Predictive role of arterial carboxyhemoglobin concentrations in ovine burn and smoke inhalation-induced lung injury

Abstract

Inhalation injury frequently occurs in burn patients and contributes to the morbidity and mortality of these injuries. Arterial carboxyhemoglobin has been proposed as an indicator of the severity of inhalation injury; however, the interrelation between arterial carboxyhemoglobin and histological alterations has not yet been investigated. Chronically instrumented sheep were subjected to a third degree burn of 40% of the total body surface area and inhalation of 48 breaths of cotton smoke. Carboxyhemoglobin was measured immediately after injury and correlated to clinical parameters of pulmonary function as well as histopathology scores from lung tissue harvested 24 hours after the injury. The injury was associated with a significant decline in pulmonary oxygenation and increases in pulmonary shunting, lung lymph flow, wet/dry weight ratio, congestion score, edema score, inflammation score, and airway obstruction scores. Carboxyhemoglobin was negatively correlated to pulmonary oxygenation and positively correlated to pulmonary shunting, lung lymph flow, and lung wet/dry weight ratio. No significant correlations could be detected between carboxyhemoglobin and histopathology scores and airway obstruction scores. Arterial carboxyhemoglobin in sheep with combined burn and inhalation injury are correlated with the degree of pulmonary failure and edema formation, but not with certain histological alterations including airway obstruction scores.

A rat model of smoke inhalation injury

“…When CO is breathed, it is absorbed into the bloodstream and combines with haemoglobin to form carboxyhaemoglobin (COHb), leading to severely impaired lung oxygenation. Until now, diagnosis of CO poisoning is based on the measurement of FCOHb (Ballard-Croft et al, 2010;Lange et al, 2011;Sugi et al, 1990). In our present study, interestingly, the FCOHb was significantly elevated and reached the peak at 2 h after smoke exposure and began to drop, which was in line with the change of PaCO 2 .…”

The acute pulmonary inflammatory response to the graded severity of smoke inhalation injury*

“…Although this feature could have profound effects on the burned patient through hypoxemic pulmonary vasoconstriction and ventilation/perfusion mismatching, we failed to note any substantial differences in the initial P:F ratio over the range of inhalation injury severities. Moreover, the anti-inflammatory effects of CO have been previously noted in the setting of burn and smoke inhalation injury, sepsis, and trauma (20–24). One might theorize that CO, if present at higher levels in patients with greater inhalation injury severities, would mute the inflammatory response to worsening injury.…”

Pulmonary microvascular hyperpermeability and expression of vascular endothelial growth factor in smoke inhalation- and pneumonia-induced acute lung injury

“…Blood gases were measured using a blood gas analyzer (Synthesis 15, Instrumentation Laboratories; Lexington, MA). PaO 2 /FiO 2 ratio, pulmonary shunt fraction (Qs/Qt), and pulmonary capillary pressure were calculated using standard equations [10]. Lung lymph flow (Q L ) was determined by collecting lymph fluids for an hour and measuring the amount with graduated test tubes.…”