Alveolar haemorrhage

Animals became restles s and developed piloerec-tion within 5 min of dosing. There then developed salivation, rapid shallow breathing, extensor spasms and convulsions. In survivors, these effects subsided within 24 h and no abnormalities were seen on sacrifice at 21 days. Animals that died usually did so within 1 to 18 h, although a few survived for 2 to 9 days. Animals that died showed congestion of the liver, small intestine and lungs, with scattered patches of inter-and intra-alveolar haemorrhages. Small circumscribed foci of acute renal tubular necrosis were occasionally seen. 

Kumar et al. (1994) exposed mice to an average CR concentration of 1008 mg m 3 daily for 15 minaday for lOdays. At5days, lungs demonstrated minimal alveolar haemorrhage and after 10 days there was moderate alveolar haemorrhage and alveolar capillary congestion and a few foci of renal cortical necrosis. 

Tanawuttiwat T, Harindhanavudhi T, Hanif S, Sahloul MZ. Amiodarone-induced alveolar haemorrhage a rare complication of a common medication. Heart Lung Circ 2010 19(7) 435-7. 

El-Fakih R, Chehab BM, Shaver T. Thiona-mide-induced vasculitis a case of alveolar haemorrhage secondary to propylthiouracil. J Intern Med 2008 264(6) 610-2. 

Study of tissue samples from lungs of Iranian casualties who died as a result of exposure to mustard gas has revealed a pattern identical with that described above. In all, tissue from four patients was studied. Alveolar capillary congestion, haemorrhage, oedema, the formation of hyaline membranes and fibrosis were seen. The casualties died as a result of multi-system organ failure and the changes in the lung parenchyma were very similar to those seen in cases of Adult Respiratory Distress Syndrome (ARDS) (Maynard, unpublished observations). 

Animals that died after the repeated exposures had moderate to marked congestion of the alveolar capillaries and intrapulmonary veins, and multiple variable sized areas of haemorrhage, both inter- and intra-alveolar a few animals had moderate pulmonary oedema (Ballantyne and Callaway, 1972). 

Phentolamine might have affected alveolar hquid clearance in haemorrhaged rats by mechanisms that are unrelated to its inhibition of the release of reactive oxygen species. For instance, phentolamine has been shown to block ATP-sensitive potassium channels in cardiac ventricular cells by a mechanism unrelated to its a-adrenergic blockade (Wilde et al. 1994). 

Both protective ventilation strategies significantly improved survival (from 30 to 100% at 24 hours), arterial blood oxygenation and pathology as determined by reduced haemorrhage, neutrophil infiltration and intra-alveolar oedema formation (Figure 4.5). ... 

The alveolar proteinosis caused by heavy exposure to silica ( acute silico-proteinosis ) and possibly by other agents (Blanc 1992) would qualify for this entity. Similarly, some instances of exogenous lipoid pneumonitis seem to correspond well to the concept of subacute toxic pneumonitis. The pulmonary haemorrhagic syndrome associated with exposure to trimellitic anhydride and, possibly, to methylene diphenyl diisocyanate is also a potential form of toxic response but, in this instance, the role of specific immunological mechanisms is likely. 

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