Toxic inhalational injury

2020 ◽  
Vol 13 (3) ◽  
pp. e232875 ◽  
Author(s):  
Victoria Davies ◽  
Jake Turner ◽  
Michael Greenway

A middle-aged patient presented with toxic inhalational injury, and was resuscitated prehospitally and treated in the emergency department for smoke inhalation, carbon monoxide (CO) exposure and cyanide poisoning with the use of antidotes. Due to the CO effects on spectrophotometry, an anaemia initially identified on blood gas analysis was thought to be artefactual, but was later confirmed by laboratory testing to be accurate. In addition, cyanide can confound haemoglobin testing due to its use in the analytical process and non-cyanide analysis is required when there is suspected exposure. Although no consensus exists on a first-line cyanide antidote choice, hydroxocobalamin is the only antidote without a serious side effect profile and/or deleterious cardiovascular effects. We propose prehospital enhanced care teams consider carrying hydroxocobalamin for early administration in toxic inhalational injury.

2008 ◽  
Vol 42 (5) ◽  
pp. 661-669 ◽  
Author(s):  
Greene Shepherd ◽  
Larissa I Velez

Objective: To review the recently approved cyanide antidote, hydroxocobalamin, and describe its role in therapy. Data Sources: Relevant publications were identified through a systematic search of PubMed using the MeSH terms and key words hydroxocobalamin and cyanide. This search was then limited to human studies published since 2000. Systematic searches were conducted through January 2008. References from identified articles were reviewed for additional pertinent human studies. Study Selection and Data Extraction: The literature search retrieved 7 studies on the safety and/or efficacy of hydroxocobalamin in humans. Four new studies were identified by the search and 3 studies were identified from the references. Data Synthesis: Studies of antidote efficacy in humans are ethically and logistically difficult. A preclinical study demonstrated that intravenous doses of hydroxocobalamin 5 g are well tolerated by volunteer subjects. Hydroxocobalamin has been shown to reduce cyanide concentrations in controlled studies of nitroprusside therapy and in heavy smokers. A retrospective study of 14 acute cyanide poisonings also demonstrated hydroxocobalamin's safety and efficacy. Two studies examining hydroxocobalamin for smoke inhalation-associated cyanide poisoning indicated a possible benefit, but they are insufficient to establish definitive criteria for use in this setting. Randomized controlled trials of hydroxocobalamin and traditional cyanide antidotes (nitrites/thiosulfate) are lacking. Conclusions: Cyanide poisoning can rapidly cause death. Having an effective antidote readily available is essential for facilities that provide emergency care. In cases of cyanide ingestion, both the nitrite/thiosulfate combination and hydroxocobalamin are effective antidotes. Hydroxocobalamin offers an improved safety profile lor children and pregnant women. Hydroxocobalamin also appears to have a better safety profile in the setting of cyanide poisoning in conjunction with smoke inhalation. However, current data are insufficient to recommend the empiric administration of hydroxocobalamin to all victims of smoke inhalation.


2006 ◽  
Vol 21 (S2) ◽  
pp. s49-s55 ◽  
Author(s):  
Marc Eckstein ◽  
Paul M. Maniscalco

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.


2011 ◽  
Vol 31 (1) ◽  
pp. 72-82 ◽  
Author(s):  
Jillian Hamel

Cyanide causes intracellular hypoxia by reversibly binding to mitochondrial cytochrome oxidase a3. Signs and symptoms of cyanide poisoning usually occur less than 1 minute after inhalation and within a few minutes after ingestion. Early manifestations include anxiety, headache, giddiness, inability to focus the eyes, and mydriasis. As hypoxia progresses, progressively lower levels of consciousness, seizures, and coma can occur. Skin may look normal or slightly ashen, and arterial oxygen saturation may be normal. Early respiratory signs include transient rapid and deep respirations. As poisoning progresses, hemodynamic status may become unstable. The key treatment is early administration of 1 of the 2 antidotes currently available in the United States: the well-known cyanide antidote kit and hydroxocobalamin. Hydroxocobalamin detoxifies cyanide by binding with it to form the renally excreted, non-toxic cyanocobalamin. Because it binds with cyanide without forming methemoglobin, hydroxocobalamin can be used to treat patients without compromising the oxygen-carrying capacity of hemoglobin.


2010 ◽  
Vol 38 (4) ◽  
pp. 69-74 ◽  
Author(s):  
Christopher P. Holstege ◽  
Joseph D. Forrester ◽  
Heather A. Borek ◽  
David T. Lawrence

2014 ◽  
Vol 17 (3) ◽  
pp. 154 ◽  
Author(s):  
Arıtürk Cem ◽  
Ustalar Serpil ◽  
Toraman Fevzi ◽  
Ökten Murat ◽  
Güllü Ümit ◽  
...  

<p><strong>Introduction:</strong> Clear guidelines for red cell transfusion during cardiac surgery have not yet been established. The current focus on blood conservation during cardiac surgery has increased the urgency to determine the minimum safe hematocrit for these patients. The aim of this study was to determine whether monitoring of cerebral regional oxygen saturation (rSO<sub>2</sub>) via near-infrared spectrometry (NIRS) is effective for assessing the cerebral effects of severe dilutional anemia during elective coronary arterial bypass graft surgery (CABG).</p><p><strong>Methods:</strong> The prospective observational study involved patients who underwent cerebral rSO<sub>2</sub> monitoring by NIRS during elective isolated first-time CABG: an anemic group (<em>N</em>=15) (minimum Hemoglobin (Hb) N=15) (Hb &gt;8 g/dL during CPB). Mean arterial pressure (MAP), pump blood flow, blood lactate level, pCO<sub>2</sub>, pO<sub>2</sub> at five time points and cross-clamp time, extracorporeal circulation time were recorded for each patient. Group results statistically were compared.</p><p><strong>Results:</strong> The anemic group had significantly lower mean preoperative Hb than the control group (10.3 mg/dL versus 14.2 mg/dL; <em>P</em> = .001). The lowest Hb levels were observed in the hypothermic period of CPB in the anemic group. None of the controls exhibited a &gt;20% decrease in cerebral rSO<sub>2</sub>. Eleven (73.3%) of the anemic patients required an increase in pump blood flow to raise their cerebral rSO<sub>2</sub>.</p><p><strong>Conclusions:</strong> In this study, the changes in cerebral rSO<sub>2</sub> in the patients with low Hb were within acceptable limits, and this was in concordance with the blood lactate levels and blood-gas analysis. It can be suggested that NIRS monitoring of cerebral rSO<sub>2</sub> can assist in decision making related to blood transfusion and dilutional anemia during CPB.</p>


Author(s):  
G.G. Khubulava ◽  
A.B. Naumov ◽  
S.P. Marchenko ◽  
O.Yu. Chupaeva ◽  
A.A. Seliverstova ◽  
...  

Respiration ◽  
2021 ◽  
pp. 1-8
Author(s):  
Clemens F. Hinke ◽  
Rudolf A. Jörres ◽  
Peter Alter ◽  
Robert Bals ◽  
Florian Bornitz ◽  
...  

<b><i>Background:</i></b> Oxygenated hemoglobin(OxyHem) is a simple-to-measure marker of oxygen content capable of predicting all-cause mortality in stable chronic obstructive pulmonary disease (COPD). <b><i>Objectives:</i></b> We aimed to analyze its predictive value during acute exacerbations of COPD (AECOPD). <b><i>Methods:</i></b> In this retrospective study, data from 227 patients discharged after severe AECOPD at RoMed Clinical Center Rosenheim, Germany, between January 2012 and March 2018, was analyzed. OxyHem (hemoglobin concentration [Hb] × fractional SpO<sub>2</sub>, g/dL) was calculated from oxygen saturation measured by pulse oximetry and hemoglobin assessed within 24 h after admission. The follow-up (1.7 ± 1.5 years) covered all-cause mortality, including readmissions for severe AECOPD. <b><i>Results:</i></b> During the follow-up period, 127 patients died, 56 due to AECOPD and 71 due to other reasons. Survivors and non-survivors showed differences in age, FVC % predicted, C-reactive protein, hemoglobin, Cr, Charlson Comorbidity Index (CCI), and OxyHem (<i>p</i> &#x3c; 0.05 each). Significant independent predictors of survival were BMI, Cr or CCI, FEV<sub>1</sub> % predicted or FVC % predicted, Hb, or OxyHem. The predictive value of OxyHem (<i>p</i> = 0.006) was superior to that of Hb or SpO<sub>2</sub> and independent of oxygen supply during blood gas analysis. OxyHem was also predictive when using a cutoff value of 12.1 g/dL identified via receiver operating characteristic curves in analyses including either the CCI (hazard ratio 1.85; 95% CI 1.20, 2.84; <i>p</i> = 0.005) or Cr (2.04; 95% CI 1.35, 3.10; <i>p</i> = 0.001) as covariates. <b><i>Conclusion:</i></b> The concentration of OxyHem provides independent, easy-to-assess information on long-term mortality risk in COPD, even if measured during acute exacerbations. It therefore seems worth to be considered for broader clinical use.


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