Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation.

STUDY OBJECTIVE: To assess outcomes in patients treated with hydroxocobalamin at the fire scene or in the ICU for suspected smoke inhalation-associated cyanide poisoning. METHODS: Adult smoke inhalation victims with suspected cyanide poisoning as determined by soot in the face, mouth, or nose or expectorations and neurologic impairment received an intravenous infusion of hydroxocobalamin 5 g (maximum 15 g) at the fire scene or in the ICU in this observational case series conducted from 1987 to 1994. Blood cyanide specimens were collected before administration of hydroxocobalamin. The threshold for cyanide toxicity was predefined as greater than or equal to 39 micromol/L. RESULTS: The sample included 69 patients (mean age 49.6 years; 33 men), of whom 39 were comatose. Out-of-hospital deaths were excluded. Fifty of the 69 patients (72%) admitted to the ICU survived after administration of hydroxocobalamin. In the group in which cyanide poisoning was confirmed a posteriori (n=42), 67% (28/42) survived after administration of hydroxocobalamin. The most common adverse events were chromaturia (n=6), pink or red skin discoloration (n=4), hypertension (n=3), erythema (n=2), and increased blood pressure (n=2). No serious adverse events were attributed to hydroxocobalamin. Laboratory tests revealed transient alterations in renal and hepatic function consistent with the critical condition of the patients and mild anemia consistent with progressive hemodilution. CONCLUSION: Empiric administration of hydroxocobalamin was associated with survival among 67% of patients confirmed a posteriori to have had cyanide poisoning. Hydroxocobalamin was well tolerated irrespective of the presence of cyanide poisoning. Hydroxocobalamin appears to be safe for the out-of-hospital treatment of presumptive cyanide poisoning from smoke inhalation.

Exosurf treatment following wood smoke inhalation.

Pulmonary surfactant deactivation is an important factor in the pathophysiology caused by wood smoke inhalation. Surfactant replacement is beneficial in treatment of surfactant-deficient neonates and possibly the adult respiratory distress syndrome (ARDS). In this study, the effect of exogenous Exosurf treatment for acute wood smoke injury was examined in four groups of rabbits. All groups were anaesthetized, placed on a ventilator, and surgically prepared for haemodynamic, peak airway pressure (P(aw)), and blood gas measurements. Rabbits were monitored for 2 h following smoke or sham smoke inhalation. At the conclusion of the experiment pulmonary oedema and surfactant function were measured. A Control group (n = 5) was followed without intervention. A Smoke group (n = 4) was ventilated with wood smoke for 3 min. A third group (Smoke+Exo, n = 4) was subjected to smoke followed by pulmonary instillation of Exosurf (5 ml/kg). Saline (5 ml/kg) was instilled into the lungs of the fourth group (n = 3) as a control for Exosurf instillation. Saline, Smoke and Smoke+Exo all significantly lowered PO2 and elevated P(aw) compared to baseline and the Control group. Exosurf treatment did not reduce the pulmonary oedema or restore surfactant function caused by smoke exposure. This study indicates that wood smoke inhalation acutely damages the lung and that administration of Exosurf by instillation is not an effective treatment.

Transient increase of serum Clara cell protein (CC16) after exposure to smoke.

OBJECTIVES: Smoke inhalation is a well known cause of airways injury in firefighting personnel. The aim of this study was to evaluate whether toxic effects of smoke on the respiratory tract can be detected by measuring Clara cell protein (CC16), a recently described serum marker of lung function. METHODS: CC16 was measured by a sensitive latex immunoassay in the serum of six voluntary firefighters from a chemical plant who had inhaled smoke from the combustion of polypropylene for about 20 minutes. The protein was measured immediately after the fire and 10 days later. The values were compared with those of six control workers examined simultaneously. RESULTS: The mean (SD) concentration of CC16 in the serum of firefighters after the fire (54.4 (34.9) micrograms/l) was significantly higher than that of controls (19.5 (11.7), P = 0.04). 10 days later, serum CC16 from firefighters had returned to the concentrations found in controls (15.9 (2.76) v 17.7 (12.5)). With the values at day 10 as a baseline, the rise of serum CC16 was estimated at 328% on average (range 100%-564%). These changes were found in the absence of any functional sign of lung impairment. CONCLUSION: Acute exposure to smoke results in a transient increase of CC16 in serum due most likely to an increased permeability of the bronchoalveolar/blood barrier. Serum CC16 seems potentially to be a new biomarker for the early detection of acute airways injury caused by smoke.

Smoke inhalation with a concurrent systemic stress results in lung alveolar injury.

Smoke inhalation causes injuries to lung airways, and, at times, alveolar inflammation also develops over approximately 24 h. The pathophysiology of parenchymal lung injuries is unknown, and it is often fatal. We hypothesized that an inflammatory stress remote from the smoke-related lung insult was required for development of alveolar injuries. Spontaneously breathing rats were exposed, head only, to smoke generated by nonflaming pyrolysis (smoldering) of Douglas fir wood (DF), polyvinylchloride (PVC), or the combination of DF+PVC. Intraperitoneal injection of sterile oyster shell glycogen 4 h before smoke inhalation was used as an extra inflammatory stimulus. Histologic examinations revealed extensive airway inflammation in all smoke-exposed groups. Glycogen peritonitis alone caused no lung injuries, and in the absence of glycogen, smoke inhalation caused neither parenchymal lung injuries, assessed by [125I]bovine serum albumin (BSA) leakage, nor neutrophil infiltration, quantified by myeloperoxidase (MPO) activity. However, in rats pretreated with glycogen and studied 24 h after exposure to smoke from burning DF+PVC, [125I]BSA permeability was increased by 232 +/- 41% (SE; n = 13), MPO activity was increased 5-fold, from 2.6 +/- 0.4 (n = 7) to 13.9 +/- 1.4 (n = 19) A460/min/g lung, and histopathologic findings included extensive pulmonary inflammation. We conclude that inhalation of certain types of smoke will trigger pulmonary injury when an inflammatory process remote from the lungs is present.