Background: Phosgene (carbonyl dichloride) gas is an indispensable chemical intermediate used in
numerous industrial processes. Acute lung injury (ALI) caused by accidental inhalation exposure to
phosgene is characterized pulmonary edema being phenotypically manifested after an asymptomatic or
more precisely phrased “clinical occult” period. Opposite to common clinical practice, protective treatment
should be given preference to curative treatment. Treatment initiated already during the asymptomatic phase
shortly after exposure requires prognostic endpoints preceding the lung edema for triage and re-triage.
Treatment strategies need to be personalized and exposure-dose related. The objective of this post-hoc
analysis of published data is to assess prognostic value of ventilation dead-space (Vd/Vt) and extravascular
lung water index (EVLWI) to guide treatment by protective PEEP supplemented by venovenous (vv)
ECMO.
Methods: This paper aims to compare the overarching published framework from systematic toxicological
research of phosgene in animal bioassays with the clinical evidence from four accidentally phosgenepoisoned workers admitted to hospital with life-threatening lung edema. Treatment focused on a
combination of protective PEEP and ECMO to reverse phosgene-induced deterioration in lung mechanics
by personalized mechanical ventilation. Endpoints selected for titration PEEP focused on endpoints
indicative of decoupling cardiopulmonary and vascular functions. To better understand any cardiogenic and
vascular disturbances, titration endpoints included calculated ventilation dead-space (Vd/Vt), measured
extravascular lung water index (EVLWI), arterial blood gases and acid-base status, systemic vascular
resistance index (SVRI), and cardiac index (CI). EVLWI and APACHE II criteria guided the course of
treatment in adjusting plateau pressure (Pplat), positive end-expiratory pressure (PEEP), and driving
pressure (ΔP).
Results: Remarkable equivalence of human data and those from controlled inhalation studies with phosgene
on rats and dogs was found. The endpoint of choice guiding PEEP ventilation and implementation of ECMO
was EVLWI. This maker of lung edema precisely reflects the increased wet lung weights in animals.
Conclusions: ECMO-supplemented PEEP not only mitigates hypoxemia at conditions of severe
ARDS and it also provides a means to reduce driving and plateau pressures minimizing ventilatorassociated lung injury.
Comparison of thermodilution measured extravascular lung water with chest radiographic assessment of pulmonary oedema in patients with acute lung injury
