Legionella pneumonia complicated by adult respiratory distress syndrome

Two patients with sporadic Legionella pneumonia complicated by adult respiratory distress syndrome (ARDS) are described. Details about the clinical course and follow-up of their chest films are provided. The outcome in both patients was favourable. Literature concerning Legionella pneumonia complicated by ARDS is reviewed.     

A clinical analysis of 18 cases with adult respiratory distress syndrome

18 cases with adult respiratory distress syndrome (ARDS) admitted to our hospital since 1985 were reported. Among them, 2 cases were mild, 10 moderate and 6 severe. All of them received a combination of treatment, including correction of primary disease, O2 therapy, medications such as corticosteroid diuretics and anti-inflammatory agents, restriction of water intake and keep of negative fluid balance. Mechanical ventilation, especially early application of PEEP, was applied in 12 cases. In general, the level of pressure was kept between 0.08-0.1 KPa. End inspiration pause (EIP) was also routinely taken. Usually, the pausing period accounted for 10% of the respiratory cycle. 2 died among the 12 cases with mechanical ventilation, whereas all of the 6 cases receiving simple artificial ventilation died. The mortality rate was 44%.     

Gram-negative sepsis and the adult respiratory distress syndrome.

Gram-negative sepsis has dramatically increased in frequency throughout the twentieth century in the United States. Currently, approximately 200,000 patients develop gram-negative sepsis each year in this country. Of these, about one-quarter develop the adult respiratory distress syndrome (ARDS). Among these critically ill patients, mortality is estimated at 60%-90%. In the complex series of events leading to acute lung injury in gram-negative sepsis, endotoxin is the proximal mediator. Although endotoxin may be capable of causing direct injury to the pulmonary endothelium, its primary role is as a trigger activating inflammatory agents, including complement, neutrophils, and platelets, and inducing the production of cytokines and arachidonic acid metabolites. The end results are impairment of the endothelial barrier, diffusely increased capillary permeability, and adherence of neutrophils to the endothelium with subsequent migration into the tissues. The consequent clinical syndrome is one of acute respiratory distress with pulmonary edema, poorly compliant lungs, and refractory hypoxemia. Endothelial injury often becomes widespread, leading to the failure of multiple organs, including the kidneys, brain, intestine, and liver. Conventional therapy consists of supplemental oxygen, positive end-expiratory pressure, inotropic agents, fluid management, and antibiotics aimed at the offending pathogen. Recent discoveries regarding the mediators of sepsis as well as the expansion of the biotechnological armamentarium have provided clinicians with a plethora of new tools with which to manipulate the host's inflammatory response. The challenge for the next decade will be to ensure the safety, efficacy, and cost-effective use of these expensive but potentially lifesaving immunomodulators, singly or in combination, as adjuvant therapy.     

A clinical and pathologic analysis of 13 cases of adult respiratory distress syndrome

The autopsy findings and clinical features of 13 cases of adult respiratory distress syndrome (ARDS) were analysed. The underlying causes consisted of malignant tumor of the hematopoietic tissue, severe infections, surgical wounds and water drowning. Although tachypnoea and dyspnoea are the chief symptoms of ARDS., we noticed, however, that at the beginning of the episode or when complicated by other factors (such as fracture of cervical vertebra with transverse paralysis), the pulmonary symptoms may be not very obvious. Histological examination showed hyperplasia and fibrosis of the alveolar epithelium in those cases with a course of more than 5 days. Such findings rendered classification of ARDS into acute and chronic types reasonable.     

Ventilation-perfusion distributions in the adult respiratory distress syndrome.

The distribution of ventilation-perfusion ratios, as determined by the multiple inert gas elimination technique, was measured in 16 patients with the adult respiratory distress syndrome. In each case, the distribution of ventilation-perfusion ratios was bimodal. The upper mode consisted of units with normal ventilation-perfusion ratios that received a mean of 52% of the cardiac output. The lower mode, which received the remainder of the cardiac output, consisted of either pure shunt or shunt plus a small number of units with very low ventilation-perfusion ratios (less than 0.01). The measured arterial PO2 and that predicted from the distribution of ventilation-perfusion ratios were very closely correlated (r = 0.93), indicating that the hypoxemia was completely explained by the measured ventilation-perfusion inequality. In 12 patients, the effect of positive end-expiratory pressure on the distribution of ventilation-perfusion ratios was also determined. The addition of positive end-expiratory pressure uniformly resulted in a decrease in blood flow to the lower mode and an increase in the ventilation of unperfused alveoli. Increasing positive end-expiratory pressure also led to a uniform decrease in cardiac output. We conclude that the hypoxemia of the adult respiratory distress syndrome is caused by the presence of shunt or units of very low ratio of ventilation to perfusion and that positive end-expiratory pressure increases the arterial PO2 by decreasing the perfusion of unventilated lung. The mechanism of this decrease is yet to be defined.     

Gonococcemia associated with adult respiratory distress syndrome.

We report a case of gonococcemia that was associated with adult respiratory distress syndrome (ARDS). To our knowledge, this is only the third reported case of ARDS associated with gonococcemia. This is the first reported case of ARDS associated with gonococcemia that was documented by positive results of blood cultures and measurements of wedge pressure obtained by a catheter in the pulmonary artery. We also believe that this is the first reported patient who required mechanical ventilation under positive end-expiratory pressure. This patient made a full recovery. Gonococcemia associated with ARDS continues to occur rarely in patients despite the prevalence of disseminated gonococcal infection. The reason for the infrequent occurrence of ARDS with disseminated gonococcal infection remains uncertain.     

The adult respiratory distress syndrome. Definition and prognosis

This article provides an expanded definition of acute lung injury and the adult respiratory distress syndrome and describes the value of using this definition for establishing prognosis by discussing the basis for the acute lung injury scoring system, the various clinical disorders that may be associated with acute lung injury and how they affect outcome, and the influence of nonpulmonary organ failure on the outcome of patients with acute lung injury.     

Clinical and pathologic comparison of adult respiratory distress syndrome and infant respiratory distress syndrome

The authors compared the clinical and pathological findings between adult respiratory distress syndrome (ARDS), and infant respiratory distress syndrome (IRDS). In ARDS, the most common causes were injury, infection, shock and acidosis. The clinical course was longer. The weight of the lungs increased markedly, the hyaline membrane formation in the alveoli was late in the clinical course, and the degree of edema in the interstitium of the lungs and microthrombosis within the blood vessels was more serious. The pathogenesis of ARDS was related to the activation of the complements and neutrophils by inflammation in which proteinase, oxygen radical, thromboxane, leukotriene and prostaglandin were released. Thus the endothelial cells of the blood vessels and capillary-alveoli membrane were damaged by these mediators. On the other hand, the main contributory factors of IRDS were suffocation of premature fetus by various reasons in the uterus and aspiration of meconium during delivery by the infant. The clinical course was shorter, alveolar hemorrhage and collapse were severe and hyaline membrane in alveoli was formed in early stage of the clinical course. Insufficiency of surfactant in premature fetus, damage of the surfactant system by hypoxia, aspiration of foreign materials and defect of the epithelial cells of infant were the pathogenic factors of IRDS, they resulted in increase of permeability of fluid and, as a result, led to pulmonary edema and atelectasis.     

A positron emission tomographic comparison of pulmonary vascular permeability during the adult respiratory distress syndrome and pneumonia

We measured extravascular density (EVD) and the pulmonary transcapillary escape rate (PTCER) for 68Ga-transferrin using positron emission tomography in 14 normal volunteers and 29 patients with radiographic infiltrates, including six patients with congestive heart failure (CHF), eight patients with the adult respiratory distress syndrome (ARDS), and 15 patients with focal pneumonia. Contralateral, radiographically normal regions were also evaluated in the patients with focal pneumonia. Mean EVD was elevated in the patients with CHF, ARDS, and pneumonia in regions of radiographic infiltrate compared with values from normal subjects (p less than 0.05), but it was not significantly different among the three patient groups. PTCER in normal subjects and in patients with CHF was not significantly different (21 +/- 11 versus 44 +/- 16 x 10(-4) min-1, respectively, p = NS). PTCER was elevated in regions of infiltrate because of either pneumonia (173 +/- 99) or ARDS (170 +/- 79). PTCER was also elevated in regions contralateral to those with focal infiltrate during pneumonia, even though these regions were radiographically normal and had normal EVD values. These results suggest that PTCER is a sensitive but nonspecific index of abnormal pulmonary vascular permeability, which may be useful for classifying patients in clinical studies of pulmonary edema.     

Ventilator-associated pneumonia complicating the acute respiratory distress syndrome

Pulmonary infections span a wide spectrum, ranging from self-limited processes (e.g., tracheobronchitis) to life-threatening infections including both community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP). Together, pneumonia and influenza rank as the sixth leading cause of death in the United States and lead all other infectious diseases in this respect. Pneumonia is the second-most-common hospital-acquired infection in the United States, accounting for 17.8% of all hospital-acquired infections and 40,000 to 70,000 deaths per year. HAP is the most common nosocomial infection occurring in patients requiring mechanical ventilation, developing in 6.5% of patients after 10 days and in 28% of patients after 30 days of ventilatory support. Patients acquiring HAP have a greater risk of mortality than comparably ill ventilated patients who do not develop pneumonia. Ventilator-associated pneumonia (VAP) specifically refers to a bacterial pneumonia developing in patients with acute respiratory failure who have been receiving mechanical ventilation for at least 48 hours. The etiologic bacteriologic agents associated with VAP typically differ based on the timing of the occurrence of the infection relative to the start of mechanical ventilation. VAP occurring within 96 hours of the onset of mechanical ventilation is usually due to antibiotic-sensitive bacteria that colonize the patient prior to hospital admission (e.g., Streptococcus pneumoniae, Haemophilus influenza, oxacillin-sensitive Staphylococcus aureus). VAP developing after 96 hours of ventilatory support is more often associated with antibiotic-resistant bacteria including oxacillin-resistant Staphylococcus aureus, Acinetobacter species and Pseudomonas aeruginosa. However, more recent data suggest that hospitalization and exposure to antibiotics prior to the start of mechanical ventilation are important risk factors for the occurrence of VAP attributed to antibiotic-resistant bacteria. Therefore, these risk factors should be considered when deciding on an appropriate empiric antibiotic regimen regardless of the onset of VAP. VAP and catheter-associated bloodstream infections are the leading causes of infection acquired in the intensive care unit (ICU) setting. Patients in the ICU have rates of HAP that are as much as five to ten times higher than the rates in general hospital wards. Additionally, like nosocomial bloodstream infections, VAP is associated with an attributable mortality beyond that accounted for by patients' severity of illness. The attributable mortality associated with VAP appears to be greatest for "high-risk' antibiotic-resistant bacteria including Pseudomonas aeruginosa and oxacillin-resistant Staphylococcus aureus. The greater hospital mortality associated with these "high-risk' pathogens has been attributed to the virulence of these bacteria and the increased occurrence of inadequate initial antibiotic treatment of VAP due to the presence of antibiotic resistance. This review provides an overview of the clinical importance of VAP. We then describe how this nosocomial infection influences the management and outcomes of patients with the acute respiratory distress syndrome (ARDS).     

Acute respiratory distress syndrome of the adult

In a 43-year-old female patient after a bland influenzal infection suddenly an acute life-threatening picture of a disease with severe dyspnoea developed. Radiologically a distinct interstitial oedema was to be seen. According to the clinical and paraclinical data the case in question was the benign for of an acute dyspnoea syndrome of the adult. Etiology and therapy of the acute dyspnoea syndrome are shown. This picture of a disease should be included into the differential-diagnostic consideration in acute conditions of dyspnoea.     

Nocardia pneumonitis and the adult respiratory distress syndrome

This report describes the progression of an acute regional Nocardia pneumonitis to diffuse pulmonary parenchymal disease in a previously healthy man. The pathophysiologic manifestations of disease evolved from that of a severe bacterial pneumonia to the adult respiratory distress syndrome. This progression may be representative of pyogenic bacterial pneumonias, which are associated with the syndrome even when the infections are adequately treated.     

Fluid balance and the adult respiratory distress syndrome

This study examined the effect of fluid balance on survival in ARDS. Of the 213 patients entered into a prospective data collection study, we evaluated 113 patients who met strict criteria for ARDS. Multiple variables were analyzed for as long as 14 days after intubation including cardiac output, pulmonary capillary wedge pressure, mean blood pressure, intake minus output (I-O), cumulative intake minus output (cum I-O), and change in weight (delta wt). We found significant differences in cum I-O and delta wt between survivors and nonsurvivors on almost every day. Survivors lost weight and had a significantly lower cum I-O compared with nonsurvivors. Logistic regression was used to determine if delta wt and cum I-O could predict survival. Patients who lost 3 kg or more weight had a much higher survival than did those who gained 3 kg or more weight (67 and 0%, respectively, on Day 14). Similar results were obtained using comparably low and high values for cum I-O. The logistic regression equations demonstrated that weight loss and low cumulative I-O correlated with improved survival. Although cause and effect relationships are difficult to determine from these types of analyses, they can be used to formulate prospective studies and predict survival in patients.     

Prognosis after recovery from adult respiratory distress syndrome.

Ten patients who survived an acute episode of the adult respiratory distress syndrome were studied on recovery. Serial pulmonary function tests performed in 3 subjects revealed a tendency toward normalization of values at 4 to 6 months after the episode, with a subsequent serial decrease in maximal mid-expiratory flow rates, and a partial reversal by bronchodilators. Of the 10 patients, 6 had dyspnea on exertion and all but one of the 6 were smokers. The ventilatory tests revealed a predominantly restrictive pattern in 2 patients and an obstructive pattern in 4. The 4 asymptomatic patients had essentially normal pulmonary function. Pathologic features of the lung, available in 3 cases, are discussed.     

Total respiratory pressure-volume curves in the adult respiratory distress syndrome

To assess the value of measuring compliance in the adult respiratory distress syndrome, sequential pressure-volume curves were obtained in 19 patients with this syndrome. Analysis of the pressure-volume curves allowed separation of the patients into the following four groups: (1) group 1 (n = 6), normal compliance measured during deflation, little hysteresis, and no inflection in the ascending limb of the pressure-volume tracing; (2) group 2 (n = 8), normal compliance during deflation, increased hysteresis, and presence of an inflection; (3) group 3 (n = 10), decreased compliance during deflation, marked hysteresis, and presence of an inflection; and (4) group 4 (n = 10), reduced compliance during deflation, no increased hysteresis, and no inflection. These patterns were correlated with the stage of the adult respiratory distress syndrome and to the pattern of the chest x-ray film. Group 2 corresponds to the initial stage of the syndrome and to pure alveolar opacities on the chest x-ray film. Group 3 is seen later in the course of the syndrome and corresponds to mixed alveolar and interstitial opacities. Group 4 corresponds to patients with end-stage adult respiratory distress syndrome (two weeks) and a predominant interstitial pattern on the chest x-ray film. Group 1 corresponds to a nearly normal chest x-ray film and to recovery.