Developing toxic pulmonary oedema

Fig. 8.5 Early developing toxic pulmonary oedema. The diffuse opacity in the lung fields is visible only after the effects of developing t3 pe 1 respiratory failure...

A typical regime is methylprednisolone 2000 mg IV or IM at 15 min, 6 and 12 h post-exposure. The dose should be repeated every 12 h for 1-5 days until the risk of developing toxic pulmonary oedema has passed. 

Regrettably there is, as yet, no known antidote to phosgene poisoning. Consequently treatment is usually directed to the main symptom - toxic pulmonary oedema - the development of which is dose-related [1374]. 

Mechanisms Underlying the Development of Toxic Pulmonary Oedema and Acute Respiratory Distress Syndrome... 

Fig. 7.2 A field hospital during the First World War. Casualties with toxic pulmonary oedema following a gas attaek outside a field hospital during the First World War. Little could be done for such cases, apart from providing bed rest during the latent period of possible development of pulmonary oedema following the exposure. (Source The National Archive)...

Proactive to mitigate and pre-empt developing type 1 respiratory failure with the development of toxic pulmonary oedema and acute respiratory distress syndrome during a latent period following exposure. 

The key lesson was the importance of the development of toxic pulmonary oedema from exposure to lung-damaging agents. 

A clinical study that was started to find out if pentostatin would improve the immunosuppressive effects of cyclophosphamide, carmustine and etoposide in bone marrow transplant patients was stopped when acute and fatal cardiovascular collapse developed in the first 2 patients. Both patients had been given cyclophosphamide 800mg/m and etoposide 200 mg/m, both every 12 hours for 8 doses, and carmustine 112 mg/m daily for 4 doses. On day 3 pentostatin 4 mg/m, given over 4 hours, was added. Within 8 to 18 hours after completion of chemotherapy both patients developed confusion, hypothermia, hypotension, respiratory distress, pulmonary oedema, and eventually fatal ventricular fibrillation within 45 to 120 minutes of the first symptoms. A later study in rats similarly found that pentostatin markedly increased the acute toxicity of cyclophosphamide. The reasons for this cardiotoxicity are not understood. Neither of the 2 patients had previously shown any evidence of cardiac abnormalities. ... 

Auscultation plays an important part in the early assessment of respiratory toxic trauma. It can detect early signs of bronchoconstriction and equally developing signs of pulmonary oedema. 

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