperresponsiveness (AHR) upon inhalational challenge with spasmogens. ASM is undoubtedly the motor driving airway responsiveness, but whether defects in its contractile properties underlie AHR is still a matter of debate. Many non-muscle changes in asthmatic airways could contribute to AHR. However, this review focuses on the potential contributions of ASM to AHR. Several of the contractile properties of ASM are discussed, including its force-generating capacity, ability to shorten, degree of stiffness, velocity of shortening and ability to relax. The rationale for any of these individual contractile properties being involved in AHR is first explained followed by a brief summary of the current literature concerning their potential contribution to AHR in asthma.