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PubMed2006

Changes in respiratory mechanics and gas exchange during the acute respiratory distress syndrome.

BACKGROUND: The time course of impairment of respiratory mechanics and gas exchange in the acute respiratory distress syndrome (ARDS) remains poorly defined. We assessed the changes in respiratory mechanics and gas exchange during ARDS. We hypothesized that due to the changes in respiratory mechanics over time, ventilatory strategies based on rigid volume or pressure limits might fail to prevent overdistension throughout the disease process. METHODS: Seventeen severe ARDS patients {PaO2/FiO2 10.1 (9.2-14.3) kPa; 76 (69-107) mmHg [median (25th-75th percentiles)] and bilateral infiltrates} were studied during the acute, intermediate, and late stages of ARDS (at 1-3, 4-6 and 7 days after diagnosis). Severity of lung injury, gas exchange, and hemodynamics were assessed. Pressure-volume (PV) curves of the respiratory system were obtained, and upper and lower inflection points (UIP, LIP) and recruitment were estimated. RESULTS: (1) UIP decreased from early to established (intermediate and late) ARDS [30 (28-30) cmH2O, 27 (25-30) cmH2O and 25 (23-28) cmH2O (P=0.014)]; (2) oxygenation improved in survivors and in patients with non-pulmonary etiology in late ARDS, whereas all patients developed hypercapnia from early to established ARDS; and (3) dead-space ventilation and pulmonary shunt were larger in patients with pulmonary etiology during late ARDS. CONCLUSION: We found a decrease in UIP from acute to established ARDS. If applied to our data, the inspiratory pressure limit advocated by the ARDSnet (30 cmH2O) would produce ventilation over the UIP, with a consequent increased risk of overdistension in 12%, 43% and 65% of our patients during the acute, intermediate and late phases of ARDS, respectively. Lung protective strategies based on fixed tidal volume or pressure limits may thus not fully avoid the risk of lung overdistension throughout ARDS.

Adult↗
PubMed1988

Respiratory syncytial virus infection: a cause of respiratory distress syndrome and pneumonia in adults.

Respiratory syncytial virus (RSV) infection, an important and sometimes lethal disease of infants and children, generally causes a milder and self-limited syndrome of cough, nasal congestion and fever in adults. While some evidence suggests that RSV may be responsible for more serious respiratory illness in the elderly and chronically ill, it has not been shown to cause life-threatening respiratory tract disease in previously healthy adults. This report describes a previously healthy woman who experienced the acute onset of right lower lobe pneumonia which rapidly progressed to the adult respiratory distress syndrome (ARDS). Acute and convalescent serology showed RSV was the cause of the respiratory tract illness. Michigan Department of Public Health records revealed six additional cases of adult bilateral pneumonia with diagnostic antibody titers to RSV, with or without coinfection with a second organism. These data suggest that RSV may be an under-recognized cause of lower respiratory tract disease in adults.

Aged↗
PubMed1976

Estimation of surfactant lecithin in amniotic fluid and prediction of respiratory distress syndrome.

The quantitative and qualitative analyses of lecithin in the human amniotic fluid in relation to the antenatal prediction of developing respiratory distress syndrome were described. Surfactant lecithin (disaturated and/or dipalmitoyl lecithin) was estimated for the first time in 42 amniotic fluid specimens of 21-42 weeks gestation. Surfactant lecithin was present in considerable amounts in specimens obtained near or at term except in the ones associated with infants who subsequently developed respiratory distress syndrome. One infant developed typical respiratory distress syndrome despite the normal total lecithin concentration of amniotic fluid at birth. The fatty acid analysis, however, revealed that the surfactant lecithin concentration was extremely low, showing a great discrepancy between total lecithin and surfactant lecithin concentrations. Thus the estimation of disaturated and/or dipalmitoyl lecithin in the amniotic fluid seems to be the most precise sign of a potential risk of respiratory distress syndrome.

Amniotic Fluid↗
PubMed2006

Limitations of clinical trials in acute lung injury and acute respiratory distress syndrome.

PURPOSE OF REVIEW: To review the challenges and limitations of randomized clinical trials in acute respiratory distress syndrome, with special emphasis on those pertaining to ventilatory management. RECENT FINDINGS: Superbly executed randomized trials of ventilatory strategy have garnered deserved attention from the critical care community and yet have illustrated the limitations of our current approach to clinical research in this area. Inexact definitions, incomplete mechanistic understanding of complex pathophysiology, inappropriate outcome variables, diverse therapeutic environments, lengthy data acquisition time and ethical constraints on trial design limit the applicability of randomized control trial methodology to acute respiratory distress syndrome and acute lung injury. As yet, clinical practice does not seem to have been greatly impacted by the implications of completed randomized controlled trials per se. Recent issues, both ethical and interpretive, regarding control group participants have raised troubling and theoretically important issues that are yet to be fully resolved. SUMMARY: Without tighter definitions of the condition under treatment, more specific targets for interventions to act upon, stratification that recognizes key interactive elements, and cointerventions based on better mechanistic understanding, randomized controlled trials of new drugs, ventilatory strategy, and other management approaches in acute respiratory distress syndrome are likely to remain a blunt instrument for investigation. As valuable as they are for calling important therapeutic principles to attention and for helping to suggest general guidelines for care, the limitations of randomized controlled trials for treating the individual with acute respiratory distress syndrome must be acknowledged.

Critical Care↗
PubMed1999

Resolution of adult respiratory distress syndrome after recovery from fulminant hepatic failure.

Adult respiratory distress syndrome (ARDS) complicating the course of fulminant hepatic failure is nearly always fatal without orthotopic liver transplantation. We report the case of a 50-year-old woman with fulminant hepatic failure and ARDS that resolved after her recovery from the acute liver failure without liver transplantation. The pathogenesis is discussed, particularly with regard to liver-lung interactions.

Female↗
PubMed1994

Prone position for ventilation in patients with severe adult respiratory distress syndrome.

We report 3 cases of severe adult respiratory distress syndrome. The patients were very difficult to oxygenate, even with the most advanced conventional mechanical ventilation techniques. In all cases oxygenation improved dramatically when the patient was turned to the prone position. Reports of the use of the prone position for ventilation are scanty, and this is the first time it has been reported in this country. The proposed mechanisms for its effectiveness are reviewed.

Adolescent↗
PubMed2001

Influence of direct and indirect etiology on acute outcome and 6-month functional recovery in acute respiratory distress syndrome.

OBJECTIVE: To assess the possibility that acute respiratory distress syndrome (ARDS) of pulmonary and nonpulmonary origins represent two distinct syndromes. DESIGN: Analysis of data collected prospectively from an inception cohort of 117 patients with ARDS. SETTING: Adult intensive care unit (ICU), university/postgraduate hospital. MEASUREMENTS AND MAIN RESULTS: Differences were sought in mortality and 6-month functional outcome between patients developing ARDS due to pulmonary (group 1) and nonpulmonary (group 2) pathology. Group 1 patients displayed a trend toward increased ICU and in-hospital mortality (42.1% vs. 23.2%, p = .10, and 47.4% vs. 27.9%, p = .11, respectively). No difference was found in ICU length of stay (46.3 +/- 4.9 vs. 39.0 +/- 4.8 days for groups 1 and 2, respectively) nor in duration of positive-pressure ventilation (26.2 +/- 4.3 vs. 20.6 +/- 3.2 days). However, the need for pressure-controlled inverse ratio ventilation was significantly greater in group 1 (16.9 +/- 3.2 vs. 9.1 +/- 1.3 days; p = .033). In survivors, reductions in total lung capacity at 6 months (68.1 +/- 4.6 vs. 61.8 +/- 4.6% predicted for groups 1 and 2, respectively; p = .4), accessible lung volume (74.4 +/- 4.4 vs. 68.9 +/- 4.9% predicted; p = .56), and forced expiratory volume (77.8 +/- 2.9 vs. 80.3 +/- 2.4% predicted; p = .57) did not differ between groups. Gas transfer coefficient was well preserved (84.5 +/- 4.6 vs. 86.6 +/- 4.7% predicted; p = .80). CONCLUSIONS: These data suggest a trend toward higher mortality and ventilatory requirements in ARDS of direct etiology, generating a hypothesis worthy of further exploration.

APACHE↗
PubMed2001

Acute respiratory distress syndrome: pharmacological treatment options in development.

The acute respiratory distress syndrome (ARDS) is a clinical syndrome with primarily supportive management options. Despite extensive basic and clinical investigations, multiple pharmacological and nonpharmacological modalities have been unsuccessful in decreasing mortality. Nonetheless, these efforts have substantially heightened our understanding of ARDS pathophysiology. Investigators continue to create new and more complex therapeutic strategies that may have significant clinical impact. Several pharmacological agents for ARDS are in development and have shown either great promise or are at most, under phase II evaluation. The order in which therapeutic options are presented in this review highlights therapeutic options other than the anti-inflammatory approach. In addition to the anti-inflammatory category, vasodilators, surfactant therapy, immunonutrition and partial liquid ventilation are all being evaluated. Within the anti-inflammatory category. new mechanistic approaches include the 'anti-inflammatory nature' of interleukin-10, the inhibitory aspects of lysophosphatidic acid on endothelial cell permeability, and the use of recombinant human anti-coagulant proteins (activated protein C and tissue factor pathway inhibitor) to reduce the inflammatory cycle that contributes to microvascular thrombi. Previous work with surfactant in ARDS had its limitations, however, these trials were of sufficient success to spawn 2 new synthetic compounds. These new synthetic surfactants incorporate mixtures of phosphatidylcholine and phosphatidylglycerol (the key phospholipids within endogenous surfactant) and either recombinant surfactant protein C or an analogue of surfactant protein B. Recently, the ARDS Network's low tidal volume study has broken the cycle of decades of negative ARDS trials and demonstrated an improvement in mortality. Through better mechanistic approach and study design, investigator compliance with exclusion criteria, and better understanding of the complexities of patient management, the next pharmacological ARDS trials will hopefully be successful and lead to further reductions in patient mortality.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Adult respiratory distress syndrome and sepsis.

In the 25 yrs since the original description of adult respiratory distress syndrome, much has been learned concerning the pathology and pathophysiology of the syndrome. Investigations into the humoral mediator of the syndrome are proceeding. Despite these advances and the advances in intensive care medicine, adult respiratory distress syndrome remains a considerable clinical challenge, especially when associated with sepsis.

Antibody Formation↗
PubMed2003

Influence of the humidification device during acute respiratory distress syndrome.

OBJECTIVE: To evaluate the effects of the humidification device on respiratory, hemodynamic and gas exchange parameters in acute respiratory distress syndrome (ARDS) patients. DESIGN: A prospective open study. SETTING: A medical intensive care unit of a university hospital. PATIENTS: Acute respiratory distress syndrome patients, with hypercapnia (PaCO(2)>60 mmHg). INTERVENTION: A progressive reduction of the humidification system dead space (DSh). The following five conditions were tested sequentially: (1). heat and moisture exchanger (internal volume=95 ml) with a tracheal closed-suction system (internal volume=25 ml; total DSh=120 ml), (2). heat and moisture exchanger (internal volume=45 ml) with the closed-suction system (DSh=70 ml), (3). heat and moisture exchanger (internal volume=25 ml) with the closed-suction system (DSh=50 ml), (4). heated humidifier with the closed-suction system (DSh=25 ml) and (5). heated humidifier alone (DSh=0 ml). Recordings were performed at baseline and every 30 min after each artificial dead-space reduction. All ventilatory settings remained constant during the measurement periods. RESULTS: Ten ARDS patients were included. A significant PaCO(2) decrease was observed at each humidification system dead-space reduction, compared to baseline: PaCO(2 )=80.3+/-20 mmHg at DSh(120) compared to PaCO(2 )=63.6+/-13 mmHg at DSh(0) ( p<0.05). No changes were observed for hemodynamic and ventilatory parameters between the different humidification devices. CONCLUSION: Artificial airway dead-space reduction allows a significant PaCO(2) reduction. Independently of any respiratory mechanical changes, this very simple maneuver may be of importance when low tidal volume ventilation is used in ARDS patients, and when PaCO(2) lowering is warranted.

Adult↗
PubMed1989

Background to neonatal respiratory distress syndrome and treatment with exogenous surfactant.

The neonatal respiratory distress syndrome (RDS), caused by surfactant deficiency, is characterized by a nonuniform distribution of tidal volumes in the lung parenchyma, epithelial necrosis in peripheral airspaces, and leakage of protein into the alveoli from areas of epithelial disruption. Studies on premature experimental animals have shown that the leakage of protein is correlated to the pressure required to ventilate the lungs, i.e. presumably to the degree of surfactant deficiency. Since the leaking material includes potent surfactant inhibitors, the underlying surfactant deficiency may become aggravated, and a vicious cycle is easily established. Lung compliance is improved, epithelial necrosis prevented, and protein leakage significantly reduced by instillation of surfactant into the airways of immature newborn experimental animals. This provides the rationale for surfactant replacement therapy in neonatal RDS.

Animals↗
PubMed1983

Adult-type respiratory distress syndrome in children. Experience with seven cases.

Adult respiratory distress syndrome (ARDS) is not well recognized in children. We report seven individuals, ranging in age from 1.5 to 16 years. The clinical picture of ARDS reached a peak in 72 hours from admission and was associated with a 28.5 per cent death rate (2/7). In no case was an organism isolated, either from bronchial washings via a flexible bronchoscope or from open lung biopsy specimen. ARDS is characterized by severe damage to the alveolar-capillary unit and probably inadequate production of lung surfactant, resulting in severe hypoxia, hypoxemia, intrapulmonary shunting, and marked decline in pulmonary compliance. The prognosis remains poor in the pediatric age group. The pathophysiology of this entity is outlined, with guidance for monitoring and therapy.

Adolescent↗
PubMed1996

Changes in lung volume and static expiratory pressure-volume diagram after surfactant rescue treatment of neonates with established respiratory distress syndrome.

The effect of natural surfactant on respiratory system mechanics in infants with respiratory distress syndrome (RDS) is incompletely understood, possibly because the analysis has usually been confined to the tidal breath. We studied 11 paralyzed neonates weighing 540 to 1,850 g before and approximately 30 min after surfactant, which was instilled at 4 to 41 h of age. Diagrams relating airway pressure to expired volume were obtained by having the infant exhale passively through a flowmeter, starting at 30 and ending at 0 cm H20 of pressure. An interrupter intermittently stopped the flow so that pressure could be recorded under static conditions. FRC was measured by sulfur hexafluoride washout, and TLC was calculated from FRC and the pressure-volume (P-V) curve. Ventilation homogeneity was assessed from the washout curve as pulmonary clearance delay (PCD). TLC increased by 10% or more in five infants, but it remained unchanged in the others. Median TLC was 19 ml/kg before and 21.5 ml/kg after surfactant (p = 0.39). The P-V curve became markedly steeper at low pressures after surfactant in most infants, the slope of the steepest segment, i.e., maximal compliance, increasing from 0.65 to 1.22 ml/cm H20/kg (medians, p = 0.008). Dynamic compliance (Cdyn) was unchanged at 0.28 ml/cm H20/kg, whereas specific dynamic compliance (Cdyn/FRC) decreased (p = 0.04). There was no significant immediate change in PCD. The findings imply that during the first 30 min surfactant acted mainly by stabilizing already ventilated air spaces.

Biological Products↗
PubMed1994

Neutrophil-generated free radicals: possible mechanisms of injury in adult respiratory distress syndrome.

The acute lung injury resulting from adult respiratory distress syndrome (ARDS) is thought to be largely mediated by activated neutrophils. Because activated neutrophils produce the superoxide radical, which is both bacterial and cytotoxic to host cells, this oxygen-derived free radical is likely responsible for at least part of the neutrophil-mediated lung injury. In a rat model of ARDS resulting from intratracheal instillation of interleukin-1, recombinant human manganous superoxide dismutase significantly decreased lung leak. One detrimental action of proteases released by adherent neutrophils may be the degradation of extracellular superoxide dismutase (ECSOD), which normally binds to the heparan sulfate on the surface the endothelium. We found that rabbit ECSOD incubated with either trypsin or activated neutrophils loses affinity for heparin. Furthermore, soluble ECSOD is elevated in the serum of patients with ARDS, consistent with this hypothesis.

Animals↗
PubMedDate not supplied

[Hemostatic-vascular interactions in the pathogenesis and the treatment of adult respiratory distress syndrome].

The complex pathophysiologic alterations occurring in adult respiratory distress syndrome (ARDS) result from the interaction of various humoral and cellular mediators. In this review we examine the events that lead to acute pulmonary injury as discussed in the recent literature as well as the correlations among humoral systems and cell activation involved in the pathogenesis of ARDS. We also consider the mechanisms inducing the appearance of adhesive molecules (ELAM-1 and ICAM-1) on the surface of endothelial cells, the importance of complement and clotting activation, and the role of monocyte-macrophages, platelets and neutrophils. The complexity of alterations among the different mediators involved in the pathogenesis of ARDS is underscored by experimental results demonstrating how the pharmacologic blockade of each system cannot completely prevent the development of lung damage. Understanding of the complex processes involved in the pathogenesis of ARDS provides new prospects for its treatment, such as inhalational nitric oxide and aerosolised prostacyclin. The most promising approach involves the use of monoclonal antibodies which may enable the selective inhibition of different mediators and endotoxins.

Humans↗
PubMed1999

Acute respiratory distress syndrome in a paediatric intensive care unit.

Acute respiratory distress syndrome (ARDS) is the final outcome of a common pathway of a variety of unrelated but massive insults to the lung. It is commonly seen in adults but also occurs in the paediatric age group. A prospective study was carried out to determine the incidence, predisposing conditions, clinical course and outcome of children with ARDS admitted to a paediatric intensive care unit (PICU). Six patients (aged 0.8 to 11 years) who fulfilled the strict criteria for ARDS were identified prospectively during a one year study period. The incidence was 1.7% of all PICU admission. The most common underlying conditions were septicemia and pneumonia. The mortality rate was 83%. Death most often occurred during the early phase of the disease. Treatment of ARDS included elimination of the cause of ARDS, early institution of mechanical ventilation with PEEP, prompt recognition and treatment of superimposed infection and careful management of additional organ failure.

Child↗