Bladder fibrosis caused by eosinophilic cystitis

A 70-years-old man with no history of allergy or genitourinary problems had bilateral hydronephrosis, a marked decrease in bladder capacity and severe eosinophilic infiltration with fibrosis of the bladder wall. A total cystoprostatectomy with ileal bladder replacement was performed. We reviewed the literature of eosinophilic cystitis for clinical presentation, diagnosis and therapeutic options.     

Acute respiratory failure revealing an idiopathic acute eosinophilic pneumonia: report of a pediatric case

Eosinophilic pneumonias are a group of heterogeneous disorders, rarely reported in children. We describe a case of a 12-year-old boy hospitalized for an acute febrile respiratory failure. Chest radiograph showed bilateral diffuse infiltrates. A pulmonary eosinophilic infiltration was confirmed by a major blood eosinophilia at 33 800/mm³ associated with increased eosinophilic rate (90%) on bronchoalveolar lavage fluid. Outcome improved markedly with mechanical ventilation and corticosteroid therapy. Laboratory screenings for parasitic or allergic disease were negative. Bone marrow smear and medullar caryotype eliminated an acute leukemia. No further visceral eosinophilic injury were found. Acute eosinophilic pneumonia should be included in etiological investigation of patients with acute respiratory distress syndrome (ARDS) even in young subjects.     

Diagnosis of acute respiratory distress syndrome in nosocomial pneumonia

Acute respiratory distress syndrome (ARDS) complicates nosocomial pneumonias (NPn) in 12% to 33% of patients with associated increases in mortality of up to 80%. A timely diagnosis of ARDS with NPn is, however, problematic. The aim of this investigation was to improve the diagnosis and treatment of the early stages of ARDS with NPn. A total of 82 cancer and multiple trauma patients were enrolled in the investigation. Patients were split into 3 groups according to standard ARDS and NPn diagnostic criteria: group 1 ("ARDS + NPn"), group 2 ("NPn"), group 3 ("no ARDS, no NPn"). ARDS was diagnosed using 3 methods: the Murray score, the American-European Consensus Conference criteria, and the V. A. Negovsky Research Institute of General Reanimatology criteria. Elevation of extravascular lung water index along with other ARDS diagnostic criteria (oxygenation index, central hemodynamic indices) was predictive of early stage of ARDS in patients with NPn. The standard diagnostic criteria for ARDS, including the Murray score, oxygenation index, and radiographic data only predicted the later stages of ARDS in NPn. Early diagnosis of ARDS with concomitant NPn in the current study was associated with improved treatment results with decreased duration of artificial ventilation and intensive care unit stay.     

An aggressive systematic strategy for acute respiratory distress syndrome caused by severe pneumonia after renal transplantation

Acute respiratory distress syndrome (ARDS) caused by pneumonia after renal transplantation was usually associated with overimmunosuppression and high mortality rate. We evaluated the efficacy of an aggressive systemic protocol including strategies improving body's immune function. Twenty-one recipients were enrolled in this study. Patients were subjected to a protocol including (i) withdrawal of most immunosuppressants, (ii) early use of immunoenhancers and continuous renal replacement therapy (CRRT), (iii) reasonable administration of antibiotic regimen, (iv) prompt mechanical ventilating strategy, and (v) adequate nutrition. Immunosuppressants were adjusted according to the value of CD4+, CD8+T lymphocytes in peripheral blood. CRRT was conducted at once when patients were admitted to the intensive care unit (ICU), regardless the graft function. Thirteen (62%) survived and eight died finally. This is a high survival rate for this kind of patients. Eighteen patients had received thymosin treatment. All patients who survived experienced renal allograft dysfunction during CRRT, but when CRRT stopped, the function of all grafts gradually recovered. No acute rejection episodes were documented during the treatment. The aggressive systemic protocol including strategies improving the body's immune function and CRRT can improve the outcome of patients with ARDS after renal transplantation. The count of CD4+, CD8+T lymphocytes of peripheral blood is useful in the adjustment of immunosuppressants and the prediction of patient outcome.     

An approach to ventilation in acute respiratory distress syndrome.

Appropriate management of patients with acute respiratory distress syndrome (ARDS) represents a challenge for physicians working in the critical care environment. Significant advances have been made in understanding the pathophysiology of ARDS. There is also an increasing appreciation of the role of ventilator-induced lung injury (VILI). VILI is most likely related to several different aspects of ventilator management: barotrauma due to high peak airway pressures, lung overdistension or volutrauma due to high transpulmonary pressures, alveolar membrane damage due to insufficient positive end expiratory pressure levels and oxygen-related cell toxicity. Various lung protective strategies have been suggested to minimize the damage caused by conventional modes of ventilation. These include the use of pressure- and volume-limited ventilation, the use of the prone position in the management of ARDS, and extracorporeal methods of oxygen delivery and carbon dioxide removal. Although the death rate resulting from ARDS has been declining over the past 10 years, there is no evidence that any specific treatment or change in approach to ventilation is the cause of this improved survival.     

Management of the acute respiratory distress syndrome

Significant advances have occurred in the knowledge of the pathogenesis of ARDS. It is now recognized that ARDS is a manifestation of a diffuse process that results from a complicated cascade of events following an initial insult or injury. Mechanical ventilation and PEEP are still important components of supportive therapy. To avoid ventilator-associated lung injury there is emphasis on targeting ventilator management based on measurement of pulmonary mechanics. For those with resistant hypoxia and severe pulmonary hypertension adjunctive modalities, such as prone positioning and low-dose iNO, may provide important benefit. Alternative modes of supporting gas exchange, such as with partial liquid ventilation and extracorporeal gas-exchange, may serve as rescue therapies. Advances in cell and molecular biology have contributed to a better understanding of the role of inflammatory cells and mediators that contribute to the acute lung injury and the pathophysiology of the syndrome that manifests as ARDS. Based on this new understanding, the potential targets for intervention to ameliorate the systemic inflammatory response have proliferated. Examples include the cytokine network and its receptors, antioxidants, and endothelins. Apart from the challenge of testing these agents in experimental models, it seems likely that determination of the optimum combination of agents will become an equally important endeavor. A particular challenge is to develop better methods of predicting which of the many at-risk patients will go on to full-blown ARDS and MODS, thereby targeting subgroups of patients most likely to benefit from anti-inflammatory therapies. Similarly, the adverse effects of immunosuppressive therapy may be diminished by improved, perhaps molecular, techniques to detect microbial pathogens and permit differentiation between Systemic inflammatory response syndrome and sepsis.     

Inflammation and the acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is a clinical syndrome of non-cardiogenic pulmonary oedema associated with bilateral pulmonary infiltrates, stiff lungs and refractory hypoxaemia. ARDS is characterized by an explosive acute inflammatory response in the lung parenchyma, leading to alveolar oedema, decreased lung compliance and, ultimately, hypoxaemia. Although our understanding of the causes and pathophysiology of ARDS has increased, the mortality rate remains in the range of 30-50%. No major advances in pharmacological therapy have been achieved. Mechanical ventilation is the main therapeutic intervention in the management of ARDS. The only approach that has been shown to reduce the inflammatory response and mortality is the use of lung-protective ventilatory strategy with a low tidal volume and high positive-end expiratory pressure. This chapter will review the current state of the literature on the pathogenesis of ARDS and ventilatory and pharmacotherapy approaches to its management.     

Supportive care in acute respiratory distress syndrome

Although the central focus of acute respiratory distress syndrome (ARDS) is the pathology within the lung, ARDS is very much a systemic disease. As such, the whole body needs care and support while the disease process within the lung runs its course. The issues of pain management, sedation, fluid balance, nutrition, metabolic and hormonal processes, infection control, and patient positioning are important for any patient in a critical care setting. For patients with ARDS, the required ventilatory support and ARDS-associated systemic inflammation mandate the above supportive measures.     

Pharmacogenetic treatment of acute respiratory distress syndrome

Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) occur due to systemic inflammatory disorders or direct injury to the lung. The occurrence of ALI/ARDS is sporadic and is not reliably predicted by the type or severity of injury. A combination of patient characteristics and mechanism of injury are responsible for the sporadic nature of ALI/ARDS and its observed phenotypic variability. Research on the pathophysiology and genetics of ALI/ARDS continues to advance, revealing critical molecular pathways in disease development and specific genetic factors that alter the expression of disease. Despite these advances, pharmacologic therapies have yet to be developed for the prevention or treatment of disease. We anticipate that continued improvement of our understanding of the genetic and pathophysiologic mechanisms underlying ALI/ARDS combined with future clinical trials will allow pharmacogenetic therapies for ALI/ARDS to be developed.     

Mechanical ventilation and acute respiratory distress syndrome

Acute respiratory distress syndrome continues to be a high-mortality condition. The role of mechanical ventilation remains primarily a supportive modality. Recent research has elucidated the adverse impact of traditional ventilation strategies on development of the disease and, ultimately, mortality. The institution of low tidal volume ventilation has been the only intervention that has resulted in definitive improvement in survival. Animal and human investigations that culminated in the Acute Respiratory Distress Syndrome Network low tidal volume study are reviewed. Current controversies in the application of mechanical ventilation including the use of positive end-expiratory pressure, recruitment maneuvers, and high frequency oscillatory ventilation are also addressed.     

Large-animal models of acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is characterized by an acute inflammatory response that compromises alveolar-capillary membrane integrity. Clinical symptoms include refractory hypoxemia, noncardiogenic edema, and decreased lung compliance. The purpose of this review is to summarize the different ARDS large-animal models in terms of similarity to the clinical disease and underlying pathophysiology. The repeated lavage, oleic acid, endotoxin, and smoke/burn ARDS models will be discussed in this review. While each model has significant benefits, none is without weaknesses. Thus, the choice of large-animal ARDS model must be carefully considered based upon the study focus and investigative team experience.     

Mechanical ventilation in acute respiratory distress syndrome

The acute respiratory distress syndrome occurs commonly in critical care. There is an increasing volume of clinical and experimental evidence that poor ventilatory technique that is injurious to the lungs can propagate the systemic inflammatory response and adversely affect mortality. Many ventilatory techniques have been hypothesized to 'protect' the lungs during mechanical ventilation, including tidal volume limitation, high positive end-expiratory pressure, pressure-controlled inverse ratio ventilation, and prone positioning. Experimental techniques include liquid ventilation, surfactant administration and extracorporeal gas exchange. Despite excellent rationale for their use, few techniques, apart from tidal volume limitation, have been shown to improve survival in randomized controlled trials.     

Pharmacologic strategies in acute respiratory distress syndrome

Treatment of the acute respiratory distress syndrome includes both supportive measures and correction of the underlying cause. Various pharmacological interventions have been proposed to limit the severity of lung injury and enhance the healing process, including exogenous surfactant, inhaled vasodilators (mainly nitric oxide), corticosteroids, prostaglandin E1, antioxidants (N-acetylcysteine), ketoconazole and other substances. Some of these interventions are administered via the airways, for example inhaled nitric oxide or liquid ventilation with perfluorocarbons. Some have beneficial effects on surrogate end-points such as pulmonary gas exchange. However, in large prospective trials none of these pharmacological approaches have resulted in significantly improved survival in acute respiratory distress syndrome patients.     

Metalloproteinase inhibition prevents acute respiratory distress syndrome

BACKGROUND: The acute respiratory distress syndrome (ARDS) occurs in patients with clearly identifiable risk factors, and its treatment remains merely supportive. We postulated that patients at risk for ARDS can be protected against lung injury by a prophylactic treatment strategy that targets neutrophil-derived proteases. We hypothesized that a chemically modified tetracycline 3 (COL-3), a potent inhibitor of neutrophil matrix metalloproteinases (MMPs) and neutrophil elastase (NE) with minimal toxicity, would prevent ARDS in our porcine endotoxin-induced ARDS model. METHODS: Yorkshire pigs were anesthetized, intubated, surgically instrumented for hemodynamic monitoring, and randomized into three groups: (1) control (n = 4), surgical instrumentation only; (2) lipopolysaccharide (LPS) (n = 4), infusion of Escherichia coli lipopolysaccharide at 100 microg/kg; and (3) COL-3 + LPS (n = 5), ingestion of COL-3 (100 mg/kg) 12 h before LPS infusion. All animals were monitored for 6 h following LPS or sham LPS infusion. Serial bronchoalveolar lavage (BAL) samples were analyzed for MMP concentration by gelatin zymography. Lung tissue was fixed for morphometric assessment at necropsy. RESULTS: LPS infusion was marked by significant (P < 0.05) physiological deterioration as compared with the control group, including increased plateau airway pressure (P(plat)) (control = 15.7 +/- 0.4 mm Hg, LPS = 23.0 +/- 1.5 mm Hg) and a decrement in arterial oxygen partial pressure (P(a)O(2)) (LPS = 66 +/- 15 mm Hg, Control = 263 +/- 25 mm Hg) 6 h following LPS or sham LPS infusion, respectively. Pretreatment with COL-3 reduced the above pathophysiological changes 6 h following LPS infusion (P(plat) = 18.5 +/- 1.7 mm Hg, P(a)O(2) = 199 +/- 35 mm Hg; P = NS vs control). MMP-9 and MMP-2 concentration in BAL fluid was significantly increased between 2 and 4 h post-LPS infusion; COL-3 reduced the increase in MMP-9 and MMP-2 concentration at all time periods. Morphometrically LPS caused a significant sequestration of neutrophils and monocytes into pulmonary tissue. Pretreatment with COL-3 ameliorated this response. The wet/dry lung weight ratio was significantly greater (P < 0.05) in the LPS group (10.1 +/- 1.0 ratio) than in either the control (6.4 +/- 0.5 ratio) or LPS+COL-3 (7.4 +/- 0.6 ratio) group. CONCLUSIONS: A single prophylactic treatment with COL-3 prevented lung injury in our model of endotoxin-induced ARDS. The proposed mechanism of COL-3 is a synergistic inhibition of the terminal neutrophil effectors MMPs and NE. Similar to the universal practice of prophylaxis against gastric stress ulceration and deep venous thromboses in trauma patients, chemically modified tetracyclines may likewise be administered to prevent acute lung injury in critically injured patients at risk of developing ARDS.     

Mortality predictors in recipients developing acute respiratory distress syndrome due to pneumonia after kidney transplantation

Background: The aim of the present study was to investigate the risk factors related to hospital mortality due to infection in kidney recipients with ARDS meeting the Berlin definition.

Methods: Univariate and multivariate logistic regression analysis were used to confirm the independent risk factors related to infection-associated mortality.

Results: From January 2001 to August 2014, a total of 94 recipients with acute respiratory dress syndrome (ARDS) caused by pneumonia following kidney transplantation were enrolled in the present study. The most common type of infection was bacterial (52/94; 55.3%), viral (25/94; 26.6%), and polymicrobial (14/94; 14.9%). The most common ARDS was diagnosed within 6 months after transplantation (76/94; 80.9%). There were 39 deaths in these recipients (39/94; 41.5%). Eleven (11.7%) patients had mild, 47 (50.0%) moderate, and 36 (38.3%) severe ARDS; mortality was 27.3, 27.7, and 63.9%, respectively. The independent predictors of infection-related mortality were serum creatinine level >1.5?mg/dL at ARDS onset (OR 3.5 (95%CI 1.2–10.1), p?=?0.018) and severe ARDS (OR 3.6 (95%CI 1.4–9.7), p?=?0.009) in the multivariate analysis.

Conclusion: Infection-related mortality in kidney transplant patients with ARDS was associated with high serum creatinine level and severe ARDS.     

Sirolimus-associated acute respiratory distress syndrome in a renal transplant recipient

Sirolimus is a new potent immunosuppressive drug used in organ transplantation; its major advantage is the absence of deterioration in renal function. Documented adverse effects include myelosuppression and hyperlipidemia. Recently several cases of sirolimus-associated interstitial pneumonitis have been reported, usually of mild severity. We report a new case that was complicated by a severe acute respiratory distress syndrome, which required several days of mechanical ventilation. No infectious or cardiogenic etiology was documented. Low sirolimus blood levels and acute CD4 lymphocytic alveolitis suggested an immune-related mechanism rather than a direct toxic effect of the drug. The patient recovered after discontinuation of sirolimus and the administration of corticosteroids.