Hydroxocobalamin-attributed risk of oxalate nephropathy: evidence is not sufficient to change the recommended management of cyanide toxicity by fire smoke inhalation

AbstractEnclosed-space smoke inhalation is the fifth most common cause of all unintentional injury deaths in the United States. Increasingly, cyanide has been recognized as a significant toxicant in many cases of smoke inhalation. However, it cannot be emergently verified. Failure to recognize the possibility of cyanide toxicity may result in inadequate treatment. Findings suggestive cyanide toxicity include: (1) a history of an enclosed-space fire scene in which smoke inhalation was likely; (2) the presence of oropharyngeal soot or carbonaceous expectorations; (3) any alteration of the level of consciousness, and particularly, otherwise inexplicable hypotension (systolic blood pressure ≤90 mmHg in adults). Prehospital studies have demonstrated the feasibility and safety of empiric treatment with hydroxocobalamin for patients with suspected smoke inhalation cyanide toxicity. Although United States Food and Drug Administration (FDA)-approved since 2006, the lack of efficacy data has stymied the routine use of this potentially lifesaving antidote. Based on a literature review and on-site observation of the Paris Fire Brigade, emergency management protocols to guide empiric and early hydroxocobalamin administration in smoke inhalation victims with high-risk presentations are proposed.

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Substance P and neutral endopeptidase in development of acute respiratory distress syndrome following fire smoke inhalation

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00388.2003 ◽

2004 ◽

Vol 287 (4) ◽

pp. L859-L866 ◽

Cited By ~ 17

Author(s):

Simon S. Wong ◽

Nina N. Sun ◽

R. Clark Lantz ◽

Mark L. Witten

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Substance P ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Time Course ◽

Distress Syndrome ◽

Neutral Endopeptidase ◽

Smoke Inhalation ◽

Plasma Extravasation ◽

Fire Smoke

To characterize the tachykininergic effects in fire smoke (FS)-induced acute respiratory distress syndrome (ARDS), we designed a series of studies in rats. Initially, 20 min of FS inhalation induced a significant increase of substance P (SP) in bronchoalveolar lavage fluid (BALF) at 1 h and persisted for 24 h after insult. Conversely, FS disrupted 51.4, 55.6, 46.3, and 43.0% enzymatic activity of neutral endopeptidase (NEP, a primary hydrolyzing enzyme for SP) 1, 6, 12, and 24 h after insult, respectively. Immunolabeling density of NEP in the airway epithelium largely disappeared 1 h after insult due to acute cell damage and shedding. These changes were also accompanied by extensive influx of albumin and granulocytes/lymphocytes in BALF. Furthermore, levels of BALF SP and tissue NEP activity dose dependently increased and decreased, respectively, following 0, low (10 min), and high (20 min) levels of FS inhalation. However, neither the time-course nor the dose-response study observed a significant change in the highest affinity neurokinin-1 receptor (NK-1R) for SP. Finally, treatment (10 mg/kg im) with SR-140333B, an NK-1R antagonist, significantly prevented 20-min FS-induced hypoxemia and pulmonary edema 24 h after insult. Further examination indicated that SR-140333B (1.0 or 10.0 mg/kg im) fully abolished early (1 h) plasma extravasation following FS. Collectively, these findings suggest that a combination of sustained SP and NEP inactivity induces an exaggerated neurogenic inflammation mediated by NK-1R, which may lead to an uncontrolled influx of protein-rich edema fluid and cells into the alveoli as a consequence of increased vascular permeability.

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Hydroxocobalamin-induced oxalate nephropathy in a patient with smoke inhalation

Kidney International Reports ◽

10.1016/j.ekir.2021.05.019 ◽

2021 ◽

Author(s):

Jordan Evans ◽

Abhishek Pandya ◽

Yanli Ding ◽

Wajeh Y. Qunibi

Keyword(s):

Smoke Inhalation ◽

Oxalate Nephropathy

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Cyanide poisoning by fire smoke inhalation

European Journal of Emergency Medicine ◽

10.1097/mej.0b013e328357170b ◽

2013 ◽

Vol 20 (1) ◽

pp. 2-9 ◽

Cited By ~ 77

Author(s):

Kurt Anseeuw ◽

Nicolas Delvau ◽

Guillermo Burillo-Putze ◽

Fabio De Iaco ◽

Götz Geldner ◽

...

Keyword(s):

Smoke Inhalation ◽

Cyanide Poisoning ◽

Fire Smoke

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Impact of forest fire smoke on the state of the central nervous system of rats

Hygiene and Sanitation ◽

10.47470/0016-9900-2021-100-11-1224-1228 ◽

2021 ◽

Vol 100 (11) ◽

pp. 1224-1228

Author(s):

Larisa M. Sosedova ◽

Vera A. Vokina ◽

Mikhail A. Novikov ◽

Elizaveta S. Andreeva ◽

Viktor S. Rukavishnikov

Keyword(s):

Forest Fire ◽

Right Hemisphere ◽

White Male ◽

Experimental Studies ◽

Smoke Inhalation ◽

Male Rats ◽

Control Group ◽

Bioelectrical Activity ◽

Average Amplitude ◽

Fire Smoke

Introduction. The adverse negative effect of forest fire smoke on human health represents a unique interdisciplinary challenge to the scientific community. The influence of forest fire smoke on locomotor activity, cognitive indices, and brain bioelectrical activity parameters in exposed rats is presented. Materials and methods. Experimental studies were carried out on outbred white male rats. The animals of the experimental group were exposed to smoke inhalation forest fire for one day. Immediately after the end of the exposure, the animals were examined, including testing in an open field and Morris water maze, as well as an electroencephalographic examination. Results. At twenty-four-hour exposure to wildfire smoke in the model, conditions showed increasing motor and research activity of male rats against the backdrop of growing anxiety. Disorders of indicators of spatial memory and navigation learning were not revealed. On the encephalogram of the exposed animals, in comparison with the control group, the δ-rhythm range predominated, more pronounced in the leads of the right hemisphere. A decrease in the power spectrum and the average amplitude β1-rhythm, as well as a tendency to decrease the average amplitude of θ-rhythm, were revealed. The indices of the primary EEG rhythms did not have statistically significant differences when compared with the control group. Conclusion. The results showed that forest fire smoke leads to changes in the bioelectric activity of brain structures and dysregulation of individual behaviour in animals, all of which may indicate the formation of increased levels of stressing beyond physiological adaptation.

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Fire smoke inhalation and cardiac disorders—Efficacy of hydroxocobalamin: Preliminary results

Burns ◽

10.1016/j.burns.2009.06.055 ◽

2009 ◽

Vol 35 ◽

pp. S14

Author(s):

J.L. Fortin ◽

T. Desmettre ◽

V. Peureux ◽

C. Manzon ◽

G. Capellier

Keyword(s):

Smoke Inhalation ◽

Preliminary Results ◽

Fire Smoke ◽

Cardiac Disorders

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Pediatric Cyanide Poisoning by Fire Smoke Inhalation

Pediatric Emergency Care ◽

10.1097/pec.0b013e3182aa4ee1 ◽

2013 ◽

Vol 29 (11) ◽

pp. 1234-1240 ◽

Cited By ~ 18

Author(s):

Santiago Mintegi ◽

Nuria Clerigue ◽

Vincenzo Tipo ◽

Eduardo Ponticiello ◽

Davide Lonati ◽

...

Keyword(s):

Smoke Inhalation ◽

Cyanide Poisoning ◽

Fire Smoke

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Focus on Smoke Inhalation—The Most Common Cause of Acute Cyanide Poisoning

Prehospital and Disaster Medicine ◽

10.1017/s1049023x00015909 ◽

2006 ◽

Vol 21 (S2) ◽

pp. s49-s55 ◽

Cited By ~ 40

Author(s):

Marc Eckstein ◽

Paul M. Maniscalco

Keyword(s):

Treatment Options ◽

Signs And Symptoms ◽

The United States ◽

Morbidity And Mortality ◽

Smoke Inhalation ◽

Closed Space ◽

Cyanide Poisoning ◽

Cyanide Antidote ◽

Prehospital Management ◽

Fire Smoke

AbstractThe contribution of smoke inhalation to cyanide-attributed morbidity and mortality arguably surpasses all other sources of acute cyanide poisoning. Research establishes that cyanide exposure is: (1) to be expected in those exposed to smoke in closed-space fires; (2) cyanide poisoning is an important cause of incapacitation and death in smoke-inhalation victims; and (3) that cyanide can act independently of, and perhaps synergistically with, carbon monoxide to cause morbidity and mortality. Effective prehospital management of smoke inhalation-associated cyanide poisoning is inhibited by: (1) a lack of awareness of fire smoke as an important cause of cyanide toxicity; (2) the absence of a rapidly returnable diagnostic test to facilitate its recognition; and (3) in the United States, the current unavailability of a cyanide antidote that can be used empirically with confidence outside of hospitals. Addressing the challenges of the prehospital management of smoke inhalation-associated cyanide poisoning entails: (1) enhancing the awareness of the problem among prehospital responders; (2) improving the ability to recognize cyanide poisoning on the basis of signs and symptoms; and (3) expanding the treatment options that are useful in the prehospital setting.

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