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Adult respiratory distress syndrome after cardiac surgery.

Adult respiratory distress syndrome, characterized by high permeability pulmonary oedema caused by endothelial cell damage, resulting in refractory hypoxemia, has a very high mortality. Cardiopulmonary bypass is said to be responsible for the development of adult respiratory distress syndrome after cardiac surgery. The present study was performed in order to identify predicting and aetiological factors of adult respiratory distress syndrome and multiple organ failure after cardiac surgery. Between January 1984 and December 1993, 3848 patients underwent cardiac surgery with cardiopulmonary bypass in the authors' institution, and were analysed in a retrospective manner. The operations performed were 3444 coronary artery bypass grafts (CABG), 267 valve and 137 combined (CABG + valve) procedures. The incidence of adult respiratory distress syndrome was 1.0% (38 of 3848) with an overall mortality rate of 68.4% (26 patients); 24 of these died from multiple organ failure. Multivariate regression analysis identified hypertension, current smoking, emergency surgery, preoperative New York Heart Association (NYHA) class 3 and 4, low postoperative cardiac output and left ventricular ejection fraction < 40% as significant, independent predictors for adult respiratory distress syndrome. Combined cardiac surgery and diffuse coronary disease were also significant predictors; cardiopulmonary bypass time was not. Thirty-six of the 38 patients that later developed adult respiratory distress syndrome had low postoperative cardiac output, 12 requiring intra-aortic balloon pump support. The remaining two had severe hypotension caused by postoperative bleeding. Twenty-six adult respiratory two had severe hypotension caused by postoperative bleeding. Twenty-six adult respiratory distress syndrome patients (68%) had confirmed gastrointestinal complication (e.g. intestinal ischaemia). Adult respiratory distress syndrome is a rare complication after cardiac surgery but is associated with a very high mortality. Preoperative predictors were identified. Cardiopulmonary bypass alone was not found to be an important factor. Postoperative low cardiac output leading to splanchnic hypoperfusion may be the most important single factor in developing adult respiratory distress syndrome after cardiac surgery.

Adult↗

Maternal alcohol ingestion and the incidence of respiratory distress syndrome.

The risk of respiratory distress syndrome in infants born to mothers with varying quantities of alcohol intake during pregnancy was assessed. In infants less than 37 weeks' gestation, there was a decreasing incidence of respiratory distress syndrome with increasing maternal alcohol consumption (p less than 0.02). In addition, in infants less than 37 weeks' gestation, maternal alcohol ingestion was associated with a decreased risk of respiratory distress syndrome even when adjusted for other factors such as smoking, gestational age, birth weight, Apgar score, and sex of the infant. It is suggested that maternal alcohol ingestion enhances the maturation of the fetal lung.

Alcohol Drinking↗

Distinguishing hantavirus pulmonary syndrome from acute respiratory distress syndrome by chest radiography: are there different radiographic manifestations of increased alveolar permeability?

Hantavirus infection may cause diffuse air space disease, termed hantavirus pulmonary syndrome (HPS). The authors sought to determine if chest radiographs could differentiate HPS from typical acute respiratory distress syndrome (ARDS). The authors identified patients with either HPS (n = 11) or acute ARDS (n = 32) and selected the earliest chest radiograph showing diffuse airspace disease, and a chest radiograph taken 24 to 48 hours previously. Thoracic and general radiologists first viewed the chest radiograph showing diffuse air space disease, and ranked the likelihood that each case represented HPS versus ARDS. Afterward, readers viewed earlier chest radiographs and rescored each case. Receiver operating characteristic (ROC) curves from both scoring sessions were generated. The mean areas under the ROC curves for the entire group was 0.83 +/- 0.12 initially, and improved to 0.87 +/- 0.09 (p < 0.05) after viewing prior chest radiographs. Receiver operating characteristic curves of thoracic radiologists described greater areas than those of general radiologists both before and after viewing prior chest radiographs; 0.95 +/- 0.01 versus 0.78 +/- 0.08 (p < 0.05) and 96 +/- 0.02 versus 0.80 +/- 0.05 (p < 0.05). The mean sensitivity and specificity of chest radiograph interpretation for HPS was 86 +/- 13% and 74 +/- 11%, respectively. Chest radiographs can differentiate HPS from ARDS. Accuracy is improved by the use of serial radiographs and more highly trained readers. The chest radiograph findings may represent differences in the extent of alveolar epithelial damage seen in HPS and ARDS.

Acute Disease↗

Neuroleptic-induced acute respiratory distress syndrome.

CONTEXT: A case of neuroleptic malignant syndrome and acute respiratory distress syndrome is presented and discussed with emphasis on the role of muscle relaxation, creatine kinase, and respiratory function tests. CASE REPORT: A 41-year-old man presented right otalgia and peripheral facial paralysis. A computed tomography scan of the skull showed a hyperdense area, 2 cm in diameter, in the pathway of the anterior intercommunicating cerebral artery. Preoperative examination revealed: pH 7.4, PaCO2 40 torr, PaO2 80 torr (room air), Hb 13.8 g/dl, blood urea nitrogen 3.2 mmol/l, and creatinine 90 mmol/l. The chest x-ray was normal. The patient had not eaten during the 12-hour period prior to anesthesia induction. Intravenous halothane, fentanyl 0.5 mg and droperidol 25 mg were used for anesthesia. After the first six hours, the PaO2 was 65 torr (normal PaCO2) with FiO2 50% (PaO2/FiO2 130), and remained at this level until the end of the operation 4 hours later, maintaining PaCO2 at 35 torr. A thrombosed aneurysm was detected and resected, and the ends of the artery were closed with clips. No vasospasm was present. This case illustrates that neuroleptic drugs can cause neuroleptic malignant syndrome associated with acute respiratory distress syndrome. Neuroleptic malignant syndrome is a disease that is difficult to diagnose. Acute respiratory distress syndrome is another manifestation of neuroleptic malignant syndrome that has not been recognized in previous reports: it may be produced by neuroleptic drugs independent of the manifestation of neuroleptic malignant syndrome. Some considerations regarding the cause and effect relationship between acute respiratory distress syndrome and neuroleptic drugs are discussed. Intensive care unit physicians should consider the possibility that patients receiving neuroleptic drugs could develop respiratory failure in the absence of other factors that might explain the syndrome.

Adult↗

Ceruloplasmin and transferrin levels are altered in serum and bronchoalveolar lavage fluid of patients with the adult respiratory distress syndrome.

The respiratory burst of neutrophils generates oxygen radicals that can result in lipid peroxidation and may contribute to acute lung injury in the adult respiratory distress syndrome (ARDS). Because ceruloplasmin and transferrin are inhibitors of lipid peroxidation and may play a role in regulating tissue injury, antigen levels of ceruloplasmin and transferrin and ceruloplasmin oxidase levels were measured in the serum and bronchoalveolar lavage fluid (BALF) of ARDS patients (n = 28), patients at risk for ARDS (n = 22), and normal control subjects (n = 45). Serum ceruloplasmin levels were similar in ARDS (mean +/- SEM) (3.8 +/- 0.3 microM) and at-risk (3.3 +/- 0.4 microM) patients compared with control subjects (3.2 +/- 0.2 microM). Serum transferrin levels were decreased in ARDS (14.9 +/- 1.7 microM) and at-risk (20.4 +/- 1.7 microM) patients compared with normal control subjects (32.9 +/- 1.2 microM), and serum transferrin levels correlated with serum unsaturated iron binding capacity (UIBC). Ceruloplasmin was detected in only one of 38 normal BALF samples (0.002 +/- 0.002 microM) and two of 13 at-risk BALF samples (0.15 +/- 0.1 microM), yet it was present in 17 of 23 ARDS BALF samples (0.9 +/- 0.2 microM). Transferrin was also increased in ARDS BALF (5.4 +/- 1.1 microM) compared with at-risk (0.7 +/- 0.5 microM) and normal (0.4 +/- 0.1 microM) samples. Ceruloplasmin that was present in the BALF and serum samples had functional oxidase activity, and purified human ceruloplasmin inhibited hydroxyl radical formation by phorbol myristate acetate (PMA)-stimulated neutrophils.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchoalveolar Lavage Fluid↗

Inhaled nitric oxide for the adult respiratory distress syndrome.

BACKGROUND: The adult respiratory distress syndrome is characterized by pulmonary hypertension and right-to-left shunting of venous blood. We investigated whether inhaling nitric oxide gas would cause selective vasodilation of ventilated lung regions, thereby reducing pulmonary hypertension and improving gas exchange. METHODS: Nine of 10 consecutive patients with severe adult respiratory distress syndrome inhaled nitric oxide in two concentrations for 40 minutes each. Hemodynamic variables, gas exchange, and ventilation-perfusion distributions were measured by means of multiple inert-gas-elimination techniques during nitric oxide inhalation; the results were compared with those obtained during intravenous infusion of prostacyclin. Seven patients were treated with continuous inhalation of nitric oxide in a concentration of 5 to 20 parts per million (ppm) for 3 to 53 days. RESULTS: Inhalation of nitric oxide in a concentration of 18 ppm reduced the mean (+/- SE) pulmonary-artery pressure from 37 +/- 3 mm Hg to 30 +/- 2 mm Hg (P = 0.008) and decreased intrapulmonary shunting from 36 +/- 5 percent to 31 +/- 5 percent (P = 0.028). The ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO2/FiO2), an index of the efficiency of arterial oxygenation, increased during nitric oxide administration from 152 +/- 15 mm Hg to 199 +/- 23 mm Hg (P = 0.008), although the mean arterial pressure and cardiac output were unchanged. Infusion of prostacyclin reduced pulmonary-artery pressure but increased intrapulmonary shunting and reduced the PaO2/FiO2 and systemic arterial pressure. Continuous nitric oxide inhalation consistently lowered the pulmonary-artery pressure and augmented the PaO2/FiO2 for 3 to 53 days. CONCLUSIONS: Inhalation of nitric oxide by patients with severe adult respiratory distress syndrome reduces the pulmonary-artery pressure and increases arterial oxygenation by improving the matching of ventilation with perfusion, without producing systemic vasodilation. Randomized, blinded trials will be required to determine whether inhaled nitric oxide will improve outcome.

Adolescent↗

Pulmonary and extrapulmonary acute respiratory distress syndrome are different.

Acute respiratory distress syndrome (ARDS) can be derived from two pathogenetic pathways: a direct insult on lung cells (pulmonary ARDS (ARDSp)) or indirectly (extrapulmonary ARDS (ARDSexp)). This review reports and discusses differences in biochemical activation, histology, morphological aspects, respiratory mechanics and response to different ventilatory strategies between ARDSp and ARDSexp. In ARDSp the direct insult primarily affects the alveolar epithelium with a local alveolar inflammatory response while in ARDSexp the indirect insult affects the vascular endothelium by inflammatory mediators through the bloodstream. Radiological pattern in ARDSp is characterised by a prevalent alveolar consolidation while the ARDSexp by a prevalent ground-glass opacification. In ARDSp the lung elastance, while in ARDSexp the chest wall and intra-abdominal chest elastance are increased. The effects of positive end-expiratory pressure, recruitment manoeuvres and prone position are clearly greater in ARDSexp. Although these two types of acute respiratory distress syndrome have different pathogenic pathways, morphological aspects, respiratory mechanics, and different response to ventilatory strategies, at the present, is still not clear, if this distinction can really ameliorate the outcome.

Airway Resistance↗

Pathophysiology of acute lung injury and the acute respiratory distress syndrome.

Since the adult respiratory distress syndrome was first described substantial progress has been made in understanding the pathogenesis of this complex syndrome. This review summarizes our current understanding of the pathophysiology of what is now termed the acute respiratory distress syndrome (ARDS) and its less severe form acute lung injury (ALI), with an emphasis on cellular and molecular mechanisms of injury that may represent potential therapeutic targets. Although it is difficult to synthesize all of these abnormalities into a single, unified, pathogenetic pathway, a theme that emerges repeatedly is that of imbalance, be it between pro- and anti-inflammatory cytokines, oxidants and antioxidants, procoagulants and anticoagulants, neutrophil recruitment and activation and mechanisms of neutrophil clearance, or proteases and protease inhibitors. Future therapies aimed at restoring the overall balance of cytokines, oxidants, coagulants, and proteases may ultimately be successful where therapies that target individual cytokines or other mediators have not.

Endothelium, Vascular↗

Partial liquid ventilation in the therapy of pediatric acute respiratory distress syndrome.

BACKGROUND: Acute respiratory failure represents life-threatening disease with persistently marked mortality and late morbidity in pre-term newborns (RDS--respiratory distress syndrome), children as well as, adults (ARDS--acute respiratory distress syndrome). We are probably in the period when better understanding of pulmonary pathophysiology enables the development of new technologies that can help in decreasing the morbidity and mortality of patients with respiratory failure. One of these unconventional methods is partial liquid ventilation (PLV). MAIN PURPOSE: The main aim of the study was to verify the possibility of treating potentially reversible respiratory failure in patients where extracorporeal life support (ECLS) was contraindicated and extracorporeal membrane oxygenation (ECMO) could not be used, or the patient had not met the criteria for ECMO. METHODS: PLV was used in 6 children totally, in 7 applications with severe hypoxemic respiratory failure. Preoxygenated perfluorocarbon Rimar 101 (Miteni, Milan, Italy) warmed to 37 degrees C was applied intratracheally in the doses which corresponds with the functional residual capacity of lungs, the dose of perfluorocarbon was repeated every hour. Following parameters were recorded before, during and after PLV: pH, blood gases, ventilator setting, alveoloarterial difference for oxygen, dynamic compliance, and indices--oxygenation index and hypoxemia score (PaO2/FiO2). The values obtained 1 hour before PLV were compared with the values during PLV; the data before PLV and in the 3rd hour of PLV were evaluated statistically. RESULTS: Statistically significant increase of pH (7.22 vs 7.34, p < 0.05) and PaO2/FiO2 (72 vs 100 Torr, p < 0.01) and decrease of FiO2 (82% vs 64%, p < 0.05) and oxygenation index (23 vs 17, p < 0.05) occurred during 3 hours of PLV. CONCLUSION: Partial liquid ventilation is an effective method for controlling ARDS in certain groups of patients with severe lung disease. (Tab. 4, Ref. 15.)

Acute Disease↗

[Special features of intensive care of toxic shock syndrome. Review and case report of a TSST-1 associated toxic-shock syndrome with adult respiratory distress syndrome and multiple organ failure from a staphylococcal panaritium].

Toxic-shock-syndrome (TSS) is an acute febrile, exanthematous illness caused by toxins such as toxic-shock-syndrome-toxine-1 (TSST-1) and other endotoxines from staphylococcus aureus with an incidence of 0,5 per 100.000 inhabitants. Patients with menstrual toxic-shock-syndrome (menstrual-TSS) usually have TSS associated with menstruation and use of a vaginal device such as tampons. Other patients with non-menstrual toxic-shock-syndrome (non-menstrual-TSS) have a focus of staphylococcal infection such as a surgical wound infection or soft tissue abscess. TSS usually presents with fever, pharyngitis, diarrhoea, vomiting, myalgia and may progress rapidly (within hours) to signs of hypovolaemic hypotension and shock. In some cases TSS is associated with multisystem failure including shock, renal failure, myocardial failure and adult respiratory distress syndrome. In its acute phase the diagnosis of TSS is often uncertain because of its initial symptoms are non-specific and numerous conditions need to be considered in the differential diagnosis. But obviously less incidence, the signs and symptoms of toxic-shock-syndrome should be recognised early to permit successful therapy. The site of infection should be adequately drained and treated with antimicrobial therapy. Possible complications including ARDS and myocardial failure require a thorough understanding of its underlying pathophysiology to ensure appropriate intensive-care treatment. Only if appropriate therapy is instituted as early as possible, most of patients will be able to survive their toxic-shock-syndrome. In other cases TSS can be a rapidly progressive and perhaps lethal ending disease because of possible multiple organe failure such as ARDS.

Adolescent↗

Clinical features and outcomes of severe acute respiratory syndrome and predictive factors for acute respiratory distress syndrome.

BACKGROUND: Severe acute respiratory syndrome (SARS) is an emerging infectious disease, and indeed, the SARS epidemic in Taiwan from March to July 2003 had a great impact. This study depicts the clinical characteristics and short-term outcomes of patients with SARS treated at Taipei Veterans General Hospital; potential predictive factors for acute respiratory distress syndrome (ARDS) are also analyzed. METHODS: This study retrospectively analyzed data for 67 SARS patients, who were grouped according to whether or not ARDS developed during the clinical course of SARS. RESULTS: There were 32 males (mean age, 50.3 years; range, 20-75 years) and 35 females (mean age, 51.1 years; range, 23-86 years). Twenty-five patients (37.3%) were health care workers. At admission, 50 patients (74.6%) had abnormal chest radiographs, and all patients developed pulmonary infiltrates during the following week. During hospitalization, lymphopenia was found in 57 patients (85.1%); and elevated levels of lactate dehydrogenase (LDH; n = 55; 83.3%), C-reactive protein (n = 55; 83.3%), aminotransferases (n = 44; 65.7%), and creatine kinase (n = 14; 20.9%) were also noted. ARDS developed in 33 patients (49.3%), who were generally older than the patients in whom ARDS did not develop, male, non-health care workers, and who generally had dyspnea at the time of diagnosis, and a history of diabetes mellitus, hypertension or cerebrovascular accident. Patients with, versus those without, ARDS also tended to present with more severe lymphopenia and leukocytosis, and with higher levels of LDH and aspartate aminotransferase. The overall mortality rate was 31.3% (21/67), whereas the rate for patients who developed ARDS was 63.6% (21/33). Multivariate analyses showed that age greater than 65 years (odds ratio, OR, 10.6; 95% confidence interval, CI, 2.1-54.1), pre-existing diabetes mellitus (OR, 13.7; 95% CI, 1.3-146.9), and elevated levels of LDH (OR, 8.4; 95% CI, 1.9-36.9) at admission, were independent predictors of ARDS. CONCLUSION: The clinical manifestations of SARS showed high variability, and were related to the underlying health status of individual patients. Importantly, the development of ARDS was associated with significant mortality, despite aggressive therapy.

Adult↗

[Study of diagnostic criteria of acute respiratory distress syndrome and multiple organ dysfunction syndrome at high altitude: revised draft of the diagnostic criteria of high acute respiratory distress syndrome drawn in Lanzhou conference].

OBJECTIVE: To compare the difference of the diagnostic parameters of acute respiratory distress syndrome/multiple organ dysfunction syndrome (ARDS/MODS) at high altitude (H-ARDS/MODS) with that on plains and reevaluate the practicality and feasibility of the diagnostic criteria of H-ARDS (Lanzhou conference, 1999). METHODS: Three hundred and sixty cases with relatively complete data were divided into three groups according to their originating altitude: control group on plains (CG, n=93), high altitude group 1 at the altitude of 1,517 m (H1G, n=223), high altitude group 2 at the altitude of 2,261-2,400 m (H2G, n=44). The ARDS/MODS scorings of the three groups were carried out according to the diagnostic criteria of Lushan Conference, Marshall (1995) and Lanzhou criteria drafted by the authors and the receiver operating characteristic curves (ROC curve) were made to predict the outcome of MODS. RESULTS: In CG group, the area of ROC, the susceptibility and specificity were 0.823, 0.833, 0.731, respectively according to Lushan criteria, which were better than those (0.815, 0.767, 0.763) according to Marshall criteria. Then in group H2G, the area of ROC, the susceptibility and specificity according to Lushan criteria were lower than those according to Marshall criteria: 0.855, 0.583, 0.969 vs 0.914, 1.000, 0.657. The optimum cutoff points of partial pressure of oxygen in artery (PaO(2))/fractional concentration of inspired oxygen (FiO(2)) were 198.32 mmHg, 131.50 mmHg and 97.58 mmHg in group CG, H1G and H2G. CONCLUSION: (1) There are significant differences between the diagnostic criteria of ARDS at high altitude and that on plains. The altitude of 1 517 m would be an important border line in diagnosing H-ARDS. (2) The drafted diagnostic criteria of ARDS at high altitude are feasible and practical in this region, but the range of the parameters is still wide, which need to be properly amended. (3) The changing tendency of the parameters of MODS at high altitude is different from that on plains, but the amount of sample needs to be accumulated further and the Lanzhou criteria needs to be perfected.

Age Factors↗

Respiratory consequences of multisystem crisis: the adult respiratory distress syndrome.

This article reviews adult respiratory distress syndrome as it is associated with multiple organ dysfunction and systemic inflammatory response. The pathophysiology of adult respiratory distress syndrome is discussed and related to the clinical presentation. Included in the clinical presentation is a discussion of respiratory and hemodynamic alterations, lung mechanics, and oxygen delivery and consumption alterations. Conventional therapeutic modalities for treatment of adult respiratory distress syndrome are reviewed in addition to new ventilatory approaches. New approaches to ventilation and oxygenation included in this article are pressure control ventilation, inverse ratio ventilation, permissive hypercapnia, and extracorporeal therapy. New pharmacologic therapy for the treatment of adult respiratory distress syndrome is also reviewed in this article.

Critical Care↗

Extensive mast cell degranulation in bovine respiratory syncytial virus-associated paroxystic respiratory distress syndrome.

Bovine respiratory syncytial virus (BRSV) infection is an important cause of outbreaks of respiratory disease among calves. This virus commonly induces mild to severe respiratory signs but, in a substantial proportion of cases, is also reported to be associated with paroxystic respiratory distress syndrome (PRDS). The pathogenesis of this 'malignant' clinical form has not been fully elucidated. The present study aimed at determining whether mast cell (MC) degranulation plays a role in the physiopathologic cascade leading to the PRDS. Paired serum samples were taken in herds during outbreaks of severe respiratory diseases (acute sera) and 3 weeks after (convalescent sera). Based on seroconversion to BRSV and clinical picture, 67 pairs of sera were selected from calves with a BRSV-associated PRDS for circulating MC tryptase determination. A MC metachromatic score was measured in post-mortem lungs from animals died from a BRSV-associated PRDS (principals) and compared with reference scores obtained from healthy lungs (controls). Levels of tryptase were significantly higher in acute sera (26.6 +/- 12.4 microg/l) compared to convalescent sera (8.4 +/- 7.8 microg/l; P<0.001). Metachromatic scores yielded significantly different results between controls and principals (P<0.01), demonstrating a significant disappearance of metachromatic granules from lung MCs in principals. Taken together, these data demonstrate the presence of an extensive MC degranulation in BRSV-associated PRDS.

Animals↗

Adult respiratory distress syndrome: a consideration with rapid respiratory decompensation in association with preeclampsia.

Adult respiratory distress syndrome, presenting as rapid respiratory decompensation in the setting of preeclampsia at 36 weeks of gestation, was managed by early hemodynamic monitoring with pulmonary artery catheterization. With confirmation of the diagnosis of preeclampsia the patient was delivered promptly; improvement of her respiratory failure was observed within 48 hours. Consideration of adult respiratory distress syndrome in the setting of preeclampsia is discussed, with emphasis on early confirmation of the diagnosis and determination of the precise mechanisms of pulmonary edema.

Adolescent↗

Mechanical ventilation and pharmacologic strategies for acute respiratory distress syndrome.

Acute or adult respiratory distress syndrome (ARDS) contributes to mortality and morbidity in the intensive care environment. Appropriate application of microprocessor-controlled mechanical ventilatory support, pathophysiology of the disease, and new pharmacologic modalities are currently being investigated. Mechanical ventilation is usually begun when respiratory failure is caused by alveolar hypoventilation or hypoxia. Primary choices for this therapy are control-mode ventilation, assist-control ventilation, pressure-control ventilation, intermittent mandatory ventilation, and synchronized intermittent mandatory ventilation with the addition of positive end-expiratory pressure. Patients who deteriorate despite these interventions may require alternative modes of ventilation. Pharmacologic agents in ARDS is important due to the multifactorial pathophysiologic and pharmacodynamic processes that are part of the disease. Clinical studies will continue to determine advantageous agents. Unfortunately, no convincing data exist that any pharmacologic or nonpharmacologic strategy is superior for the support of these patients or results in a better outcome than others.

Adult↗