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PubMed1998

Maternal mortality associated with adult respiratory distress syndrome.

BACKGROUND: Pregnancy-related adult respiratory distress syndrome (ARDS) can lead to maternal mortality and morbidity. METHODS: Records of all pregnant patients diagnosed with ARDS over a 14-year period were reviewed and the cases were stratified into survivors and nonsurvivors. RESULTS: Forty-one cases were identified and 31 survived (maternal mortality rate of 24.4%). Adult respiratory distress syndrome was diagnosed in the antepartum period in 23 (56.1%) of the patients and the majority of these cases occurred in the third trimester (73.9%). There was no statistically significant difference in demographic characteristics, preexisting diseases, or probable precipitating cause for the development of ARDS between the two groups. The cause of death among the nonsurvivors included multisystem organ failure, sepsis, cardiac arrest, and disseminated intravascular coagulopathy. CONCLUSION: Pregnancy-related ARDS continues to be associated with a high maternal mortality rate (25%). Unfortunately, the etiology for ARDS during pregnancy is not predictive of maternal outcome.

Adolescent↗
PubMed2006

[Effects of macrophage migration inhibitory factor in pathogenesis of acute respiratory distress syndrome in children].

OBJECTIVE: Acute respiratory distress syndrome (ARDS) is usually diagnosed on the basis of clinical manifestations. However, a sensitive and effective biochemical index is important for early diagnosis of ARDS. It has been confirmed that macrophage migration inhibitory factor (MIF) expression is increased in patients with ARDS (adults and children). The present study aimed to investigate the expression and pathogenic role of MIF in children with ARDS by determining the serum level of MIF and expression of MIF in lung tissues. METHODS: Totally 18 children with ARDS, who were diagnosed in the department of pediatrics, the People's Hospital of Nanhai District, and 8 healthy children (control) were enrolled into the study. The serum level of MIF in ARDS children and normal children were measured by using enzyme-linked immunosorbent assay (ELISA). Peripheral blood mononuclear cell (PBMC) MIF expression was determined by flow-cytometry. The expression of MIF mRNA and protein in lung tissues were detected by using double-staining immunohistochemistry and in situ hybridization. RESULTS: (1) The serum level of MIF and PBMC MIF expression were (2040 +/- 146) microg/L and (8.98 +/- 2.76)%, respectively in ARDS children, which were significantly higher than those in the healthy children [(53 +/- 31) microg/L and (0.97 +/- 0.28)%, (P < 0.01)]. (2) In situ hybridization and immunohistochemistry showed that the number of KP(1)(+) cells and the percentages of MIF(+) expressed cells and MIF mRNA expressed cells were (229 +/- 87)/mm(2), (31.4 +/- 7.8)% and (34.71 +/- 8.91)%, respectively in the bronchoalveolar lavage fluid of ARDS children, which were significantly higher than those in the healthy children [(11 +/- 6)/mm(2), (1.9 +/- 0.8)% and (1.17 +/- 0.16)%, P < 0.01)]. (3) The number of KP(1)(+) cells and the percentages of MIF(+) expressed cells and MIF mRNA expressed cells were (319 +/- 129)/mm(2), (41.7 +/- 11.6)% and (45.13 +/- 13.2)% in ARDS lungs interstitium, which were significantly higher than those in the healthy children [(11 +/- 6)/mm(2), (1.9 +/- 0.8)% and (1.40 +/- 0.25)%, (P < 0.01)]. CONCLUSIONS: The level of MIF increased in serum and lung interstitium in ARDS children. Macrophage infiltration was demonstrated in lung interstitium and bronchoalveolar lavage fluid of ARDS children, MIF was expressed and significantly associated with the number of macrophage, which suggest that MIF plays an important role in the pathogenesis of ARDS. The level of MIF expression and macrophage infiltration can be regarded as a sensitive and effective biochemical index in the early diagnosis of ARDS.

Biomarkers↗
PubMed1989

Surfactant replacement therapy: impact on hospital charges for premature infants with respiratory distress syndrome.

Surfactant replacement therapy for neonatal respiratory distress syndrome has the potential to reduce morbidity and mortality of very premature infants. To investigate whether surfactant replacement therapy will also reduce hospital charges for these infants, we compared the hospital charges incurred by a group of patients treated with surfactant with charges of control patients. Mortality in the surfactant-treated group (8%) was significantly decreased compared with the control patients (29%). Average daily hospital charges in the surfactant-treated patients were 25% less than for the control patients. Most of the savings in daily hospital charges were due to a 52% reduction in daily charges for laboratory, x-ray, respiratory therapy, and other ancillary services. Similarly, ancillary charges for the first full week of hospitalization were significantly reduced by $1,883 for patients who received surfactant therapy. Analysis of the charges for the entire hospitalization revealed that surfactant-treated patients had a significantly smaller proportion of their charges that resulted from ancillary services and an increased proportion due to room charges. The average total hospital charges for the two groups were similar, but the total hospital charges to produce a surviving infant were $18,500 less in the surfactant-treated group than the charges to produce a survivor from the control group. It is likely that, in addition to a reduction in neonatal mortality and morbidity from respiratory distress syndrome, surfactant replacement therapy may also significantly reduce charges for ancillary services for these patients. In this way, surfactant therapy may be cost-effective by improving survival without increasing overall hospital costs.

Economics, Hospital↗
PubMed1999

Pressure limited ventilation with permissive hypoxia and nitric oxide in the treatment of adult respiratory distress syndrome.

In the management of adult respiratory distress syndrome pressure limited mechanical ventilation may protect the lungs from overdistention injury. Unacceptable hypoxia may be avoided by adding nitric oxide to the inspiratory gas, and thus make pressure limited ventilation easier to perform. There exists no consensus about an acceptable lower limit of SaO2, and in the present case we gave preference to pressure limitation at the cost of oxygenation. A young woman with severe adult respiratory distress syndrome was set on pressure limited mechanical ventilation with peak pressures of 35-38 cm H2O, PEEP of 10-12 cm H2O, and FiO2 of 0.95 with 20 ppm nitric oxide. SaO2 varied between 75 and 85%, and cardiac output ranged between 5.2 and 7.5 L min-1. Oxygen consumption was in the upper normal range, and she did not became acidotic. After 3 days, she started to improve. In conclusion, it seems that hypoxia might be well tolerated as long as the circulation is not compromised. It might prove beneficial to accept some hypoxia to avoid ventilator induced lung damage.

Adult↗
PubMed2003

One-year outcomes in survivors of the acute respiratory distress syndrome.

BACKGROUND: As more patients survive the acute respiratory distress syndrome, an understanding of the long-term outcomes of this condition is needed. METHODS: We evaluated 109 survivors of the acute respiratory distress syndrome 3, 6, and 12 months after discharge from the intensive care unit. At each visit, patients were interviewed and underwent a physical examination, pulmonary-function testing, a six-minute-walk test, and a quality-of-life evaluation. RESULTS: Patients who survived the acute respiratory distress syndrome were young (median age, 45 years) and severely ill (median Acute Physiology, Age, and Chronic Health Evaluation score, 23) and had a long stay in the intensive care unit (median, 25 days). Patients had lost 18 percent of their base-line body weight by the time they were discharged from the intensive care unit and stated that muscle weakness and fatigue were the reasons for their functional limitation. Lung volume and spirometric measurements were normal by 6 months, but carbon monoxide diffusion capacity remained low throughout the 12-month follow-up. No patients required supplemental oxygen at 12 months, but 6 percent of patients had arterial oxygen saturation values below 88 percent during exercise. The median score for the physical role domain of the Medical Outcomes Study 36-item Short-Form General Health Survey (a health-related quality-of-life measure) increased from 0 at 3 months to 25 at 12 months (score in the normal population, 84). The distance walked in six minutes increased from a median of 281 m at 3 months to 422 m at 12 months; all values were lower than predicted. The absence of systemic corticosteroid treatment, the absence of illness acquired during the intensive care unit stay, and rapid resolution of lung injury and multiorgan dysfunction were associated with better functional status during the one-year follow-up. CONCLUSIONS: Survivors of the acute respiratory distress syndrome have persistent functional disability one year after discharge from the intensive care unit. Most patients have extrapulmonary conditions, with muscle wasting and weakness being most prominent.

APACHE↗
PubMed2005

Effects of high versus low positive end-expiratory pressures in acute respiratory distress syndrome.

A recent study by the Acute Respiratory Distress Syndrome Network compared the traditional lower end-expiratory pressure strategy with a higher end-expiratory pressure strategy in patients with the acute respiratory distress syndrome ventilated with low tidal volumes. Clinical outcomes were similar whether lower or higher positive end-expiratory pressure (PEEP) levels were used. We applied both the lower (9 +/- 2 cm H2O) and higher (16 +/- 1 cm H2O) PEEP strategy in 19 patients. In nine recruiters, the higher end-expiratory pressure strategy resulted in significant alveolar recruitment (587 +/- 158 ml), improvement in arterial oxygen partial pressure/inspired oxygen fraction ratio (from 150 +/- 36 to 396 +/- 138), and reduction in static lung elastance (from 23 +/- 3 to 20 +/- 2 cm H2O/L). In 10 nonrecruiters, alveolar recruitment was minimal, oxygenation did not improve, and static lung elastance significantly increased (from 26 +/- 5 to 28 +/- 6 cm H2O/L). The increase in oxygenation, the reduction in static lung elastance, and the shape of the volume-pressure curve during the lower PEEP strategy were independently associated with alveolar recruitment. In conclusion, the protocol proposed by the Acute Respiratory Distress Syndrome Network, lacking solid physiologic basis, frequently fails to induce alveolar recruitment and may increase the risk of alveolar overinflation.

Adult↗
PubMed1992

[The effects of prostacyclin on oxygen transport in adult respiratory distress syndrome].

BACKGROUND: Patients with the adult respiratory distress syndrome (ARDS) present a deficit of tissue oxygenation which may be unmasked if increases in oxygen uptake (VO2) are observed when increases in oxygen delivery (DO2) are induced. Prostacyclin is a drug to which microvasodilator effects have been attributed and it has been proposed as an efficient agent for increasing histic enhancement of oxygen. METHODS: An infusion of prostacyclin was administered to 13 patients diagnosed with ARDS at doses of 10, 20, and 30 ng/kg per minute monitored with a Swan-Gatz catheter. RESULTS: The values are expressed as the percentage median of the increase with p less than 0.05 being considered as statistically significant. Prostacyclin significantly increased DO2 (10, 18 and 15% at the different doses). The VO2 rose significantly only following the first dose (13%). There was a correlation between the increase of DO2 and that of VO2 following the administration of the first dose (r = 0.70, p = 0.017. An important systemic vasodilator and pulmonary effect was observed accompanied by increases in the pulmonary (20, 56 and 59%) and reductions of PaO2 (-33.5, -40 and -48%) which may have been due to inhibition of hypoxic vasoconstriction. CONCLUSIONS: Prostacyclin is efficient for unmasking a lack of oxygen in patients with adult respiratory distress syndrome. The deleterious effects of this drug on systemic hemodynamics and on gaseous interchange makes not only the monitorization of arterial pressure but also of the parameters of gaseous interchanges necessary in these patients.

Adult↗
PubMedDate not supplied

Nitrovasodilator therapy for severe respiratory distress syndrome.

Improved gas exchange in infants with severe respiratory distress syndrome has been reported in association with infusion of nitroprusside and during inhalation of nitric oxide. To evaluate the association between nitrovasodilator therapy and clinical improvement in premature neonates with severe respiratory distress syndrome, we reviewed the courses of 22 infants with severe respiratory distress syndrome who were treated with sodium nitroprusside for at least 24 hours. These infants had birth weights of 2049 +/- 828 gm (range 720 to 3430 gm), gestational ages of 32.5 +/- 3.5 weeks (range 25 to 38 weeks), high ventilator settings before treatment (FIO2 of 100%, peak inspiratory pressures of 37.8 +/- 6.1 cm H2O [range 30 to 50 cm H2O], and mean airway pressures of 18.0 +/- 3.3 cm H2O [range 12.3 to 26 cm H2O]), and low pretreatment PaO2 of 49.3 +/- 9.4 mm Hg (range 27 to 69 mm Hg). Baseline oxygenation indexes were 39.4 +/- 12.1 (range 18.6 to 66.7). Nitroprusside infusion was temporally associated with increased PaO2, decreased PaCO2, and reduced oxygenation index. Potentially beneficial changes were inconsistent in infants with pulmonary interstitial emphysema and were greatest in infants treated with end-expiratory pressures of at least 4 cm H2O. These observations provide a basis for the hypothesis that nitrovasodilator therapy produces improvement in gas exchange in premature infants with severe respiratory distress syndrome.

Humans↗
PubMed2005

Umbilical cord blood and neonatal endothelin-1 levels in preterm newborns with and without respiratory distress syndrome.

Increased pulmonary vascular resistance in preterm newborn infants with respiratory distress syndrome is suggested, and endothelin-1 plays an important role in pulmonary vascular reactivity in newborns. We determined umbilical cord blood and neonatal (second sample) levels of endothelin-1 in 18 preterm newborns with respiratory distress syndrome who had no clinical or echocardiographic diagnosis of pulmonary hypertension and 22 without respiratory distress syndrome (gestational ages: 31.4 +/- 1.6 and 29.3 +/- 2.3 weeks, respectively). Umbilical cord blood and a second blood sample taken 18 to 40 h after birth were used for endothelin-1 determination by enzyme immunoassay. Median umbilical cord blood endothelin-1 levels were similar in both groups (control: 10.9 and respiratory distress syndrome: 11.4 pg/mL) and were significantly higher than in the second sample (control: 1.7 pg/mL and respiratory distress syndrome: 3.5 pg/mL, P < 0.001 for both groups). Median endothelin-1 levels in the second sample were significantly higher in children with respiratory distress syndrome than in control infants (P < 0.001). There were significant positive correlations between second sample endothelin-1 and Score for Neonatal Acute Physiology and Perinatal Extension II (r = 0.36, P = 0.02), and duration of mechanical ventilation (r = 0.64, P = 0.02). A slower decline of endothelin-1 from birth to 40 h of life was observed in newborns with respiratory distress syndrome when compared to controls. A significant correlation between neonatal endothelin-1 levels and some illness-severity signs suggests that endothelin-1 plays a role in the natural course of respiratory distress syndrome in preterm newborns.

Analysis of Variance↗
PubMed1998

The relation of pneumothorax and other air leaks to mortality in the acute respiratory distress syndrome.

BACKGROUND: In patients with the acute respiratory distress syndrome, pneumothorax and other air leaks - any extrusion of air outside the tracheobronchial tree - have been attributed to high ventilatory pressures or volumes and linked to increased mortality. METHODS: We analyzed data from a prospective trial of aerosolized synthetic surfactant in 725 patients with the acute respiratory distress syndrome induced by sepsis. We compared the ventilatory pressures and volumes in the patients without any air leaks (the highest values during the five-day study) with the pressures and volumes in those with pneumothorax or with any air leaks (the highest values during the 16- and 24-hour periods before the complication developed). RESULTS: Fifty patients (6.9 percent) had pneumothorax and 77 (10.6 percent) had pneumothorax or other air leaks. There were no significant differences between patients with air leaks and those without air leaks in any pressure or volume examined. Overall mortality at 30 days was 40.0 percent (95 percent confidence interval, 36.4 to 43.6); among the patients with pneumothorax, it was 46.0 percent (95 percent confidence interval, 32.2 to 59.8), and among those without pneumothorax, it was 39.3 percent (95 percent confidence interval, 35.6 to 43.0; P=0.35). The mortality rate was 45.5 percent (95 percent confidence interval, 34.4 to 56.6) in the group with any air leaks and 39.0 percent (95 percent confidence interval, 35.3 to 42.8) in the group without air leaks (P=0.28). CONCLUSIONS: In patients with sepsis-induced acute respiratory distress syndrome who were receiving mechanical ventilation with conventional pressures and volumes, there were no significant correlations between high ventilatory pressures or volumes and the development of pneumothorax or other air leaks. Pneumothorax or other air leaks were not associated with a significantly increased mortality rate.

Adult↗
PubMed2004

Partial liquid ventilation for preventing death and morbidity in adults with acute lung injury and acute respiratory distress syndrome.

BACKGROUND: Acute lung injury (ALI), and acute respiratory distress syndrome (ARDS), are syndromes of severe respiratory failure. Adults with ALI or ARDS have high mortality and significant morbidity. Partial liquid ventilation (PLV) may be better (i.e., cause less lung damage) for these patients than other forms of respiratory support. Uncontrolled studies in adults have shown improvement in gas exchange and lung compliance with partial liquid ventilation. OBJECTIVES: To assess whether partial liquid ventilation reduces morbidity and mortality in adults with ALI or ARDS. SEARCH STRATEGY: We searched The Cochrane Central Register of Controlled Trials (CENTRAL), The Cochrane Library Issue 2, 2004; MEDLINE (1966 to May 2004); and CINAHL (1982 to May 2004); intensive care journals and conference proceedings; reference lists and unpublished literature. SELECTION CRITERIA: Randomized controlled trials which compared partial liquid ventilation with other forms of ventilation, in adults (16 years old or greater) with ALI or ARDS, reporting one or more of the following: mortality; duration of mechanical ventilation, respiratory support, oxygen therapy, stay in the intensive care unit, or stay in hospital; infection; long term cognitive impairment or health related quality of life; long term lung function; or cost. DATA COLLECTION AND ANALYSIS: Two reviewers independently evaluated the quality of the relevant studies and extracted the data from the included studies. MAIN RESULTS: Problems with the inadequacy of the primary report of the one included study do not allow us to report any quantitative results for patients with ALI or ARDS. The only outcome we considered to be of clinical significance and reported for all enrolled patients (i.e., patients with ALI and ARDS and less severe respiratory insufficiency) was 28 day mortality. There was no statistically significant difference between groups for this outcome with a relative risk for 28 day mortality in the PLV group of 1.15 (95% confidence intervals of 0.64 to 2.10). REVIEWERS' CONCLUSIONS: There is no evidence from randomized controlled trials to support or refute the use of partial liquid ventilation in adults with ALI or ARDS; adequately powered, high quality randomized controlled trials are still needed to assess its efficacy. Clinically relevant outcome measures should be assessed (especially mortality at discharge and later, duration of respiratory support and hospital stay, and long term cognitive and quality of life outcomes) and the studies should be published in full.

Adult↗
PubMed2005

Sequential cardiac troponin T following delivery and its relationship with myocardial performance in neonates with respiratory distress syndrome.

We measured serial cardiac troponin T in babies with respiratory distress syndrome and in "healthy" controls (no cardiorespiratory support required). We investigated relationships between cardiac troponin T and myocardial performance in respiratory distress syndrome. This was a prospective observational study at a large tertiary maternity unit that recruited 104 "healthy" babies from whom individual samples were collected. A further 24 infants with respiratory distress syndrome and 14 "healthy" preterm infants had serial sampling over the first three days. We measured fractional shortening in 14 of the infants with respiratory distress syndrome. Cardiac troponin T rose from a median (interquartile range) of 10 (10-11) pg/mL on day one to 34 (22-46) pg/mL by day three, p=0.005, in "healthy" babies. In respiratory distress syndrome levels were higher, 91 (46-135) pg/mL at 6 (5-7) hours of age, p<0.001, and remained so for all three days. In babies with respiratory distress syndrome on day one cardiac troponin T correlated negatively with fractional shortening, Rho=-0.831, p<0.001, but this correlation did not persist. In "healthy" babies there is a minimal rise of cardiac troponin T by day 3. In respiratory distress syndrome there is an early and sustained elevation of cardiac troponin T, with a negative relationship with fraction shortening, suggesting significant myocardial damage of antenatal/intrapartum origin, giving rise to measurable dysfunction.

Cardiotonic Agents↗
PubMed2003

[Management of the acute respiratory distress syndrome].

OBJECTIVE: To review the current support and treatment strategies of the acute respiratory distress syndrome. DATA SOURCES: Original data from our research laboratory and from representative scientific articles on acute respiratory distress syndrome and acute lung Injury searched through Medline. SUMMARY OF THE FINDINGS: Despite advances in the understanding of the pathogenesis of acute respiratory distress syndrome, this syndrome still results in significant morbidity and mortality. Mechanical ventilation, the main therapeutic modality for acute respiratory distress syndrome, is no longer considered simply a support modality, but a therapy capable of influencing the course of the disease. New ventilation strategies, such as high-frequency oscillatory ventilation appear to be promising. This text reviews the current knowledge of acute respiratory distress syndrome management, including conventional and non-conventional ventilation, the use of surfactant, nitric oxide, modulators of inflammation, extracorporeal membrane oxygenation and prone position. CONCLUSIONS: The last decade was marked by significant advances, such as the concept of protective ventilation for acute respiratory distress syndrome. The benefit of alternative strategies, such as high-frequency oscillatory ventilation, the use of surfactant and immunomodulators continue to be the target of study.

Adrenal Cortex Hormones↗
PubMed2001

Ventilator-induced lung injury and the evolution of lung-protective strategies in acute respiratory distress syndrome.

Traditional ventilator management of acute respiratory distress syndrome (ARDS), emphasizing normalization of blood gases, promoted high rates of conventional barotrauma. Research revealed a broader range of ventilator-induced lung injury, physiologically and histopathologically indistinguishable from ARDS itself. It is now known that overdistention and cyclic inflation of injured lung can exacerbate lung injury and probably promote systemic inflammation, effects minimized by low tidal volumes/plateau pressures and by application of positive end-expiratory pressure. No compelling data suggest a safe interval for nonprotective ventilation in humans; historically defined "low" tidal volumes may remain excessive for certain patients. Protective ventilation, however, entails carbon dioxide accumulation ("permissive hypercapnia"). Despite extensive study, debate remains, even over whether consequent respiratory acidosis is harmful, tolerable with physiologic adaptation, or intrinsically adaptive. Its gross systemic effects seem generally tolerated by critically ill patients; however, subsets, including those with ischemic heart disease, left or right heart failure, pulmonary hypertension, or cranial injury, may be at higher risk. In controlled trials demonstrating mortality benefit from lung-protective ventilation, acidosis was more tightly controlled than in negative studies. Decreased acidosis-associated dyspnea probably explains reduced use of sedatives and paralytics noted in those trials. There may thus be disparate goals in ARDS management: rapid institution of a restrictive ventilatory strategy, and avoidance of significant acidosis. We review data pertaining to ARDS physiology, ventilator-induced lung injury, lung-protective ventilatory strategies, and the physiology of respiratory acidosis. Tracheal gas insufflation is considered as a means to reconcile the clinical goals of ventilatory reduction and control of acidosis.

Acidosis, Respiratory↗
PubMed2001

Lung collapse during low tidal volume ventilation in acute respiratory distress syndrome.

BACKGROUND: Current ventilator management for acute respiratory distress syndrome (ARDS) incorporates low tidal volume (V(T)) ventilation in order to limit ventilator-induced lung injury. Low V(T) ventilation in supine patients, without the use of intermittent hyperinflations, may cause small airway closure, progressive atelectasis, and secretion retention. Use of high positive end-expiratory pressure (PEEP) levels with low V(T) ventilation may not counter this effect, because regional differences in intra-abdominal hydrostatic pressure may diminish the volume-stabilizing effects of PEEP. CASE SUMMARY: A 35-year-old man with abdominal compartment syndrome (intra-abdominal pressure > 48 cm H2O developed ARDS and was treated with V(T) of 4.5 mL/kg and PEEP of 20 cm H2O. Despite aggressive fluid therapy, appropriate airway humidification and tracheal suctioning, the patient developed complete bronchial obstruction, involving the entire right lung and left upper lobe. After bronchoscopy the patient was placed on a higher V(T) (7.0 mL/kg). Intermittent PEEP was instituted at 30 cm H2O for 2 breaths every 3 minutes. This intermittently raised the end-inspiratory plateau pressure from 38 cm H2O to 50 cm H2O. With the same airway humidity and tracheal suctioning practices bronchial obstruction did not reoccur. CONCLUSION: Low V(T) ventilation in ARDS may increase the risk of small airway closure and retained secretions. This adverse effect highlights the importance of pulmonary hygiene measures in ARDS during lung-protective ventilation.

Adult↗
PubMed1999

Ventilatory support in the acute respiratory distress syndrome.

Ventilatory support in the acute respiratory distress syndrome (ARDS) has undergone considerable transformation in the 1990s. Current approaches include lung protective techniques which, while attempting to recruit and maintain lung volume, limit the shear stresses associated with ventilation by avoiding both alveolar overdistension and cyclical end-expiratory collapse. In addition, gas exchange targets have been liberalized and ventilatory conduct is much more tailored to individual pulmonary mechanics. Assessment of the inspiratory volume-pressure (V-P) curve provides information which can direct ventilator settings. Recent information from clinical trials has provided new insights into appropriate ventilatory modification and set the foundation for future clinical investigations.

Humans↗
PubMed2004

Prone positioning in the patient who has acute respiratory distress syndrome: the art and science.

Acute respiratory distress syndrome (ARDS) remains a significant contributor to the morbidity and mortality of patients in the ICU. A variety of treatments are used to support the lung of the patient who has ARDS and improve gas exchange during the acute injury phase. It seems, however, that the simple, safe, and noninvasive act of prone positioning of the critically ill patient who has ARDS may improve gas exchange while preventing potential complications of high positive end-expiratory pressure, volutrauma, and oxygen toxicity. This article provides the critical care nurse with the physiologic rationale for use of the prone position, indications and contraindications for use, safe strategies for prone positioning, and care techniques and monitoring methods of the patient who is in the prone position.

Critical Care↗
PubMed1997

Acute respiratory distress syndrome in children.

The adult (acute) respiratory distress syndrome is a significant cause of morbidity in children. The mortality rates remain elevated, greater than 50%, and even greater than 80% in patients with underlying malignancies. The therapeutic interventions remain mainly supportive. Strategies of conventional mechanical ventilation are directed toward the use of high positive end-expiratory pressures, low positive inspiratory pressure, and permissive hypercapnia. High-frequency oscillatory ventilation and tracheal insufflation are not yet used extensively, although they should contribute to less aggressive ventilation. Surfactant replacement, nitric oxide inhalation, and partial liquid ventilation seem to be promising technologies, but controlled clinical studies are necessary before their wide-spread use. Extracorporeal membrane oxygenation remains the alternative technology in case of failure of conventional support.

Animals↗