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PubMed1986

Current perspectives on iatrogenic neonatal respiratory distress syndrome.

Iatrogenic respiratory distress syndrome (RDS) continues to result in significant morbidity and mortality. In this series of 176 cases of neonatal RDS, 8 (4.6%) resulted from errors in obstetric management: poor documentation of fetal maturity prior to elective delivery (6 cases), elective cesarean section with premature rupture of the membranes at 33 weeks of gestation (1) and failure to attempt tocolysis at 32 weeks of gestation (1). One neonatal death occurred among the eight cases. The authors encourage others to analyze their experiences in order to identify this important health care problem.

Cesarean Section↗

PubMed2006

Epidemiology of acute lung injury and acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a heterogeneous disorder that may be triggered by myriad etiologies (both pulmonary and extrapulmonary). Mortality rates for ARDS range from 30 to 75%, and most deaths are a consequence of multiorgan failure (MOF). Since the sentinel description of ARDS in 1967, criteria for the diagnosis of this entity were refined. In 1992, diagnostic criteria for ARDS were published in an American-European Consensus Conference and the term ACUTE LUNG INJURY (ALI) was adopted to encompass patients with a spectrum of less severe forms of the same pathological entity. This review discusses limitations of various criteria utilized to diagnosis ARDS and ALI, and why some criteria may be problematic when designing clinical trials. Also discussed are the myriad causes of ARDS, incidence, epidemiology, mortality, and factors that influence outcome.

Humans↗

PubMed1985

Current concepts regarding adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) is a multietiologic acute and progressive pulmonary dysfunction that may be precipitated by any of a number of pathogenic agents. Clinical and experimental studies suggest that activation of complement and blood neutrophils plays a significant role in the development of pulmonary vascular injury, which is an important pathophysiological feature of ARDS. Although the specific cellular and biochemical mechanisms resulting in the development of ARDS are unknown, it has been suggested that oxygen-derived free radicals generated from complement-activated granulocytes may be involved, directly or indirectly, in the destruction of lung vascular endothelium and alveolar tissue matrix. This hypothesis is supported by recent experimental studies showing that acute lung injury secondary to systemic complement activation can largely be prevented by interventions that scavenge for hydroxyl radicals or restrict availability of ionic iron.

Animals↗

PubMed2006

Pharmacological therapy for acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is an Inflammatory process caused by a variety of direct and indirect injuries to the lungs. Despite improvements in supportive care and advances in ventilator management, mortality in patients with ARDS remains high. Multiple pharmacological interventions have been investigated but have not shown improved survival. Clinical trials using corticosterolds, prostaglandins, nitric oxide, prostacyclin, surfactant, lisofylline, ketoconazole, N-acetylcystelne, and fish oil have been unable to show a statistically significant Improvement in patient mortality. As more is understood about the pathophyslology of ARDS, treatment strategies such as increasing alveolar fluid clearance through activation of sodium channels, enhancing repair of alveolar epithelium with growth factors, inhibiting fibrin deposition, blocking proinflammatory transcription factors, preventing the effect of potent vasocontrictors such as endothelin, and using antibodies against key inflammatory cytokines are being explored. This review focuses on the pharmacological treatments studied clinically, proposed reasons for their lack of success, and new concepts emerging in ARDS therapy.

Anti-Inflammatory Agents↗

PubMed1989

Expression of the 35kDa and low molecular weight surfactant-associated proteins in the lungs of infants dying with respiratory distress syndrome.

Newborn respiratory distress syndrome (RDS) results from a deficiency of pulmonary surfactant. Surfactant has three ultrastructural forms: lamellar bodies, which, when secreted from Type II pneumocytes, transform into tubular myelin; tubular myelin in turn gives rise to the phospholipid monolayer at the air-fluid interface in the alveolus that constitutes functional surfactant. It has been shown previously that the lungs of infants dying from RDS lacked tubular myelin despite the presence of abundant lamellar bodies, whereas the lungs of control infants dying from other causes had both tubular myelin and lamellar bodies. An abnormality in the conversion of lamellar bodies to tubular myelin in RDS was proposed as a possible explanation for this finding. To evaluate the role of surfactant proteins (SPs) in this conversion, the authors re-examined the lungs of 11 RDS infants and 10 control infants for reactivity with antisera to high and low molecular weight SPs. In control infants, abundant intense staining with antisera to both types of SPs was found, but in the RDS lungs, staining was weaker than that in controls and less intense for high molecular weight compared to low molecular weight SPs. In lungs from patients with RDS, although staining increased with increasing gestational and post-natal ages, the intensity was less than control levels at all ages. The correlation of deficiency of SPs in RDS with lack of tubular myelin suggests that SPs may be involved in the conversion of normal lamellar bodies to tubular myelin and that the deficiency of SPs could explain the persistent respiratory distress in the presence of surfactant phospholipid synthesis.

Anti-Infective Agents↗

PubMed1985

A case of pneumonia presenting with the acute respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) or high permeability pulmonary oedema (HPPE) is an uncommon presentation of a viral pneumonia and usually occurs in the setting of a fulminant or severe viral pneumonia. High permeability pulmonary oedema (HPPE) can be loosely defined as those forms of pulmonary oedema with normal cardiac function associated with the accumulation of protein-rich fluid in the interstitial or intraalveolar spaces. Through the years, a number of phrases have been used to describe this entity: white lung, shock lung, wet lung, adult hyaline membrane disease, ARDS and others. The aetiology is varied but the clinical, radiologic and pathologic pictures are similar. In fact the pathologic picture is so consistent from patient to patient regardless of aetiology that it has been suggested that the term HPPE be used in place of the other commonly used ones. A case of HPPE of possible viral aetiology who responded to prompt intervention with a successful outcome, is described here.

Acute Disease↗

PubMed2000

Use of extracorporeal membrane oxygenation to rescue a child with acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) carries a high mortality of about 60%. The results of conventional treatments for ARDS are poor. We report the use of extracorporeal membrane oxygenation (ECMO) to rescue a child with ARDS. The patient, a 7-year-old boy, underwent a Ross procedure and mitral valvuloplasty because of severe aortic and mild mitral regurgitation. ARDS due to massive transfusion and prolonged cardiopulmonary bypass developed in the early postoperative period. Hypoxemia persisted despite conventional treatments, including pressure-controlled ventilation and high-frequency ventilation. Finally, venovenous ECMO was used to rescue the patient. With ECMO support, gas exchange was well maintained with a lower ventilator setting, and ventilator-induced lung injuries were avoided. ECMO was used for 183 hours, at which point the boy was weaned without complications. His recovery was uneventful. At the latest follow-up, 6 months after the operation, he was in New York Heart Association function class I and had no complaints of lung disease. This case suggests that venovenous ECMO can be a rescue method for patients with ARDS that is refractory to conventional treatments.

Child↗

PubMed2004

Quality of life, emotional, and cognitive function following acute respiratory distress syndrome.

Acute Respiratory Distress Syndrome (ARDS) is characterized by lung injury and hypoxemia, has a high mortality rate, and is associated with significant morbidity including cognitive and emotional sequelae and decreased quality of life. There is limited information regarding which of these factors are associated with decreased quality of life. This study assessed the relationships between quality of life, cognitive and emotional function in ARDS survivors at 1-year post-hospital discharge. Sixty-six ARDS survivors were administered a battery of neuropsychological tests, measures of emotional function and quality of life 1 year post-hospital discharge. At 1 year 45% of the ARDS patients had cognitive sequelae and 29% had mild to moderate symptoms of depression and anxiety. Depression, anxiety, and intensive care unit length of stay were significantly correlated with decreased quality of life. Cognitive impairments did not correlate with decreased quality of life. Illness severity and emotional function, but not cognitive sequelae, are associated with decreased quality of life 1 year following ARDS. ARDS is common and may result in significant cognitive and emotional morbidity and decreased quality of life.

Adolescent↗

PubMed2004

Osteopontin is strongly expressed by alveolar macrophages in the lungs of acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is characterized by an intense inflammatory response in the lung parenchyma. Recent studies suggest that excessive nitric oxide (NO) production mediated by inducible NO synthase (iNOS) in macrophages is partially involved in mediating acute lung injury in ARDS. On the other hand, osteopontin (OPN) is a cytokine which is capable of inhibiting NO production by suppressing iNOS mRNA expression in macrophages. In this study, we investigated the expression of OPN in the lungs of 10 patients with ARDS. In most patients, OPN is strongly expressed on alveolar macrophages. In addition, we produced a murine model for ARDS by intratracheal administration of lipopolysaccharide and investigated the expression of endogenous OPN and iNOS in the lungs of ARDS mice. Immunostaining demonstrated that in vivo OPN protein was coinduced with iNOS protein predominantly in the accumulating alveolar macrophages. OPN mRNA expression was also coinduced with iNOS mRNA, but was induced more slowly than iNOS mRNA in the lungs of ARDS mice. These results suggested that OPN, which may reduce NO production of macrophages by inhibiting iNOS expression, is significantly induced and expressed on alveolar macrophages in the lungs of ARDS. It is possible that OPN is partially involved in playing a protective role against excessive production of NO in ARDS.

Adult↗

PubMed2004

Two-year cognitive, emotional, and quality-of-life outcomes in acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) has a high mortality and is associated with significant morbidity. Prior outcome studies have focused predominant on short-term outcomes (6-12 months). We assessed longitudinal neurocognitive, emotional, and quality of life in ARDS survivors at hospital discharge, and 1 and 2 years after hospital discharge using neuropsychologic tests and emotional and quality-of-life questionnaires. Neurocognitive sequelae occurred in 73% (54 of 74) of ARDS survivors at hospital discharge, 46% (30 of 66) at 1 year, and 47% (29 of 62) at 2 years. ARDS survivors report moderate to severe depression (16% and 23%) and anxiety (24% and 23%) at 1 and 2 years, respectively. The ARDS survivors had decreased quality of life, with the physical domains improving at 1 year, with no additional change at 2 years. Role emotional, pain, and general health did not change from hospital discharge to 2 years. Mental health improved during the first year and declined at 2 years. ARDS results in significant neurocognitive and emotional morbidity and decreased quality of life that persists at least 2 years after hospital discharge. ARDS can cause significant long-term, brain-related morbidity manifest by neurocognitive impairments and decreased quality of life.

Adolescent↗

PubMed2003

Selective pulmonary vasodilation in acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is characterized by a marked maldistribution of pulmonary perfusion in favor of nonventilated, atelectatic areas of the lungs, and it is the main cause of pulmonary right-to-left shunting and hypoxemia. Therapeutic interventions to selectively influence pulmonary perfusion in ARDS became feasible with the introduction of inhaled nitric oxide, which provided a means not only to reduce pulmonary hypertension, but also to improve matching of ventilation to perfusion and, thus, hypoxemia. Clinical studies in ARDS subsequently demonstrated that the combination of inhaled nitric oxide with other interventions, such as positive end-expiratory pressure and prone positioning, yielded beneficial and additive effects on arterial oxygenation. Although the available randomized, controlled trials of this novel concept have so far failed to show an improved outcome in ARDS, inhaled nitric oxide is a clinically valuable option for the treatment of severe refractory hypoxemia in ARDS, and largely promoted the concept of selective pulmonary vasodilation in intensive care practice. Currently, aerosolization of various vasodilators, in particular prostaglandins, is under evaluation in models of acute lung injury and human ARDS. Ongoing research aims to augment the effectiveness of vasodilators with specific inhibitors of phosphodiesterases or by combination with intravenous vasoconstrictors. Consequently, several alternative ways to selectively modulate pulmonary vascular tone in patients with ARDS may be available in the near future. Cost-benefit analysis of these therapeutic options will largely determine their future perspective.

Administration, Inhalation↗

PubMed1991

Surfactant chemical composition and biophysical activity in acute respiratory distress syndrome.

Acute Respiratory Distress Syndrome (ARDS) is characterized by lung injury and damage to the alveolar type II cells. This study sought to determine if endogenous surfactant is altered in ARDS. Bronchoalveolar lavage was performed in patients at-risk to develop ARDS (AR, n = 20), with ARDS (A, n = 66) and in normal subjects (N, n = 29). The crude surfactant pellet was analyzed for total phospholipids (PL), individual phospholipids, SP-A, SP-B, and minimum surface tension (STmin). PL was decreased in both AR and A (3.48 +/- 0.61 and 2.47 +/- 0.40 mumol/ml, respectively) compared to N (7.99 +/- 0.60 mumol/ml). Phosphatidylcholine was decreased in A (62.64 +/- 2.20% PL) compared to N (76.27 +/- 2.05% PL). Phosphatidylglycerol was 11.58 +/- 1.21% PL in N and was decreased to 6.48 +/- 1.43% PL in A. SP-A was 123.64 +/- 20.66 micrograms/ml in N and was decreased to 49.28 +/- 21.68 micrograms/ml in AR and to 29.88 +/- 8.49 micrograms/ml in A. SP-B was 1.28 +/- 0.33 micrograms/ml in N and was decreased to 0.57 +/- 0.24 micrograms/ml in A. STmin was increased in AR (15.1 +/- 2.53 dyn/cm) and A (29.04 +/- 2.05 dyn/cm) compared to N (7.44 +/- 1.61 dyn/cm). These data demonstrate that the chemical composition and functional activity of surfactant is altered in ARDS. Several of these alterations also occur in AR, suggesting that these abnormalities occur early in the disease process.

Acute Disease↗

PubMed2002

Tumor necrosis factor-alpha and angiostatin are mediators of endothelial cytotoxicity in bronchoalveolar lavages of patients with acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is characterized by an extensive alveolar capillary leak, permitting contact between intra-alveolar factors and the endothelium. To investigate whether factors contained in the alveolar milieu induce cell death in human lung microvascular endothelial cells, we exposed these cells in vitro to bronchoalveolar lavage fluid (BALF) supernatants from control patients, patients at risk of developing ARDS, and patients with early- and late-phase ARDS. In contrast to BALF from control patients, a significant cytotoxicity was found in BALF from patients at risk of developing ARDS, with late-phase ARDS, and especially from patients with early-phase ARDS. Subsequently, we determined the levels of factors known to exert cytotoxicity in endothelial cells, i.e., tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1, and angiostatin. BALF from patients at risk of developing ARDS, with early-phase ARDS, and with late-phase ARDS, contained increased levels of TNF-alpha and angiostatin, but not of TGF-beta1, as compared with BALF from control patients. Whereas inhibition of TGF-beta1 had no effect in this setting, neutralization of TNF-alpha or angiostatin inhibited the cytotoxic activity on endothelial cells of part of the early-phase ARDS BALF. These results indicate that TNF-alpha and angiostatin may contribute to ARDS-related endothelial injury.

Acute Disease↗

PubMed1988

Activation of the contact system of plasma proteolysis in the adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) is a complex pulmonary clinicopathologic condition associated with pulmonary endothelial injury and blood coagulation activation. In patients with ARDS from all causes, factor VII levels were significantly reduced. Patients with ARDS caused by sepsis had more evidence of intravascular coagulation and fibrinolysis than did patients with trauma-related ARDS by having significantly (p less than or equal to 0.05) increased prothrombin times, activated partial thromboplastin times, and fibrin degradation products, and decreased antithrombin III concentration. We sought to determine whether the proteins of the contact system of plasma proteolysis (factor XII, prekallikrein, high molecular weight kininogen, and C1 inhibitor) were also activated after acute lung injury. Patients with ARDS caused by either trauma or sepsis had significantly (p less than or equal to 0.01) reduced factor XII levels, high molecular weight kininogen functional activity, prekallikrein activity, and prekallikrein antigen levels compared with controls. In both the sepsis-related and trauma-related ARDS groups, C1 inhibitor activity was significantly reduced but C1 inhibitor antigen levels were significantly elevated from control. These findings showed that the proteins of the contact system were more extensively activated in ARDS than were the proteins that contribute to later reactions in intravascular coagulation and fibrinolysis. Activation of the contact system proteins could be the result of endothelial injury occurring as part of ARDS. Intravascular coagulation and fibrinolysis in patients with ARDS also arise from components independent from contact system activation.

Blood Coagulation↗

PubMed2002

Direct hemoperfusion using a polymyxin B immobilized column improves acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is characterized by a high mortality rate. We have studied whether direct hemoperfusion using a polymyxin B immobilized fiber column (PMX-DHP) is effective for acute lung injury (ALI) and ARDS. Two ALI and eighteen ARDS patients were evaluated, four congestive heart failure (CHF) patients were evaluated as cardiogenic pulmonary edema, and we retrospectively compared the outcome with ten patients with ARDS who had been hospitalized between 1990 and 1998 as the untreated group. PMX-DHP was carried out twice at a rate of 80-100 ml/minute for 2 hours, with a time interval of approximately 24 hours. We monitored systolic blood pressure (BP), diastolic BP, and the PaO(2)/FIO(2) (PF) ratio before and after PMX-DHP treatment. The mortality was classified if patients were alive at day 30 after initiating PMX-DHP. The mortality of ARDS patients was approximately 20%. Systolic BP increased significantly from 106 +/- 20 to 135 +/- 21 and to 125 +/- 20 mmHg on the following day. Diastolic BP increased from 61 +/- 16 to 78 +/- 15, and to 72 +/- 12 mmHg. The PF ratio increased significantly from 125 +/- 54 to 153 +/- 73, and 163 +/- 78 Torr. CHF patients did not reveal improvement of systolic, diastolic BP, and PF ratio after PMX-DHP. Eight of ten patients in the untreated group died through exacerbated ARDS. In ARDS patients, PMX-DHP improved circulatory disturbance and oxygenation despite the underlying diseases. The mortality improved compared with that before induction of PMX-DHP.

Aged↗

PubMed2001

Cytokine balance in the lungs of patients with acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) involves an intense inflammatory response in the lungs, with accumulation of both pro- and antiinflammatory cytokines in bronchoalveolar lavage fluid (BALF). Our goal was to determine how the balance between pro- and antiinflammatory mediators in the lungs changes before and after the onset of ARDS. We identified 23 patients at risk for ARDS and 46 with established ARDS and performed serial bronchoalveolar lavage (BAL). We used immunoassays to measure tumor necrosis factor alpha (TNF-alpha) and soluble TNF-alpha receptors I and II; interleukin 1 beta (IL-1 beta), IL-1 beta receptor antagonist, and soluble IL-1 receptor II; IL-6 and soluble IL-6 receptor; and IL-10. We used sensitive bioassays to measure net TNF-alpha, IL-1 beta, and IL-6 activity. Although individual cytokines increased before and after onset of ARDS, greater increases occurred in cognate receptors and/or antagonists, so that molar ratios of agonists/antagonists declined dramatically at the onset of ARDS. The molar ratios remained low for 7 d or longer, limiting the activity of soluble IL-1 beta and TNF-alpha in the lungs at the onset of ARDS. This significant antiinflammatory response early in ARDS may provide a key mechanism for limiting the net inflammatory response in the lungs.

Adult↗

PubMed1998

A placebo-controlled randomized trial of antithrombin therapy in neonatal respiratory distress syndrome.

Neonatal respiratory distress syndrome (RDS) is associated with decreased plasma activity of antithrombin (AT) and increased formation of thrombin. We tested whether AT reduces thrombin formation, improves gas exchange, and decreases the duration of mechanical ventilation and supplemental oxygen. One hundred twenty-two infants were randomized to pasteurized AT concentrate or to placebo. Two ml/kg (equivalent to 100 IU AT/kg) were followed by 1 ml/kg (50 IU/kg) every 6 h for 48 h. Outcome measures included plasma AT activity, thrombin-AT (TAT) complex, prothrombin fragment (F1+2), the ratio of arterial to alveolar oxygen pressure [(a/A)PO2], and the ventilator efficiency index (VEI). In the AT group (n = 61), mean (SD) birth weight was 1,198 (301) g, mean (SD) gestational age (GA) was 28.3 (2.0) wk, 54% were male. In the placebo group (n = 61), mean (SD) birth weight was 1,201 (315) g, mean (SD) GA was 28.8 (2. 3) wk, 51% were male. In treated infants, AT activity was raised to means of 1.69 and 2.25 U/ml at 24 and 48 h, respectively. Corresponding means in control infants were 0.37 and 0.44 U/ml (p < 0.0001). F1+2, but not TAT, was significantly reduced by AT (p = 0. 004). VEI and (a/A)PO2 were similar in both groups throughout the first week of life. Median days receiving mechanical ventilation were 7.1 (AT) versus 4.8 (placebo), p = 0.0014. Median days receiving supplemental oxygen were 7.9 (AT) versus 5.5 (placebo), p < 0.0001. There were seven (11.5%) deaths in the AT group and three (4.9%) deaths in the placebo group. We conclude that treatment with AT cannot be recommended in premature infants with RDS.

Antithrombin III↗

PubMed1994

Antithrombin III deficiency in neonatal respiratory distress syndrome.

Neonatal respiratory distress syndrome (RDS) is an acute lung injury believed to result primarily from surfactant deficiency in the immature lung. Although surfactant replacement therapy has improved the outcome of this disease, RDS remains a major cause of neonatal mortality and morbidity. Preliminary experimental evidence suggests that unopposed intravascular thrombin activity may contribute to the progression of RDS by promoting high permeability pulmonary oedema and pulmonary hypertension. In the extravascular lung compartment, polymerizing fibrin may inhibit surfactant function. In addition, interstitial and alveolar thrombin formation and resulting fibrin deposition may contribute to the development of chronic lung disease through amplification of inflammation and fibrosis. There is good evidence that extravascular coagulation occurs during the course of RDS. Fibrin is a major component of the hyaline membranes, which are a hallmark of acute lung injury, and which can be regarded as locally produced clots. It has been less certain whether neonatal RDS is also associated with intravascular activation of the coagulation system. Although low levels of antithrombin III (AT III) have been reported in infants with RDS, direct evidence of increased intravascular thrombin formation has been lacking. However, recently, plasma concentrations of thrombin-antithrombin III (TAT) complexes have been measured in infants with RDS and correlated with RDS severity. TAT formation was significantly increased in severe neonatal RDS, while free AT III activity was decreased. These data are consistent with increased thrombin generation and resulting AT III consumption. Therefore, to regulate thrombin activity, infants with severe RDS may benefit from replacement therapy with AT III concentrate. This hypothesis has been strengthened by experiments that have demonstrated the efficacy of thrombin inhibition in several animal models of acute lung injury. However, controlled clinical trials will be required to determine whether thrombin is just a coincidental marker of neonatal RDS, or whether unopposed thrombin activity exacerbates the disease process.

Animals↗