Fire smoke inhalation in pregnancy

2007 ◽  
Vol 27 (5) ◽  
pp. 525-526
Author(s):  
S. Gopu ◽  
H. Y. Wan Hussein ◽  
S. Ray
Keyword(s):  
Smoke Inhalation ◽  
Fire Smoke ◽  
In Pregnancy

Health Impacts of Fire Smoke Inhalation

2008 ◽  
Vol 20 (8) ◽  
pp. 761-766 ◽  
Author(s):  
M. Stefanidou ◽  
S. Athanaselis ◽  
C. Spiliopoulou
Keyword(s):  
Smoke Inhalation ◽  
Health Impacts ◽  
Fire Smoke

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

2004 ◽  
Vol 287 (4) ◽  
pp. L859-L866 ◽  
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.

Cyanide poisoning by fire smoke inhalation

2013 ◽  
Vol 20 (1) ◽  
pp. 2-9 ◽  
Author(s):  
Kurt Anseeuw ◽  
Nicolas Delvau ◽  
Guillermo Burillo-Putze ◽  
Fabio De Iaco ◽  
Götz Geldner ◽  
...  
Keyword(s):  
Smoke Inhalation ◽  
Cyanide Poisoning ◽  
Fire Smoke

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

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.

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

Burns ◽  
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

Pediatric Cyanide Poisoning by Fire Smoke Inhalation

2013 ◽  
Vol 29 (11) ◽  
pp. 1234-1240 ◽  
Author(s):  
Santiago Mintegi ◽  
Nuria Clerigue ◽  
Vincenzo Tipo ◽  
Eduardo Ponticiello ◽  
Davide Lonati ◽  
...  
Keyword(s):  
Smoke Inhalation ◽  
Cyanide Poisoning ◽  
Fire Smoke

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

2006 ◽  
Vol 21 (S2) ◽  
pp. s49-s55 ◽  
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.

scholarly journals PENGGUNAAN JOB SAFETY ANALYSIS DALAM IDENTIFIKASI RISIKO KECELAKAAN KERJA DI BAGIAN WORKSHOP PT. TOTAL DWI DAYA KOTA SEMARANG

2015 ◽  
Vol 4 (4) ◽  
Author(s):  
Tegar Bramasto ◽  
Intan Zainafree
Keyword(s):  
Occupational Diseases ◽  
Secondary Data ◽  
Safety Analysis ◽  
Smoke Inhalation ◽  
Primary Data ◽  
Working Process ◽  
Descriptive Research ◽  
Fire Smoke ◽  
Accident Data ◽  
Job Safety

Abstrak   Setiap tempat kerja selalu mempunyai risiko kemungkinan terjadinya kecelakaan dan penyakit akibat kerja. Sebagai upaya pengendalian risiko kecelakaan dan penyakit akibat kerja, perlu diidentifikasi sumber bahaya yang ada di tempat kerja dan dievaluasi tingkat risikonya serta dilakukan pengendalian yang memadai. Insiden kecelakaan dan cedera di tempat kerja dapat dikurangi dengan penggunaan Job Safety Analysis. Tujuan dari penelitian ini adalah untuk mengetahui potensi bahaya serta pengendalian yang tepat pada bagian workshop PT. Total Dwi Daya. Penelitian ini adalah penelitian deskriptif kualitatif dengan pendekatan observasional. Data yang digunakan dalam penelitian adalah data primer hasil observasi pada proses kerja dan wawancara kepada supervisor, serta data sekunder yang digunakan yaitu instruksi kerja dan data kecelakaan kerja. Dari hasil penelitian didapatkan bahwa risiko kecelakaan kerja yang terdapat pada bagian workshop yaitu: kejang otot, terkena plat jatuh, terkilir, terpeleset,terjepit plat, terjepit mesin, tersengat listrik, terbentur mesin, tersayat plat, tersambar plat, terkena permukaan panas, terkena api, menghirup asap, tersandung kabel, terkena gerinda, terkena percikan api, tersambar pipa, terkena mata bor, tertimpa, terkena steelwool, terkena paku, tersandung plat, terkena pisau dan tergores. Saran untuk PT. Total Dwi Daya yaitu peningkatan pengawasan terhadap pekerja serta pelatihan pembuatan Job Safety Analysis   Abstract   Every workplace always have risk and possibility of accidents and occupational diseases. In an effort to control the risk of accidents and occupational diseases, sources of hazards that exist in the workplace need to be identified, evaluated its level of risk and proper control. The incident of accident and injury at work can be reduced by using Job Safety Analysis. The purpose of this research was to understand the potential of danger and right control of it in workshop division Total Dwi Daya Corporation. Thisstudy was using qualitative descriptive research with observational approach. Primary data used in this research were observation in working process and interview with supervisor. Secondary data were work instruction and accident data. Conclusion of this research, potential dangers found in workshop division were: muscle spasms, hit by fallen plate, sprains, slips, squished by plate, squished by machine, electric shock, collide, cut by plate, strucked by plate, exposed to hot surfaces, exposed to fire, smoke inhalation, tripping over wires, grinding exposed, exposed to sparks, struck pipe, drill hit, exposed nails and scraped. Suggestions for Total Dwi Daya Corporation are raising a control of workers and training Job Safety Analysis training.  

Delayed onset pulmonary edema following toxic smoke inhalation; a systematic review

2018 ◽  
Vol 17 (4) ◽  
pp. 203-211
Author(s):  
Daniel M. Björkbom ◽  
◽  
Mikkel Brabrand ◽  
Keyword(s):  
Pulmonary Edema ◽  
Burn Injury ◽  
De Novo ◽  
Inhalation Injury ◽  
Smoke Inhalation ◽  
Cochrane Library ◽  
Post Injury ◽  
Delayed Onset ◽  
Wide Range ◽  
Fire Smoke

Background: Fire smoke inhalation cause a wide range of symptoms immediately or after a relatively asymptomatic period. In this review, we will focus on delayed onset pulmonary edema (DOPE); the incidence and duration of potential delay. As the symptoms may not present immediately, seemingly healthy patients could be inadvertently be sent home. Therefore, many authors recommend observation for 6-24 hours depending on the extent of inhalation injury. Methods: A systematic literature search in Embase, Medline, and Cochrane library was performed on 14 April 2016. All studies describing smoke exposure and delayed pulmonary edema were included. Additional relevant studies were identified snowballing based on included studies. Results: We included seven studies, with a total of 135 patients, describing pulmonary edema. Symptoms generally developed after a relatively asymptomatic period (up to 36 hours post-injury) until mechanical ventilation was needed. However, pulmonary edema developing after 36 hours was most likely due to other factors related to burn injury (excessive intravenous fluids, de novo heart failure, infection or problems related to intubation). Conclusion: Delayed onset pulmonary edema can develop as late as 36 hours postinjury after a relatively uneventful phase. But it would have been rare to have been completely asymptomatic before developing pulmonary edema.

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