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PubMedDate not supplied

[Possible use of serum calcitonin in septic patients at risk of acute respiratory distress syndrome].

The acute respiratory distress syndrome (ARDS) is a late complication in critically ill patients and its diagnosis is usually made when the syndrome is fully established. There is an increased interest in developing early markers that may help to identify ARDS in its initial stages. Calcitonin was recently reported as a useful serum marker to identify burned patients at risk for respiratory failure. We report a case with abdominal sepsis and ARDS, whose serum calcitonin level was 1000 pg/mL without other known clinical causes of hypercalcitoninemia and who died in multiorganic failure. The possible mechanisms of hypercalcitoninemia and its possible utility as marker of ARDS in critically ill patients is discussed.

Abscess↗

PubMed1987

Activation of the complement system in the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is an acute pulmonary disorder characterized by the accumulation of neutrophils within the lower respiratory tract. Because activation of the complement system can generate C5a, a potent neutrophil chemoattractant, complement activation was assessed in both serum and bronchoalveolar lavage fluid obtained from 10 patients with ARDS and compared with that from normal control subjects. Crossed immunoelectrophoresis was used to determine activation of the complement components C3 and properdin factor B (PFB), and radioimmunoassay was used to determine the presence of C5a. Complement activation was not detected either in the plasma or in the lung epithelial lining fluid of the control subjects. In contrast, evidence of C3 activation was found in the plasma of 50% of the patients with ARDS when initially studied; likewise, C3 activation, PFB activation, and C5a could all be detected in the epithelial lining fluid of all patients with ARDS with a single exception. Follow-up bronchoalveolar lavages revealed decreased amounts of C3 activation and C5a 2 to 7 days after the onset of ARDS, and the complement activation had resolved when the patients with ARDS had completely recovered. To determine if the C5a in bronchoalveolar lavage fluid could be responsible for the influx of neutrophils observed in ARDS, epithelial lining fluids obtained from both normal control subjects and from patients with ARDS were fractionated by molecular sieve chromatography. Two distinct fractions of chemotactic activity were found in the ARDS bronchoalveolar lavage fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Fluids↗

PubMed1987

A clinical study of the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a syndrome of diffuse lung injury with a high mortality rate. We evaluated retrospectively 35 adult patients with ARDS. Their overall mortality rate was 69% and was related to their age (32 +/- 14 yr in survivors and 54 +/- 15 yr in nonsurvivors; p less than .001) and to the number of complications during their illness (1.4 complications in survivors, 2.6 in nonsurvivors; p less than .005). The ARDS patients, due to an infectious etiology, incurred a 75% mortality rate, while those with a noninfectious etiology of ARDS had a 55% mortality rate (nonsignificant). Neither a simplified acute physiology score nor a respiratory failure severity index was significantly different between survivors and nonsurvivors on admission. The mean PEEP level on admission in survivors was 8.1 +/- 4.6 cm H2O and in nonsurvivors 3.7 +/- 3.9 cm H2O (p less than .025). We conclude that the age of the patients and superimposed multiple system organ failure are probably related with the still high mortality rate of this syndrome.

Acute Kidney Injury↗

PubMed2006

Infection in pediatric acute respiratory distress syndrome.

Pediatric acute respiratory distress syndrome (ARDS) is a severe lung injury caused by pneumonia, sepsis, and trauma. ARDS results from inflammation and pulmonary capillary leak causing major changes in lung architecture and function. It has a low incidence, but its severity and duration cause major morbidity, mortality, and use of resources. Any organism can cause ARDS. Susceptible populations develop the syndrome more often and have worse outcomes. Aggressive diagnosis and intensive treatment are essential to good outcomes in ARDS caused by infection. The prognosis for survival is good, but morbidity after the syndrome is a major burden.

Child↗

PubMed1990

The adult respiratory distress syndrome.

The adult respiratory distress syndrome remains an enigmatic disorder with a high mortality rate, although it can sometimes be managed effectively. Recognizing the conditions with which it is associated is the first step in preventing its occurrence. Decreasing the risk factors of developing ARDS remains the fundamental goal of initial management. Once the syndrome has developed in a particular patient, the clinician's goals in management are to stabilize the patient, avoid further insults, maximize the support therapies available, and be cognizant of and avoid the potential adverse effects of these supportive therapies.

Humans↗

PubMed1977

Current concepts of the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a sequel to pulmonary injury that may be direct, closed chest trauma or indirect, through air or vascular passages, aspiration, or fat embolization. An understanding of this syndrome is essential for the oral surgeon who not only manages severe maxillofacial injuries but is also a member of a trauma team that manages multisystem injuries. Emphasis on pathophysiologic pathways resulting in ARDS is presented with a discussion on oxygenation and ventilation abnormalities. Application of these guidelines will assist the oral surgeon in understanding the management of patients with this acute progressive syndrome.

Adrenal Cortex Hormones↗

PubMed1996

[Influence of surfactants on hemodynamics during neonatal respiratory distress syndrome].

The neonatal respiratory distress syndrome tends to delay the circulatory adaptation to extra-uterine life and leads to systematic hypotension. Haemodynamic changes following the instillation of surfactant are not stereotyped. They depend on the type of surfactant, the time of the instillation, the degree of prematurity, the severity of the respiratory disease and the mode of instillation. They are characterized by a transient haemodynamic instability with variable consequences on arterial pressure and systemic blood flow. The use of surfactant tends to decrease pulmonary arterial resistances and pulmonary arterial pressures but this effect is variable and is not obviously accompanied by long-term deleterious effect on the arterial duct. Haemodynamics and blood gases changes due to surfactant instillation have a variable effect on cerebral blood flow. The potential role of blood gas and haemodynamics changes on the occurrence of pulmonary haemorrhage or cerebral damage following instillation of surfactant remains poorly established but has to be taken into account.

Cerebrovascular Circulation↗

PubMed1996

Acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) is a serious and complex clinical problem that often threatens the lives of patients. Emerging clinical data suggest that the survival of patients with this disorder may have improved during the last two decades, presumably because of advances in supportive medical care. Among the supportive therapies used to treat patients with ARDS, none is more complex than mechanical ventilation. New strategies for administering mechanical ventilation to patients with ARDS may reduce the occurrence of iatrogenic volotrauma and oxygen toxicity, accounting in part for the recently observed improvements in patient survival. Prevention and cure of ARDS have remained elusive goals because of the lack of specific therapies directed against the known pathogenic factors. Ongoing investigations are aimed at identifying specific therapies to interrupt the mechanisms of inflammation and lung injury responsible for this syndrome. Until such therapies become available, clinicians caring for patients with ARDS should attempt to minimize additional morbidity and mortality resulting from nosocomial infections and iatrogenic injuries.

Humans↗

PubMed1982

Complications associated with the adult respiratory distress syndrome.

The adult respiratory distress syndrome is frequently fatal. Attempts to decrease mortality must include attention to pulmonary and extrapulmonary complications of this syndrome. Pulmonary complications include pulmonary emboli, barotrauma, fibrosis, and pneumonia. Mechanical ventilation, Swan-Ganz catheters, and tracheal intubation also result in pulmonary complications. Extrapulmonary complications such as gastrointestinal hemorrhage, renal failure, infection, and thrombocytopenia may increase mortality. The incidence of gastrointestinal hemorrhage can be reduced with prophylactic antacids. Likewise, the incidence of pulmonary emboli can be reduced with low dose heparin. Careful attention to patients' urine output, fluid, and electrolyte status as well as vigorous cardiovascular support are also essential to decrease renal complications. Early diagnosis, aggressive treatment, and prophylaxis of complications should increase survival.

Adult↗

PubMed1989

The adult respiratory distress syndrome.

The adult respiratory distress syndrome is a condition of life-threatening organ failure triggered by blood-borne factors and challenges which arrive via the airways. Vascular damage is a necessary, but often not sufficient criterion for ARDS, which is observed in an acute and chronic form. There is a consensus that neutrophils and their products contribute to the pathogenesis of the syndrome, and that lung vascular tone regulation and endothelial and epithelial cell permeability are affected in ARDS. Whereas the precise roles of individual mediators for the development of ARDS are still ill-defined, a synergism between lipid mediators and other injurious principles is recognized. Chronic ARDS is a proliferative disorder which may require different treatment strategies than acute ARDS. Specific treatment modalities which inhibit the interaction between activated neutrophils and the lung endothelium, and surfactant replacement might have a future as early therapy approaches.

Adult↗

PubMed1989

Immunoreactive interleukin-1 in bronchoalveolar lavage fluid of high-risk patients and patients with the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is characterized by increased neutrophils and macrophages in bronchoalveolar lavage (BAL) fluid. Interleukin-1 (IL-1), an inflammatory mediator produced by macrophages, has been shown to be chemotactic for neutrophils and to stimulate lymphocyte activation and proliferation of fibroblasts. BAL was performed in patients with ARDS, patients at high risk to develop ARDS, and in normal nonsmokers. After removal of cells and surfactant-complexed lipids by centrifugation, the remaining supernatant was concentrated by ultrafiltration utilizing membranes retaining substances greater than 5000 daltons. The concentrate was assayed for immunoreactive IL-1 beta by a radioimmunoassay method. Patients with ARDS (n = 9) had an IL-1 level of 184 +/- 67 pg/ml, high-risk patients (n = 9) had 172 +/- 62 pg/ml, and normals (n = 10) had 4 +/- 1 pg/ml. There was a significant (p less than or equal to .05) increase in IL-1 in the ARDS and risk groups compared to normals. IL-1 was detected in serum from patients with ARDS (n = 19), high risk (n = 19), and normals (n = 8), but no difference was noted among the three groups. BAL cell differentials revealed that neutrophils were increased (p less than .05) in both the ARDS (59 +/- 10%) and high-risk (65 +/- 8%) groups compared to normals (2 +/- 1%). There was a correlation (r = 0.64, p less than .001) between IL-1 levels and BAL protein concentration. BAL IL-1 levels were highest in patients with the fully developed syndrome but were also elevated in patients at high risk. The absence of significant amounts of IL-1 in serum suggests that it may be produced within the lung.

Adult↗

PubMed1982

A brief review of the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is seen with increasing frequency. It is associated with a variety of conditions even in the absence of preexisting pulmonary diseases. The treatment often includes intubation, using positive-end expiratory pressure (PEEP), and other ancillary support. The mortality rate is high, and physicians caring for such patients should be on guard for disseminated intravascular coagulation, gastrointestinal hemorrhage, and infection.

Adult↗

PubMed1997

Markers for predicting the development of acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) is a relatively common, inflammatory lung disorder that is associated with major morbidity and high mortality. The pathogenesis of ARDS is complex, and unfortunately, the development of ARDS in an individual patient is difficult to anticipate. In this chapter, we outline the rationale for why accurately predicting the development of ARDS would be valuable. We also review the accumulated data on approaches for predicting ARDS and discuss the potential difficulties in establishing predictive markers.

Biomarkers↗

PubMed1985

The adult respiratory distress syndrome.

The Adult Respiratory Distress Syndrome is a complication of many illnesses such as sepsis, pneumonia and trauma afflicting over 150,000 patients per year. While progress in intensive care medicine has increased the survival rates in many of these underlying illnesses, major obstacles remain in the successful therapy of ARDS. Animal and human investigations shed light on the pathophysiology of the illness that is allowing researchers to formulate promising new treatment strategies.

Adrenal Cortex Hormones↗

PubMed2006

Evaluation of serum cortisol levels in a relatively large and mature group of ventilated and nonventilated preterm infants with respiratory distress syndrome.

Severity of respiratory distress syndrome (RDS) and mechanical ventilation may affect the endogenous cortisol secretion in preterm infants. The aim of this study was to compare the serum cortisol concentrations of a relatively large and mature group of preterm infants with RDS who are ventilated or nonventilated and control preterm infants without RDS. Infants (group I) of comparable gestational ages without RDS served as controls. Infants with RDS who did not need ventilator support and surfactant therapy were considered to have mild RDS (group II). Those requiring mechanical ventilation and surfactant therapy were considered to have severe RDS (group III). Serum cortisol levels were determined after birth and on day 3 of life. The study groups consisted of 79 preterm infants with gestational ages ranging from 31 to 36 weeks, and birthweights ranging from 1086 to 1685 g. All preterm infants showed high cortisol levels after delivery regardless of respiratory distress (group I, n = 25, 34.1 +/- 10.7 microg/dL; group II, n = 23, 33.6 +/- 12.0 microg/dL; and group III, n = 31, 36.4 +/- 12.3 microg/dL). In group III, the cortisol levels (50.8 +/- 16.8 microg/dL) were higher than in group II (40.4 +/- 10.5 microg/dL) and in controls (22.0 +/- 7.2 microg/dL), and the cortisol levels of controls were lower than in group II on day 3 of life. Although the cortisol levels in severe and mild RDS infants increased significantly from their corresponding levels on day 1, they decreased in controls. The cortisol levels on day 3 of life were not significantly different in infants with poor outcome compared with infants with better outcome. Severity of RDS and mechanical ventilation were related to serum cortisol levels of preterm infants. Our study suggests that large and mature preterm infants who are ventilated and/or more severely ill release more cortisol than those less severely ill.

Birth Weight↗

PubMed2002

Association between increased levels of IL-2 and IL-15 and outcome in patients with early acute respiratory distress syndrome.

BACKGROUND: Acute respiratory distress syndrome remains a serious, often fatal, condition, despite progress in modern critical care treatment. Cytokines play an important role in the pathogenesis of the syndrome, although their role in the evolution and outcome has not been clearly elucidated. We explored whether the measurement of serum and bronchoalveolar lavage IL-2 and IL-15 at the time of hospital admission can predict the outcome of this syndrome. METHODS: Serum and bronchoalveolar lavage levels of IL-2 and IL-15 were measured in eight patients with ARDS (group A) and 26 patients on high risk for ARDS development who never developed ARDS (group B) from samples obtained at the time of admission. RESULTS: Serum IL-2 (P > 0.05) and IL-15 (P < 0.05) levels were higher in group A than in group B. Serum levels of both cytokines were higher in patients who did not survive in both of the groups A and B compared to those who survived (P < 0.05, and P < 0.0001, respectively). The only significant change in BALF was the higher level of IL-15 in surviving group A patients (P < 0.05) when compared with the non survivors of the same group. For a serum cut-off level of 173 pg mL(-1) for IL-2 and 250 pg mL(-1) for IL-15, they exhibited a very high positive predictive value (PPV), negative predictive value (NPV), sensitivity and specificity for survival (100% in all). A positive correlation was found between serum levels of both cytokines and APACHE II score (IL-2, r = 0.61, and IL-15, r = 0.62, respectively, and P < 0.0001 for both). CONCLUSION: Determination of serum IL-2 and IL-15 levels may be a valuable and simple aid to improve identification of patients with ARDS or at risk for ARDS who are at high risk of subsequent mortality.

APACHE↗

PubMed1993

Antilipid mediator and antioxidant therapy in adult respiratory distress syndrome.

The adult respiratory distress syndrome is now thought to be caused by or complicated by a variety of mediators for which potential antagonists exist. Lung dysfunction could be prevented by antagonists to metabolites of membrane phospholipids. Examples of such metabolites include thromboxane, prostacyclin, leukotrienes, and platelet-activating factor. Oxidant stress can also produce cytotoxicity through membrane lipid peroxidation, as evidenced by the generation of isoprostanes. N-acetylcysteine, by repletion of the endogenous antioxidant glutathione, may represent a novel approach to the therapy of acute lung injury.

Acetylcysteine↗

PubMedDate not supplied

The adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) represents a common denominator of acute lung injury leading to alveolar flooding, decreased lung compliance, and altered gas transport. In the absence of specific etiology and therapy, the management of ARDS remains largely supportive. Ubiquitous use of intermittent positive-pressure ventilation with positive end-expiratory pressure (PEEP) improves arterial oxygenation but with some risk of pulmonary barotrauma and decreased cardiac output. The recent understanding of lung inflation as a modulator of right heart afterload and the effect of the right ventricle on global cardiac performance continues to redefine optimal patterns of ventilatory and hemodynamic intervention in ARDS.

Capillary Permeability↗