Airway edema

Leuko trienes are bronchoconstrictive substances released by the body during the inflammatory process. When leukotriene production is inhibited, bronchodilation is facilitated. Zileuton acts by decreasing tire formation of leukotrienes. Although the result is tire same, montelukast and zafirlukast work in a manner slightly differently from that of zileuton. Montelukast and zafirlukast are considered leukotriene receptor antagonists because they inhibit leukotriene receptor sites in the respiratory tract, preventing airway edema and facilitating bronchodilation. 

Th2 lymphocytes are one of the primary factors initiating and perpetuating the inflammatory response.7 In addition, proinflammatory mediators such as the leukotrienes generated during mast cell degranulation can increase vascular permeability, leading to airway edema and increased mucus production.8 Eosinophilic infiltration of the airways is a hallmark of asthma, and activated eosinophils can cause bronchoconstriction and AHR.9... 

Airway obstruction manifests itself as symptoms such as chest tightness, cough, and wheezing. Airway obstruction can be caused by multiple factors including airway smooth muscle constriction, airway edema, mucus hypersecretion, and airway remodeling. Airway smooth muscle tone is maintained by an interaction between sympathetic, parasympathetic, and non-adrenergic mechanisms. Acute bronchoconstriction usually... 

The 5-lipoxygenase pathway of arachidonic acid metabolism is responsible for production of cysteinyl leukotrienes. Leukotrienes C4, D4, and E4 are released during inflammatory processes in the lung and produce broncho-spasm, mucus secretion, microvascular permeability, and airway edema. 

Uncontrolled asthma can progress to an acute state where inflammation, airway edema, excessive mucus accumulation, and severe bronchospasm result in profound airway narrowing that is poorly responsive to usual bronchodilator therapy. 

Leukotrienes are products of arachidonic acid metabolism and are released from mast cells and eosinophils. Leukotrienes and leukotriene receptor occupation have been correlated with airway edema, smooth muscle contraction, and altered cellular activity associated with the inflammatory process, which contribute to the signs and symptoms of asthma. 

Besides neuropeptides, nitric oxide is an inflammatory mediator in the airways, which is also a vasodilator and a neurotransmitter. Nitric oxide is produced by the enzymatic action of nitric oxide synthetase on L-arginine. Airways contain this enzyme in three different forms, two of which termed neuronal and endothelial nitric oxide synthetase are constitutive whereas the third form called inducible nitric oxide synthetase is inducible. The inflammatory cytokines including IL-1 and TNF-a augment the expression of inducible nitric oxide synthetase in human airway epithelial cells. Nitric oxide causes bronchodilation as a result of the relaxation of bronchial smooth muscles. It has also been suggested that nitric oxide is the neurotransmitter of the inhibitory NANC bronchodilation. The detrimental effects of nitric oxide include airway inflammation and vasodilation. It causes airway edema by increasing the erudition of plasma due to increased blood flow to postcapillary venules. The increased blood flow may also contribute to an increased mucus secretion. The role of nitric oxide in inflammatory responses has not yet been established. 

Acute upper airway edema has been observed after a single dose of azathioprine (10). 

Jungling AS, Shangraw RE. Massive airway edema after azathioprine. Anesthesiology 2000 92(3) 888-90. 

In a retrospective chart analysis in a Greek ENT department 42 patients with allergic reactions to E. elaterium, including upper airway edema, were identified (7). Treatment with glucocorticoids and antihistamines resulted in full recovery in all cases. 

Kloutsos G, Balatsouras DG, Kaberos AC, Kandhoros D, Ferekidis E, Economou C. Upper airway edema resulting from use of Ecballium elaterium. Laryngoscope 2001 lll(9) 1652-5. 

Cohen S, Liu KH, Marx GF. Upper airway edema — an anaphylactoid reaction to succinylcholine Anesthesiology 1982 56(6) 467-8. 

Martling, C.R and Lundbetg, J.M. (1988). Capsaicin sensitive afferents contribute to acute airway edema following tracheal instillation of hydrtxhloric acid or gastric juice in the tat. Anesthesiology 68, 350-356. 

Murai, M., Morimoto, H., Maeda, Y. and Fujii, T. (1992). Effects of the tripeptide substance P antagonist, FRl 13680, on airway constriction and airway edema induced by neurokinins in guinea pigs. Eur. J. Pharmacol. 217, 23-29. 

In the workplace, occupational asthma has been reported. Aspiration may result in upper airway edema and considerable respiratory distress. Again, low phosphate detergents will produce oral, esophageal, and respiratory tract burns due to their alkaline nature. 

Stridor caused by upper-airway injury and edema (progressive airway edema may result in acute airway obstmction). 

Maintain an open airway and perform endotracheal Intubation If airway edema is progressive (see pp 1-7). Treat bronchospasm (see p 8) and pulmonary edema (p 7) it they occur. 

Remain alert for progressive upper-airway edema or obstruction, and be prepared to intubate the trachea and assist ventilation if necessary (see pp 1-7). 

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