Acute respiratory distress syndrome pulmonary edema

Monitor for evidence of cerebral edema, noncardiogenic (permeability) pulmonary edema, acute respiratory distress syndrome, hyperchloremic metabolic acidosis, and vascular thrombosis... 

M29. Miller, E. J., Cohen, A. B and Matthay, M. A., Increased interleukin-8 concentrations in the pulmonary edema fluid of patients with acute respiratory distress syndrome from sepsis. Crit. Care Med. 24, 1448-1454 (1996). 

Suggested Alternatives for Differential Diagnosis Drug induced noncardiac pulmonary edema, acute respiratory distress syndrome, pneumonic plague, tularemia, Q fever, and viral influenza. 

Suggested Alternatives for Differential Diagnosis Acute respiratory distress syndrome, congestive heart failure, pulmonary edema, AIDS, pneumonia, cardiogenic shock, septic shock, phosgene toxicity, phosphine toxicity, salicylate toxicity with pulmonary edema, influenza, plague, tularemia, and anthrax. 

In reaction to a report of pulmonary edema and hypoglycemia (SEDA-24, 488) it has been noted that in many cases, one or more seizures precede pulmonary edema (acute respiratory distress syndrome), suggesting a neurogenic mechanism (65). 

In adults, a severe form of lung injury can develop in association with sepsis, pneumonia, and injury to the lungs due to trauma or surgery. This catastrophic disorder is known as acute respiratory distress syndrome (ARDS) and has a mortality rate of more than 40%. In ARDS, one of the major problems is a massive influx of activated neurophils which damage both vascular endothelium and alveolar epithelium and result in massive pulmonary edema and impairment of surfactant function. Neutrophil proteinases (e.g., elastase) break down surfactant proteins. A potential therapeutic strategy in ARDS involves administration of both surfactant and antiproteinases (e.g., recombinant a I -antitrypsin). 

Acute respiratory distress syndrome (ARDS) is a syndrome presenting with bilateral pulmonary infiltrates, high oxygen requirements (Pao2/Fi02 <200 mm Hg), and noncardiogenic pulmonary edema. 

Drug overdose Heroin overdose has been associated with pulmonary and immune system complications in 16 patients hospitalized because of overdose with heroin and other psychoactive drugs Pulmonary complications included pneumonia, non-cardiogenic pulmonary edema, acute respiratory distress syndrome, and aspiration of gastric contents. Immune system reaction complications included lower concentrations of IgG, IgA, IgM, and the complement component C3 and reduced CD4 lymphocyte and CD56-bearing lymphocyte counts. 

Many strategies can be used to repair defects in the airways, and this could be used to heat airway diseases varying from common (COPD, pulmonary edema, repair of tumor-connected defects) to less common (acute respiratory distress syndrome, bron-chomalacia, CF, pulmonary hypertension). Stem/progenitor cell therapy provides a potentially novel approach to this problem. Although practical results are scarce, the interest in this field is growing. 

Respiratory failure may be classified as hypoxemic (type 1) or hypercapnic (type II or ventilatory failure) (3), either of which may be acute and chronic. Hypoxemic respiratory failure is due to failure of the lungs, caused by acute (cardiogenic pulmonary edema, pneumonia, acute respiratory distress syndrome) or chronic (emphysema, interstitial limg disorders) diseases (Tables 1 and 2). It is characterized by hypoxemia with normocapnia or hypocapnia. In these conditions central respiratory drive is high and there is sufficient alveolar ventilation (VA) to eliminate CO2 and prevent hypercapnia. 

Chest wall compliance may be reduced in kyphoscoliosis, fibrothorax, or spinal cord injury and lung compliance may be reduced in pulmonary edema, pulmonary fibrosis, and acute respiratory distress syndrome (ARDS) and COPD in the presence of hyperinflation. Airway secretions or bronchoconstriction may contribute to increased airway resistance. Respiratory drive and muscle function may be compromised by anesthetics, sedation, coma, or hypercapnia, and muscle dysfunction may occur in the presence of malnutrition, hypophosphatemia, disuse atrophy, sepsis, myopathies, or limited oxygen delivery (9). The factors that led to a tracheostomy must be optimized prior to decannulation. 

P. falciparum malaria is a life-threatening emergency. Complications include hypoglycemia, acute renal failure, pulmonary edema, severe anemia (high parasitism), thrombocytopenia, heart failure, cerebral congestion, seizures, coma, and adult respiratory distress syndrome. 

The commonest form of lung damage is an interstitial alveolitis, although pneumonitis and bronchiolitis obhter-ans have also been reported, as have sohtary localized fibrotic lesions, non-cardiac pulmonary edema, pleural effusions, acute respiratory failure, acute pleuritic chest pain, and adult respiratory distress syndrome (SEDA-17, 220) (SEDA-18, 201) (66-68). Amiodarone has also been reported to cause impairment of lung function, even in patients who do not develop pneumonitis (69), and preexisting impairment of lung function may constitute a contraindication to amiodarone. 

Transfusion-related acute lung injury is an infrequent but life-threatening complication, clinically indistinguishable from adult respiratory distress syndrome (ARDS). It can occur after the administration of whole blood, erythrocytes, fresh frozen plasma, or cryoprecipitate, all of which contain variable amounts of plasma. In transfusion-related acute lung injury the symptoms of ARDS (dyspnea, pulmonary edema, severe hypoxia, fever, and hypotension) occur within 1-6 hours from the start of transfusion and usually subside within 1-4 days (44). These symptoms can vary from mild to severe and they lead to death in 5-10% of cases. The reaction may be more frequent than reported because confounding factors can mask the symptoms (45). 

The syndrome of acute hypotension, adult respiratory distress syndrome, non-cardiogenic pulmonary edema, anemia, coagulopathy, and anaphylactic reactions after the administration of dextran 70 is referred to as the dextran syndrome (36-39). Factors other than acute volume overload due to intravascular absorption of dextran are thought to account for the syndrome. A combination of diverse pathophysiological factors may be responsible, namely direct pulmonary toxicity, activation of the coagulation cascade, release of vasoactive mediators, hypotension, pulmonary edema, intravascular intravasation of fluids, dilution of blood, and impaired renal and hepatic clearance. Cases of pulmonary edema are described under the section Respiratory. 

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