The acute respiratory distress syndrome (ARDS) is an inflammatory disease of the lungs characterized clinically by bilateral pulmonary infiltrates, decreased pulmonary compliance and hypoxemia. Although supportive care for ARDS seems to have improved over the past few decades, few studies have shown that any treatment can decrease mortality for this deadly syndrome. In the 4 May 2000 issue of New England Journal of Medicine, the results of an NIH-sponsored trial were presented; they demonstrated that the use of a ventilatory strategy that minimizes ventilator-induced lung injury leads to a 22% decrease in mortality. The implications of this study with respect to clinical practice, further ARDS studies and clinical research in the critical care setting are discussed.

The acute respiratory distress syndrome (ARDS) is a frequent, life-threatening disease in which a marked increase in alveolar surface tension has been repeatedly observed. It is caused by factors including a lack of surface-active compounds, changes in the phospholipid, fatty acid, neutral lipid, and surfactant apoprotein composition, imbalance of the extracellular surfactant subtype distribution, inhibition of surfactant function by plasma protein leakage, incorporation of surfactant phospholipids and apoproteins into polymerizing fibrin, and damage/inhibition of surfactant compounds by inflammatory mediators. There is now good evidence that these surfactant abnormalities promote alveolar instability and collapse and, consequently, loss of compliance and the profound gas exchange abnormalities seen in ARDS. An acute improvement of gas exchange properties together with a far-reaching restoration of surfactant properties was encountered in recently performed pilot studies. Here we summarize what is known about the kind and severity of surfactant changes occuring in ARDS, the contribution of these changes to lung failure, and the role of surfactant administration for therapy of ARDS.

Several studies indicate that organ failure is the leading cause of death in surgical patients. An excessive inflammatory response followed by a dramatic paralysis of cell-mediated immunity following major surgery appears to be responsible for the increased susceptibility to subsequent sepsis. In view of this, most of the scientific and medical research has been directed towards measuring the progression and inter-relationship of mediators following major surgery. Furthermore, the effect of those mediators on cell-mediated immune responses has been studied. This article will focus on the effect of blood loss and surgical injury on cell-mediated immune responses in experimental studies utilizing models of trauma and hemorrhagic shock, which have defined effects on the immunoinflammatory response. Subsequently these findings will be correlated with data generated from surgical patients. The results of these studies may generate new approaches for the treatment of immunodepression following major surgery, thus reducing the susceptibility to infection and increasing the survival rate of the critical ill surgical patient.

This dataset contains statewide counts for every diagnosis, procedure, and external cause of injury/morbidity code reported on the ambulatory surgery data. Diagnosis codes are reported using ICD-9-CM or ICD-10-CM. Procedure codes are reported using CPT-4. External cause of injury/morbidity codes are reported using ICD-9-CM or ICD-10-CM. ICD-10 replaced ICD-9, effective October 1, 2015. Note: Physician-owned ambulatory surgery clinics do not report their data to HCAI and, therefore, are not included in the statewide frequencies.

There is increasing evidence for a close link between the upper and the lower respiratory tracts and the fact that rhinitis has an important impact on asthma. Several clinical and experimental observations suggest a similar immunopathology between the upper and lower airways in allergic subjects. The common inflammatory process that develops in the respiratory tract explains some of the complex interactions among different clinical diseases such as rhinitis, sinusitis, asthma, bronchial hyperresponsiveness and viral infections. There are also non-inflammatory mechanisms that may contribute to the link between rhinitis and asthma. Moreover, the outcomes of various pharmacological treatments of rhinitis have recently provided further support for the hypothesis of the united airways. We discuss some of the recent observations on the nose-lung interaction and some of the novel therapeutic approaches used to treat rhinitis and asthma that arise from this.

Background: Nosocomial pneumonia (NP) is a common complication in mechanically-ventilated patients and is considered to be one of the most common causes of morbidity and mortality. However, assessment of the associated mortality is not staightforward as it shares several risk factors with NP that confound the relationship. The aim of this study was to evaluate the impact of NP on the mortality rate in an intensive care unit. During the study period (January-December 1995) all patients under mechanical ventilation for a period > 48 h (n = 314) were prospectively evaluated, and the prognostic factors of NP, which have been identified in previous studies, were recorded. Results: Pneumonia was diagnosed in 82 patients. The overall mortality rate was 34% for patients with NP compared to 17% in those without NP. Multivariate analysis selected the following three prognostic factors as being significantly associated with a higher risk of death: the presence of multiple organ failure [odds ratio (OR) 6.71, 95% CI, P < 0.001]; the presence of adult respiratory distress syndrome (ARDS) (OR 3.03, 95% CI, P < 0.01), and simplified acute physiology score (SAPS)> 9(OR 2.89, 95% CI, P < 0.05). Conclusions: In mechanically-ventilated patients NP does not represent an independent risk factor for mortality. Markers of severity of illness were the strongest predictors for mortality.

Focusing on diffuse (interstitial) lung disease: a rapidly evolving field

This dataset contains statewide counts for every diagnosis, procedure, and external cause of injury/morbidity code reported on the ambulatory surgery data. Diagnosis codes are reported using ICD-9-CM or ICD-10-CM. Procedure codes are reported using CPT-4. External cause of injury/morbidity codes are reported using ICD-9-CM or ICD-10-CM. ICD-10 replaced ICD-9, effective October 1, 2015. Note: Physician-owned ambulatory surgery clinics do not report their data to HCAI and, therefore, are not included in the statewide frequencies.