PubMed and Embase were searched for all available years till April 2010 and 584 papers were identified and considered.
EXPERIMENTAL STUDIES: Because of the nature of the injury, there have been no human trials of patients exposed to
phosgene. Multiple small and large animal studies have been performed to examine potential treatments of
phosgene-induced
acute lung injury, but many of these used isolated organ models, pretreatment regimens, or clinically improbable doses. Recent studies in large animals using both realistic time frames and dosing regimens have improved our knowledge, but clinical guidance remains based on incomplete data. Management of a small-scale, confirmed exposure. In the circumstance of a small-scale, confirmed industrial release where a few individuals are exposed and present rapidly, an intravenous bolus of high-dose
corticosteroid (e.g.,
methylprednisolone 1 g) should be considered, although there are no experimental data to support this recommendation. The evidence is that there is no benefit from nebulized
steroid even when administered 1 h after exposure, or
methylprednisolone if administered intravenously ≥6 h after exposure. Consideration should also be given to administration of nebulized
acetylcysteine 1-2 g, though there is no substantive evidence of benefit outside a small animal, isolated lung model and there is a possibility of adverse effects. If the oxygen saturation falls below 94%, patients should receive the lowest concentration of supplemental
oxygen to maintain their SaO(2) in the normal range. Once patients require
oxygen, nebulized β-agonists [e.g.,
salbutamol (
albuterol) 5 mg by
nebulizer every 4 h] may reduce
lung inflammation if administered within 1 h of exposure. Elective intubation should be considered early using an ARDSnet protective ventilation strategy. Management of a large-scale, non-confirmed exposure. In the circumstances of a large-scale industrial or urban release, not all patients presenting will have been exposed and health services are likely to be highly stretched. In this situation, patients should not be treated immediately as there is no evidence that delaying
therapy causes harm, rather they should be rested and observed with regular physical examination and measurement of peripheral
oxygen saturations. Once a patient's oxygen saturation falls below 94%, treatment with the lowest concentration of
oxygen required to maintain their
oxygen saturations in the normal range should be started. Once
oxygen has been started, nebulized β-agonists [e.g.,
salbutamol (
albuterol) 5 mg by
nebulizer every 4 h] may reduce
lung inflammation if administered within 1 h of exposure, though delayed administration which is likely following a large-scale release has not been tested formally. There is no benefit from nebulized
steroid even when administered 1 h after exposure, or high-dose
corticosteroid if administered intravenously ≥6 h after exposure. Although there are no experimental data to support this recommendation, an intravenous bolus of high-dose
corticosteroid (e.g.,
methylprednisolone 1 g) may be considered if presentation is <6 h and resources allow. Depending on the numbers of casualties presenting, invasive ventilation should be initiated either electively once symptoms present (especially where there is a short latent period, indicating likelihood of more significant injury), or delayed until required. Ventilation should be with high
positive end expiratory pressure, ARDSnet recommended ventilation.
CONCLUSIONS: