The current revolution in communications technology provides an opportunity for novel approaches to management of medical illness. As economic imperatives lead to a progressive reduction in the time that health-care providers spend with their patients, computerized, telephone-linked communication systems offer an inexpensive, widely available alternative with which patients and providers can maintain contact. Such systems may be particularly useful for providing ongoing monitoring and education of patients with chronic illnesses such as COPD. In this article, we describe the general application of telephone-linked communication systems in the health-care setting. We then present in detail one such system, which provides telephone-linked care for COPD (TLC-COPD). The operation of the system is described, as are its theoretical underpinnings in social learning theory. A randomized clinical trial currently is being performed to study the effects of the TLC-COPD system. The rationale for expected improvements in disease control and quality of life, and for a reduction in acute health-care utilization, is discussed.

Asthma is a chronic inflammatory disease of the airways. Anti-inflammatory drug therapy, primarily using corticosteroids, is now considered the first-line treatment in the management of all grades of asthma severity. Although corticosteroids are believed to be the most potent anti-inflammatory agents available, they do not suppress all inflammatory mediators involved in the asthmatic response. Leukotrienes, which are lipid mediators generated from the metabolism of arachidonic acid, play an important role in the pathogenesis of asthma. They produce bronchospasm, increase bronchial hyperresponsiveness, mucus production, and mucosal edema, and enhance airway smooth muscle cell proliferation and eosinophil recruitment into the airways, and their synthesis or release is unaffected by corticosteroid administration. The use of leukotriene synthesis inhibitors or leukotriene receptor antagonists as anti-inflammatory therapies in asthma has therefore been investigated. Beneficial effects of leukotriene-modifying drugs have been demonstrated in the management of all grades of asthma severity, and there is evidence that certain patient groups (such as those with exercise-induced asthma or aspirin-induced asthma) may be particularly suitable for such therapy.

Mechanical ventilation (MV) can be lifesaving by maintaining gas exchange until the underlying disorders are corrected, but it is associated with numerous organ-system complications, which can significantly affect the outcome of critically ill patients. Like other organ systems, GI complications may be directly attributable to MV, but most are a reflection of the severity of the underlying disease that required intensive care. The interactions of the underlying critical illness and MV with the GI tract are complex and can manifest in a variety of clinical pictures. Incorporated in this review are discussions of the most prevalent GI complications associated with MV, and current diagnosis and management of these problems.

Clinical trials have established the superiority of the implantable cardioverter-defibrillator (ICD) over antiarrhythmic drug therapy in survivors of sudden cardiac death and in high-risk patients with coronary artery disease. The ICD has evolved to overcome the limitation of earlier devices that required thoracotomy for implantation and were fraught with inappropriate shock delivery. Current ICDs are implanted in a similar manner to cardiac pacemakers and incorporate sophisticated rhythm-discrimination algorithms to prevent inappropriate therapy. Managing the patient with an ICD requires an understanding of the multiprogrammable features of modern devices. Drug interactions and potential sources of electromagnetic interference may adversely affect ICD function. Driving restrictions may be necessary under certain conditions. The cost-effectiveness of ICD therapy appears favorable, given the marked survival benefit seen in randomized trials relative to antiarrhythmic drug treatment. The growing number of ICD recipients necessitates an understanding of the specialized features of the modern ICD and the role of device therapy in clinical practice.

To critically review the available data on the diagnostic evaluation, risk stratification, and therapeutic management of patients with acute exacerbations of COPD.

We report a patient with diffuse malignant pleural mesothelioma showing marked elevation of neutrophils. The level of serum granulocyte-colony stimulating factor (G-CSF) was elevated (138 pg/mL; normal range, < 20 pg/mL). The patient died 6 weeks after disease progression had been noted, and immunohistochemistry using a specific monoclonal antibody against recombinant G-CSF at autopsy demonstrated that the malignant mesothelioma cells actually produced G-CSF. Only three cases of malignant pleural mesothelioma, including the current patient, have been reported to produce G-CSF. We demonstrated an elevated serum level of G-CSF and G-CSF-bearing tumor cells by immunochemistry.

We describe a case of long-term administration of nitric oxide (NO) in a 32-year-old man who was admitted with exertional dyspnea and anasarca. A diagnosis of primary pulmonary hypertension was made. An acute vasodilator trial with inhaled NO showed a 5% reduction of the mean pulmonary artery pressure. Long-term NO inhalation therapy was initiated. Twenty days later, the dyspnea improved, the anasarca resolved, and the PaO(2) level increased. After 12 months of NO therapy, the patient remained stable and no signs of toxicity or tachyphylaxis were observed. To our knowledge, this is the first report of 1 year of continuously inhaled NO in an adult patient with primary pulmonary hypertension. These findings suggest that prolonged NO therapy might be an effective alternative, at a lower cost, to the continuous IV infusion of epoprostenol.

We describe a rare case of a 29-year-old woman with chronic eosinophilic pneumonia (CEP) presenting with massive bilateral pleural effusion leading to respiratory failure, a complication that was not reported before with CEP. The patient was successfully managed with ventilatory support and steroid therapy. On long-term follow-up, she remained well, receiving a low maintenance dose of prednisone without evidence of relapse of the disease.

We present the case of a 32-year-old woman with high-grade right pulmonary artery stenosis secondary to fibrous mediastinitis. The patient was managed with balloon angioplasty and stent placement. Only 15 cases of this nature have been reported in the literature, and this is one of the first to be managed with endovascular stent placement.

The antimicrobial resistance problem in hospitals continues to worsen. In particular, extended-spectrum beta-lactamase-producing Klebsiella pneumoniae (ESBL-KP) and vancomycin-resistant enterococci (VRE) are significant causes of morbidity and mortality among critically ill patients. Treating infections caused by these pathogens presents therapeutic dilemmas. The association between broad-spectrum beta-lactam overutilization and selection for ESBL-KP has been appreciated for some time; several institutions have reported a decrease in the prevalence of ESBL-KP with a shift in antibiotic utilization from third-generation cephalosporins to other broad-spectrum drugs. Currently, optimal treatment of ESBL-KP includes the carbapenems, but widespread use of these drugs is expensive and may be associated with further selection of antibiotic resistance and/or superinfection with other inherently resistant pathogens. VRE are especially difficult organisms to treat because of their inherent and acquired resistance to most currently available antibiotics. The prevalence of VRE has also been documented to decrease upon a shift in antibiotic use from third-generation cephalosporins to broad-spectrum antibiotics of other classes. Thus, antibiotic utilization measures appear to contribute to the control of the emergence of multidrug-resistant pathogens such as ESBL-KP and VRE.

Effective host defense against bacterial infection is dependent on the activation and recruitment of phagocytic cells. The initiation, maintenance, and resolution of this inflammatory response in the setting of bacterial pneumonia is dependent on the expression of cytokines. As the complexities of the host-pathogen interaction are further dissected and unraveled, immunologic manipulation of cytokine expression will likely become an important adjuvant therapy in the treatment of serious lung infections.

Hospital-acquired pneumonia (HAP) is associated with high morbidity and mortality. Early, appropriate, and adequate empiric therapy can increase the chance of survival. In 1995, the American Thoracic Society provided guidelines for the initial treatment of immunocompetent HAP patients, which is one of the principal HAP management approaches available to physicians today. However, these guidelines have several important limitations, including a lack of recommendations for duration of therapy and no recognition of newer drugs such as cefepime, trovafloxacin, and meropenem. Furthermore, they fail to distinguish among similar compounds (ie, beta-lactam/beta-lactamase inhibitor combinations) or to recommend specific antibiotics. The clinician using these guidelines needs to address local patterns of antimicrobial resistance, especially in ICUs. Effective computerized antibiotic management programs that incorporate information on local patterns of antimicrobial resistance can assist physicians in empiric therapy decision making, improve patient quality of care, and reduce medical costs.

Multiple surveillance studies have demonstrated that resistance among prevalent pathogens is increasing at an alarming rate, leading to greater patient morbidity and mortality from nosocomial infections. Among Gram-positive organisms, the most important resistant pathogens are methicillin- (oxacillin-)resistant Staphylococcus aureus, beta-lactam-resistant and multidrug-resistant pneumococci, and vancomycin-resistant enterococci. Important causes of Gram-negative resistance include extended-spectrum beta-lactamases (ESBLs) in Klebsiella pneumoniae, Escherichia coli, and Proteus mirabilis, high-level third-generation cephalosporin (Amp C) beta-lactamase resistance among Enterobacter species and Citrobacter freundii, and multidrug-resistance genes observed in Pseudomonas aeruginosa, Acinetobacter, and Stenotrophomonas maltophilia. In selecting an empiric treatment for a nosocomial infection, one should consider the prevalent resistance patterns. Antimicrobials used for the treatment of nosocomial infections should be effective against any likely resistant pathogens and should not further promote the development of resistance. Recent data suggest that because of ESBLs and high-level amp C beta-lactamase resistances, use of third-generation cephalosporins may be ineffective in many patients with nosocomial infections. In addition, use of these agents may allow overgrowth of inherently resistant enterococci. The role of fluoroquinolones in the empiric treatment of nosocomial infections is also being limited by new resistance patterns and increasing resistance levels. Available antimicrobials with good activity against many resistant pathogens include the carbapenems, piperacillin/tazobactam, and cefepime. In addition, several new agents with good activity against Gram-positive organisms are in development or have been recently released. Appropriate antimicrobial selection, surveillance systems, and effective infection-control procedures are key partners in limiting antimicrobial-resistant pathogen occurrence and spread.

Pneumonia complicates hospitalization in 0.5 to 2.0% of patients and is associated with considerable morbidity and mortality. Risk factors for hospital-acquired pneumonia (HAP) include mechanical ventilation for > 48 h, residence in an ICU, duration of ICU or hospital stay, severity of underlying illness, and presence of comorbidities. Pseudomonas aeruginosa, Staphylococcus aureus, and Enterobacter are the most common causes of HAP. Nearly half of HAP cases are polymicrobial. In patients receiving mechanical ventilation, P aeruginosa, Acinetobacter, methicillin-resistant S aureus, and other antibiotic-resistant bacteria assume increasing importance. Optimal therapy for HAP should take into account severity of illness, demographics, specific pathogens involved, and risk factors for antimicrobial resistance. When P aeruginosa is implicated, monotherapy, even with broad-spectrum antibiotics, is associated with rapid evolution of resistance and a high rate of clinical failures. For pseudomonal HAP, we advise combination therapy with an antipseudomonal beta-lactam plus an aminoglycoside or a fluoroquinolone (eg, ciprofloxacin).

This case report documents an uncommon cause of bilateral diaphragmatic paralysis resulting from phrenic nerve injury during cervical chiropractic manipulation. Several months after the initial injury, our patient remains short of breath and has difficulty breathing in the supine position. Other causes of diaphragmatic paralysis and phrenic nerve injury are reviewed.

Gene therapy for pulmonary disease has attracted a great deal of attention since the first report of successful gene delivery 10 years ago. Potential indications for gene therapy include chronic illnesses such as cystic fibrosis and alpha(1)-antitrypsin deficiency, and acute illnesses such as acute transplant rejection and chemotherapy-induced lung injury. The key technological impediment to successful gene therapy is vector optimization. Viral vectors, including adenovirus and adeno-associated virus, have relatively low efficiency in vivo. In addition, adenovirus has been associated with a brisk inflammatory response and limited duration of expression in the lung. Nonviral vectors, particularly liposomes, have also been tried, with limited expression efficiency and some toxicity. Although work is ongoing to improve adenoviral and adeno-associated viral vectors and test other viral and nonviral vectors, an ideal vector has not yet been identified. Several important barriers to successful gene therapy, including the host inflammatory response, promotor down-regulation, tissue-specific targeting, and physical barriers to gene delivery in the airway, will need to be overcome. Despite these daunting problems, several human gene therapy trials have been completed, using adenovirus, adeno-associated virus, and liposomes. In general, these trials have been focused on safety, and have shown that there is dose-dependent inflammation in response to adenovirus. Adeno-associated virus appears to cause little inflammation. Demonstration of successful gene delivery and transcription has been quite variable in human trials. In general, the level of expression of transgene appears to be quite low. In summary, although there is great promise for gene therapy in the lung, significant challenges remain in translating this technology to successful human therapy.