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PubMed1982

[Adult respiratory distress syndrome in childhood].

Adult respiratory distress syndrome is becoming more frequent in pediatric age. There are several factors involved in its' etiology. Sepsis is almost invariably present in all patients. Basic mechanism is an increase of pulmonary capillary permeability with production of acute non cardiogenic oedema. The decrease in compliance and functional residual capacity produce a respiratory failure with hypoxemia non-responsive to the increase in FiO2. Pulmonary hypertension and low cardiac output appear once the syndrome has developed. In its' management, cardiorespiratory monitoring is essential. Prophylaxis is based on early treatment of the essential pathological process. Corticoids are only effective if they are administered before development of pulmonary oedema. The treatment is based on: a) Moderate water restriction. b) Early respiratory assistance using PEEP or CPAP. c) Maintenance of adequate oxygen transport. The extracorporeal oxygenation guarantees the oxygen exchange but it does not affect survival. Mortality is 95%. Patients who survive have minimal pulmonary sequelae.

Carbon Dioxide↗
PubMed2006

Mechanisms of acute lung injury/acute respiratory distress syndrome.

Acute lung injury/acute respiratory distress syndrome is a clinical syndrome that describes a single common end point: severe injury to the alveolar capillary membrane and the development of proteinaceous edema. Forty years of clinical and basic science research have elaborated many of the pathophysiologic mechanisms that link initiating insults to the development of alveolar membrane failure. A combination of genetics, comorbid conditions, inciting events, and factors yet to be discovered may uniquely alter the expression of these mechanisms in the individual patient.

Animals↗
PubMed1994

Effect of continuous negative extrathoracic pressure on respiratory mechanics and timing in infants recovering from neonatal respiratory distress syndrome.

Changes in respiratory mechanics and timing produced by continuous negative extrathoracic pressure (CNEP) of -0.6 kPa were assessed in 18 infants recovering from neonatal respiratory distress syndrome. The median gestational age was 28 wk (range 24-36 wk). All infants were recruited before discharge from neonatal intensive care and were measured at a median postnatal age of 58 d (range 10-127 d) and a median weight of 2.67 kg (range 1.99-3.77 kg). All had been treated for respiratory distress syndrome; 11 were diagnosed as having chronic lung disease. At the time of the study, all infants were stable breathing room air. There was a significant decrease of the respiratory rate in all but one infant from 63.6 +/- 10.0 to 49.3 +/- 9.1 breaths per min (mean +/- SD) during CNEP. This was predominantly due to a marked prolongation of the expiratory time. Passive respiratory mechanics were assessed using airway occlusion techniques. Whereas respiratory system compliance (Crs) did not change in the infants with a normal baseline measurement, there was a significant improvement of Crs in the 11 infants with low Crs values in atmosphere: In the latter, all of whom were very-low-birth-weight infants, Crs assessed by the multiple occlusion technique (mean +/- SD) corrected for body weight increased from 7.9 +/- 1.5 to 9.4 +/- 1.9 mL.kPa-1.kg-1 in CNEP (p = 0.012). There was no consistent change in respiratory system resistance in this population of 18 infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed2006

Brain atrophy and cognitive impairment in survivors of Acute Respiratory Distress Syndrome.

PRIMARY OBJECTIVES: Acute Respiratory Distress Syndrome (ARDS) is characterized by severe acute lung injury, hypoxemia and is associated with neurological and cognitive impairments. This study assessed quantitative brain and ventricular volumes in survivors of ARDS with brain computed tomography (CT) scans compared to normal controls. It also compared the medical and cognitive outcome data of patients with ARDS with and without CT scans. RESEARCH DESIGN: Observational cohort study. METHODS: Sixty-six consecutive acute respiratory distress patients, of which 15 patients with ARDS underwent brain CT and 51 patients had no brain imaging. Brain CT scans from 15 survivors of ARDS were compared to age- and sex-matched normal controls. Clinical radiological findings and ventricular volumes, brain volume and generalized brain atrophy. RESULTS: The patients with ARDS and brain imaging had cognitive impairments, significant brain atrophy, ventricular enlargement and 53% had atrophy or lesions by radiological report. CONCLUSIONS: Clinicians need to be aware that ARDS can cause significant long-term brain-related morbidity manifest by brain atrophy, lesions and neurocognitive impairments.

Acute Disease↗
PubMed2001

Implementation of a low tidal volume ventilation protocol for patients with acute lung injury or acute respiratory distress syndrome.

The ARDS (acute respiratory distress syndrome) Network study found 22% lower mortality in acute lung injury and ARDS patients ventilated with low tidal volumes (V(T)) than in those ventilated with traditional V(T) ventilation. Several points should be considered when using the low V(T) protocol for clinical practice. Prior to implementation, hemodynamic and acid-base status, minute ventilation, and adequacy of sedation should be assessed to minimize the potential for intolerance. The volume-preset, assist-control mode is recommended for better control of V(T), and the respiratory rate should be increased as V(T) is reduced, so as to maintain minute ventilation and prevent acute hypercapnia. When unavoidable, hypercapnia should be induced slowly. Ventilator inspiratory flow (V(I)) and trigger sensitivity settings should be optimized to limit the increase in work of breathing and dyspnea. When dyspnea results in double-triggered breaths, V(T) can be titrated to 7-8 mL/kg, provided end-inspiratory plateau pressure is < or = 30 cm H(2)O. In severe acidosis (pH < 7.15) V(T) also can be increased. However, every effort should be made to maintain plateau pressure and V(T) goals by buffering severe acidosis and treating patient-ventilator asynchrony with sedation. Evaluation for weaning should occur when adequate oxygenation can be maintained on 40% oxygen and a positive end-expiratory pressure of 8 cm H(2)O. Pressure support levels between 5 and 20 cm H(2)O (above 5 cm H(2)O positive end-expiratory pressure) are used for weaning and titrated to keep the respiratory rate < 35 breaths/min. Pressure support levels should be weaned aggressively, as long as the protocol's weaning tolerance criteria can be maintained.

Acute Disease↗
PubMed1993

Adult respiratory distress syndrome in children.

Adult respiratory distress syndrome or ARDS as coined by Ashbaugh et al in 1967, has been a great challenge in the field of critical care since then. It is a clinical entity which can be caused by various insults at any age. There have been several case reports of ARDS involving infants and children in the past 10 years, but pediatric ARDS is still not well recognized in Taiwan. A review of admissions to the pediatric intensive care unit in the past 2 years shows that 11 of the cases were included as pediatric ARDS combined with the expanded definition of Murray et al, and that each patient had an acute lung injury score greater than 2.5. Clinical manifestations also presented acute pulmonary distress indicating ARDS. The distribution of age ranged from 13 months to 11 years. The predisposing insults included sepsis, gastrointestinal bleeding with shock and massive blood transfusion, central nervous system infection, major trauma, near drowning, fulminant hepatitis and chemotherapy for acute leukemia. All received mechanical ventilatory support. The average peak inspiratory pressure was 46.7 +/- 6.4 cmH2O and the mean value of maximal PEEP used was 11.9 +/- 4.4 cmH2 O. Three patients developed barotrauma. Two patients survived and nine expired, a mortality rate of 82%. It is important for physicians caring for infants and children with respiratory failure to consider the diagnosis and initiate adequate ventilatory support and other resuscitation management.

Child↗
PubMed2000

Phenotypic characterization of alveolar monocyte recruitment in acute respiratory distress syndrome.

In 49 acute respiratory distress syndrome (ARDS) patients, the phenotype of alveolar macrophages (AMs) was analyzed by flow cytometry. Bronchoalveolar lavage (BAL) was performed within 24 h after intubation and on days 3-5, 9-12, and 18-21 of mechanical ventilation. The 27E10(high)/CD11b(high)/CD71(low)/ 25F9(low)/HLA DR(low)/RM3/1(low) AM population in the first BAL indicated extensive monocyte influx into the alveolar compartment. There was no evidence of increased local AM proliferation as assessed by nuclear Ki67 staining. Sequential BAL revealed two distinct patient groups. In one, a decrease in 27E10 and CD11b and an increase in CD71, 25F9, HLA DR, and RM3/1 suggested a reduction in monocyte influx and maturation of recruited cells into AMs, whereas the second group displayed sustained monocyte recruitment. In the first BAL from all patients, monocyte chemoattractant protein (MCP)-1 was increased, and AMs displayed elevated MCP-1 gene expression. In sequential BALs, a decrease in MCP-1 coincided with the disappearance of monocyte-like AMs, whereas persistent upregulation of MCP-1 paralleled ongoing monocyte influx. A highly significant correlation between BAL fluid MCP-1 concentration, the predominance of monocyte-like AMs, and the severity of respiratory failure was noted.

Adult↗
PubMed1996

Advances in conventional and innovative therapies for respiratory distress syndrome in children.

Adult respiratory distress syndrome is a phenomenon encountered by many pediatric critical care nurses. Care of these complex patients is multifaceted and requires an in-depth understanding of pathophysiology and therapeutic intervention. Several innovative treatments are now available as biomedical and technical advances have evolved. Outcomes will improve as clinicians improve patient selection, identify therapeutic endpoints, and risk/benefits. This article addresses the current understanding of pathophysiology, innovative treatments, and nursing care issues.

Age Factors↗
PubMed2002

Respiratory reovirus 1/L induction of diffuse alveolar damage: pulmonary fibrosis is not modulated by corticosteroids in acute respiratory distress syndrome in mice.

Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by diffuse alveolar damage (DAD) secondary to an intense host inflammatory response of the lung to a pulmonary or extrapulmonary infectious or noninfectious insult. We have previously described a unique animal model in which CBA/J mice infected with reovirus 1/L develop ARDS. This model recapitulates the histopathological changes observed in human ARDS, which consist of the overlapping phases of exudation, including the formation of hyaline membranes, regeneration, and healing via repair with fibrosis. In this report, we show that the development of DAD in the acute phase of the disease and intraalveolar fibrosis in the late phase of the disease was not modulated by treatment with methylprednisolone (MPS). In the presence or absence of MPS, the majority of cells infiltrating the lungs after reovirus 1/L infection were polymorphonuclear leukocytes and macrophages. A number of key proinflammatory and anti-inflammatory cytokines/chemokines that are observed in the BAL fluid of ARDS patients were also found in the lungs of mice after reovirus 1/L infection and were not modulated by MPS. These include interferon-gamma, interleukin-10, and monocyte chemoattractant protein. The histopathology, cytokine/chemokine expression, and response to corticosteroids in reovirus 1/L-induced ARDS are similar to what is observed in human patients, making this a clinically relevant model.

Animals↗
PubMed1983

Adult respiratory distress syndrome--a review.

Adult respiratory distress syndrome (ARDS) represents a common pathway of damage to the lungs by a wide variety of different agents. The important aetiological factors and mechanisms of lung injury are considered. Electron microscopic features as well as light microscopy are described. Factors that may modify the pathological picture are discussed. Probably the most important of these is oxygen. This gas is said to produce interstitial pulmonary fibrosis but this concept is once again questioned.

Bronchopneumonia↗
PubMedDate not supplied

Adult respiratory distress syndrome.

ARDS or acute respiratory distress syndrome continues to be a considerable critical care challenge. Mortality has not decreased significantly over the last more than 30 years. This article presents an overview of origin, evaluation, and treatment of ARDS. Recent findings relative to onset and precipitators of ARDS have led to changes in evaluation and treatment plans. Clinical and radiologic descriptors in assessment of the patient with ARDS are discussed. Ventilatory modes and nursing interventions to optimize patient outcomes are identified. The challenges of outcomes issues presented offer opportunities for further study.

Blood Gas Analysis↗
PubMed1999

Continuous dose furosemide as a therapeutic approach to acute respiratory distress syndrome (ARDS).

BACKGROUND: Acute respiratory distress syndrome (ARDS) is seen in a variety of clinical settings in critically ill patients. ARDS has been defined as a clinical syndrome characterized by progressive hypoxemia, tachypnea, and generalized patchy bilateral pulmonary infiltrates in the absence of cardiac failure. Furosemide has been shown to improve pulmonary gas exchange and intrapulmonary shunt in animal models of ARDS by preferential perfusion of nonedematous lung units. We hypothesized that continuous dose furosemide would improve lung injury during resuscitation from oleic acid-induced lung injury in canines. METHODS: Ten mongrel dogs were anesthetized and given intravenous oleic acid (0.1 mg/kg) to induce lung injury. Once lung injury was established (2 h) the control animals (n = 6) were continued on standard supportive therapy, and the study animals (n = 4) were started on continuous dose furosemide at 0.2 mg/kg/h. Cardiac filling pressures were maintained in all animals by infusion of isotonic saline solution. Data collected included lung injury score (LIS), cardiac index (CI), stroke volume index (SVI), pulmonary capillary wedge pressure (PCWP), urine output (UO), volume of resuscitation (VR), and pulmonary shunt fraction (Qs/Qt). Data were collected at baseline, established lung injury (2 h), and end of protocol (6 h). Data were compared between groups at various stages of the model using one-way analysis of variance with repeated measures. RESULTS: All 10 animals survived the protocol. There was no difference between the experimental and control groups at baseline or established lung injury (2 h) for CI, SVI, PCWP, or VR. There was a significant improvement in PO2/FIO2 and reduction of PEEP values in the furosemide group. There was also a statistically significant difference between experimental and control groups in LIS, Qs/Qt, and urine volumes. CONCLUSIONS: Continuous dose furosemide therapy improves LIS, PO2/FIO2, and Qs/Qt and decreases PEEP requirements in this oleic acid model of ARDS.

Animals↗
PubMed1981

Cesarean section indication and the risk of respiratory distress syndrome.

The frequency of respiratory distress syndrome (RDS) was assessed according to indications for delivery and the presence of antecedent labor among 236 newborns delivered by cesarean section. The presence of labor preceding cesarean section did not reduce the risk of RDS significantly, although a trend, not statistically significant, was noted in this direction. Of the delivery indications evaluated, only abruptio placentae appeared to be associated with an increased risk of RDS. However, prematurity was shown to be a possible confounding variable in this regard. These data suggest that the risk of RDS associated with cesarean section is related to the mode of delivery per se and not necessarily to any of the associated factors evaluated in this study.

Birth Weight↗
PubMed1997

[Current aspects of acute respiratory distress syndrome in children].

Acute respiratory distress syndrome (ARDS) is a frequent condition in pediatric intensive care units. The mortality remains high despite advances in conventional mechanical ventilation and aetiological treatment. Several animal studies have documented lung injury during mechanical ventilation with high tidal volume, and clinical investigations have shown that in human ARDS, most ventilation is distributed to the small areas of remaining aerated lung resulting in overdistension of these areas and lung injury ("baby lung" theory). Nevertheless the usefulness of extrapulmonary gas exchange remains much debated. New ventilatory strategies have been developed in order to reduce ventilator-induced lung injury and to improve systemic oxygenation but multicentric randomized clinical trials are needed before these strategies can be validated.

Acute Disease↗
PubMed1993

[The role of oxygen radicals in adult respiratory distress syndrome].

A traumatic adult respiratory distress syndrome (ARDS) model was made with 3 intravenous bolus of homologous bone marrow extract in rabbits. Variables were then measured including the metabolites of oxygen radicals in plasma and expired gases, serum lactic dehydrogenase (LDH) isoenzymes and plasma fibronectin (Fn). A two peak increase was found in expired ethane and plasma conjugated dienes following decrease of periphery white blood and polymorphonuclear neutrophil (PMN) differential count; continuous increase of serum LDH3 and severe descent of plasma Fn were also found after the trauma. The above results suggest that PMN releasing oxygen radicals play an important role in RDS pathogenesis; and expired ethane, circulating conjugated dienes, LDH3 and Fn may be useful for making diagnosis and prognosis assessment of ARDS.

Animals↗
PubMed1990

Acute respiratory distress syndrome (ARDS).

The acute respiratory distress syndrome (ARDS) is a common clinical catastrophe following acute lung injury. A multiplicity of clinical states can lead to ARDS. A new classification system has been proposed to deal with associated organ system failure and varying degrees of acute lung injury. ARDS is a permeability and inflammatory edema with damage and destruction at the air blood interface. Many cellular and humoral mediators probably attack the lung's surfactant system which in turn enhances edema formation. Supportive care with mechanical ventilation and positive end expiratory pressure results with the salvage of less than 50% of patients. Lung regeneration requires weeks or months to become complete in those who survive. Thus far no individual pharmacological agents have been shown to alter prognosis. Controlled clinical trials are required to evaluate new and older pharmacological agents alone or in combination, and surfactant replacement.

Humans↗
PubMed1999

Acute respiratory distress syndrome.

Outcome in acute respiratory distress syndrome (ARDS) is influenced by a number of factors, including the nature of the precipitating condition and the extent to which multiorgan failure ensues. Most studies of potential therapeutic interventions have been unsuccessful due to the enrollment of limited numbers of patients with a wide variety of pathologies of varying severity. Moreover, the value of initiating single-agent interventions at varying time points in what is an evolving and complex inflammatory process must be questioned. Mortality may therefore represent an inappropriate end-point for clinical trials, which are increasingly focusing on ventilator-free days. Despite these uncertainties, survival appears to be improving, possibly due to the application of supportive techniques in a protocol-driven fashion to patients in whom the underlying condition has been rigorously treated.

Clinical Trials as Topic↗