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 ◽  

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.

Perfusion ◽  
2001 ◽  
Vol 16 (6) ◽  
pp. 460-468 ◽  
Author(s):  
J A Murphy ◽  
C M Savage ◽  
S K Alpard ◽  
D J Deyo ◽  
J B Jayroe ◽  
...  

The purpose of this study was to compare low-dose (LD) and high-dose (HD) systemic heparinization in a prospective randomized study of arteriovenous carbon dioxide removal (AVCO2R) during acute respiratory distress syndrome, using a commercially available heparin-coated oxygenator. Adult sheep ( n = 13) received an LD50 smoke inhalation and 40% TBSA third degree cutaneous flame burn injury. At 40-48 h post-injury, animals underwent cannulation of the carotid artery and jugular vein and were then randomized to HD heparin (activated clotting time, ACT > 300 s, n = 6) and LD heparin (ACT > 200 s, n = 7) and placed on AVCO2R for approximately 72 h using an oxygenator with the Trillium Bio-Passive Surface™. Mean ACTs were significantly different, as expected (HD: 446 ± 26 s, LD: 213 ± 12 s, p < 0.05). AVCO2R shunt flow averaged approximately 13% of cardiac output with mean CO2 removal similar in HD and LD, p = NS. The hematocrit, platelet count, and fibrin degradation products for the two groups were not different. No differences in thrombosis or bleeding were noted. In conclusion, LD systemic heparin (ACT < 200 s) with a heparin-coated oxygenator does not increase thrombogenicity during AVCO2R for smoke/burn-induced severe lung injury in sheep.


2008 ◽  
Vol 105 (2) ◽  
pp. 678-684 ◽  
Author(s):  
Akio Mizutani ◽  
Perenlei Enkhbaatar ◽  
Aimalohi Esechie ◽  
Lillian D. Traber ◽  
Robert A. Cox ◽  
...  

The morbidity and mortality of burn victims increase when burn injury is combined with smoke inhalation. The goal of the present study was to develop a murine model of burn and smoke inhalation injury to more precisely reveal the mechanistic aspects of these pathological changes. The burn injury mouse group received a 40% total body surface area third-degree burn alone, the smoke inhalation injury mouse group received two 30-s exposures of cotton smoke alone, and the combined burn and smoke inhalation injury mouse group received both the burn and the smoke inhalation injury. Animal survival was monitored for 120 h. Survival rates in the burn injury group, the smoke inhalation injury group, and the combined injury group were 70%, 60%, and 30%, respectively. Mice that received combined burn and smoke injury developed greater lung damage as evidenced by histological changes (septal thickening and interstitial edema) and higher lung water content. These mice also displayed more severely impaired pulmonary gas exchange [arterial Po2(PaO2)/inspired O2fraction (FiO2) < 200]. Lung myeloperoxidase activity was significantly higher in burn and smoke-injured animals compared with the other three experimental groups. Plasma NO2−/NO3−, lung inducible nitric oxide synthase (iNOS) activity, and iNOS mRNA increased with injury; however, the burn and smoke injury group exhibited a higher response. Severity of burn and smoke inhalation injury was associated with more pronounced production of nitric oxide and accumulation of activated leukocytes in lung tissue. The murine model of burn and smoke inhalation injury allows us to better understand pathophysiological mechanisms underlying cardiopulmonary morbidity secondary to burn and smoke inhalation injury.


2020 ◽  
Vol 41 (Supplement_1) ◽  
pp. S97-S98
Author(s):  
Joshua Frost ◽  
Grant Sorensen ◽  
Nicole Van Spronsen ◽  
Jordan Howell ◽  
Donna Ayala ◽  
...  

Abstract Introduction Smoke inhalation injury is strongly associated with increased morbidity/mortality. Bronchoscopy is used to diagnosis smoke inhalation injury, but its interpretation is subjective. This study sought to assess diagnostic significance of physical exam, history, location, and adjunct studies characteristically performed on patients suspected of smoke inhalation by comparing these findings to outcomes. The primary goal was to examine variables that could be used to create an accurate smoke inhalation injury scoring system in order to develop an objective method that considers the severity of inhalation injury. Methods This retrospective study evaluated demographics, clinical presentation, carboxyhemoglobin level, intubation on arrival, bronchoscopy, comorbidities, hospital course, and outcomes associated with smoke inhalation. Bronchoscopy findings included: red mucosa, carbon particles at carina, and numerical score (1–4). The primary outcome was resuscitation fluid required in the first 24 hours of treatment compared to that predicted by the modified Brooke formula (2cc*weight in kg* Total Burn Surface Area). If the patient received more fluid than predicted, this was considered positive for smoke inhalation. Differences between predictor/outcome variables were determined using Wilcoxon rank sum test for continuous variables and Chi-squared test for categorical. Results A positive bronchoscopy score was defined on the condition of having positive physical exam finding and/or bronchoscopy score 1–4. Physical exam findings consisted of soot or carbon sputum present on the patient along with hoarseness, wheezing, or a red oropharynx on physical exam. If the patient met one of these conditions, we considered this a positive result. Inclusion criteria: age 18–89, admission from 1/1/2004 and 5/31/18, and diagnosis of smoke inhalation injury/burn injury. There was a significant difference in positive bronchoscopy between those positive for our condition of inhalation injury and no injury (p&lt; 0.001; Table 1). Patients with a positive bronchoscopy score were 9 times more likely (OR=9.91, 95% CI = 2.8–35.01) to be diagnosed with inhalation injury as compared to those without a positive bronchoscopy score. Conclusions These results display the importance of bronchoscopy in suspected smoke inhalation injury and reinforce the need for an objective bronchoscopy assessment. Future studies can build upon these results by creating an objective scoring system to guide providers performing bronchoscopy. Applicability of Research to Practice Due to the 9-fold benefit of performing bronchoscopy, it should be the primary tool used to assess potential smoke inhalation injury; other tests may be secondary in nature.


1999 ◽  
Vol 5 (S2) ◽  
pp. 1176-1177
Author(s):  
P.C. Langlinais ◽  
D.W. Mozingo ◽  
M.A. Dubick ◽  
S.C. Carden ◽  
C.W. Goodwin

Inhalation injury is present in 32-38% of patients with severe burns and is associated with an increase of 20-84% above the mortality expected based on age and burn size alone. Most previous studies of smoke inhalation injury have utilized large animals such as the sheep and we have previously reported a TEM and SEM study of lung injury in the sheep. The present observations are part of a study to develop a small animal combined model of smoke inhalation and surface burn.Adult, male Sprague-Dawley rats were used. Animals were anesthetized and randomly assigned to one of four groups. Groups 1 and 2 received a 20% total body area surface (TBSA) full thickness scald burns while groups 3 and 4 were sham treated. Five hours after burn injury, rats were placed in a nose only exposure device and half of each group was exposured to either room air alone or room temperature tree bark smoke for 16.25 minutes.


2020 ◽  
Vol 48 (2) ◽  
pp. 89-92
Author(s):  
John E Greenwood

Early excision of deep burn eschar and the expeditious closure of the resultant wounds have become established as gold standard burn care. However, early burn excision has been accepted as up to four days post injury based on a series of misconceptions, not least that the patient is too unwell to undergo surgery and tolerate anaesthesia too soon after injury. There are several reasons why immediate burn excision yields superior survival outcomes, and these are expounded in this article. The systemic pathophysiology following major burn injury, especially when complicated by the respiratory pathophysiology accompanying smoke inhalation, evolves. The hours immediately after burn injury offer several windows of surgical opportunity, windows closed by the pathophysiological events that peak 24 hours later and make surgery and anaesthesia at that time both dangerous and ill-advised.


1988 ◽  
Vol 64 (3) ◽  
pp. 1121-1133 ◽  
Author(s):  
C. A. Hales ◽  
P. W. Barkin ◽  
W. Jung ◽  
E. Trautman ◽  
D. Lamborghini ◽  
...  

The chemical toxins in smoke and not the heat are responsible for the pulmonary edema of smoke inhalation. We developed a synthetic smoke composed of carbon particles (mean diameter of 4.3 microns) to which toxins known to be in smoke, such as HCl or acrolein, could be added one at a time. We delivered synthetic smoke to dogs for 10 min and monitored extravascular lung water (EVLW) accumulation thereafter with a double-indicator thermodilution technique. Final EVLW correlated highly with gravimetric values (r = 0.93, P less than 0.01). HCl in concentrations of 0.1-6 N when added to heated carbon (120 degrees C) and cooled to 39 degrees C produced airway damage but no pulmonary edema. Acrolein, in contrast, produced airway damage but also pulmonary edema, whereas capillary wedge pressures remained stable. Low-dose acrolein smoke (less than 200 ppm) produced edema in two of five animals with a 2- to 4-h delay. Intermediate-dose acrolein smoke (200-300 ppm) always produced edema at an average of 147 ± 57 min after smoke, whereas high-dose acrolein (greater than 300 ppm) produced edema at 65 ± 16 min after smoke. Thus acrolein but not HCl, when presented as a synthetic smoke, produced a delayed-onset, noncardiogenic, and peribronchiolar edema in a roughly dose-dependent fashion.


2003 ◽  
Vol 105 (5) ◽  
pp. 621-628 ◽  
Author(s):  
Perenlei ENKHBAATAR ◽  
Kazunori MURAKAMI ◽  
Katsumi SHIMODA ◽  
John SALSBURY ◽  
Robert COX ◽  
...  

Massive cutaneous burn combined with smoke inhalation causes high mortality in fire victims. Cyclo-oxygenase (COX) and inducible nitric oxide (NO) synthase (iNOS) have been shown to be up-regulated in burn injury. Ketorolac, a non-steroidal, anti-inflammatory agent (NSAID), inhibits prostaglandin and thromboxane synthesis through inhibition of COX. NSAIDs have been shown to down-regulate iNOS. Thus we hypothesized that treatment with ketorolac would attenuate burn/smoke-related cardiopulmonary derangements. We conducted a fully controlled long-term laboratory investigation in an Intensive Care Unit setting. Eighteen female sheep were surgically prepared for chronic study. After a recovery period of 5 days, a tracheotomy was performed under ketamine/halothane anaesthesia. Sheep were given a 40% total body surface third-degree burn and insufflated with cotton smoke (48 breaths, <40 °C). Sheep were divided into three groups: sham (not injured and not treated; n=6), control (injured, but not treated; n=6) and treated (injured and administered ketorolac 60 mg/day; n=6). The sham group had stable cardiopulmonary and systemic haemodynamics. Control animals showed depressed cardiopulmonary function, decreased pulmonary gas exchange, increased pulmonary microvascular leakage and decreased left ventricle stroke work index with elevated left atrial pressure. Systemic vascular leak in control animals was evidenced by robust haemoconcentration (haematocrit and fluid net balance). Treatment with ketorolac prevented all of these morbidities. Post-treatment with ketorolac also resulted in significant inhibition of elevated plasma nitrite/nitrate levels in control animals. These results suggest that ketorolac may ameliorate cardiopulmonary morbidity, at least in part, by inhibiting excessive NO.


1999 ◽  
Vol 86 (4) ◽  
pp. 1151-1159 ◽  
Author(s):  
Hiroyuki Sakurai ◽  
Frank C. Schmalstieg ◽  
Lillian D. Traber ◽  
Hal K. Hawkins ◽  
Daniel L. Traber

The effects of a monoclonal antibody against L-selectin [leukoctye adhesion molecule (LAM)1–3] on microvascular fluid flux were determined in conscious sheep subjected to a combined injury of 40% third-degree burn and smoke inhalation. This combined injury induced a rapid increase in systemic prefemoral lymph flow (sQ˙lymph) from the burned area and a delayed-onset increase in lung lymph flow. The initial increase in sQ˙lymphwas associated with an elevation of the lymph-to-plasma oncotic pressure ratio; consequently, it leads to a predominant increase in the systemic soft tissue permeability index (sPI). In an untreated control group, the increased sPI was sustained beyond 24 h after injury. Pretreatment with LAM1–3 resulted in earlier recovery from the increased sPI, although the initial responses in sQ˙lymphand sPI were identical to those in the nontreatment group. The delayed-onset lung permeability changes were significantly attenuated by pretreatment with LAM1–3. These findings indicate that both leukocyte-dependent and -independent mechanisms are involved in the pathogenesis that occurs after combined injury with burn and smoke inhalation.


2020 ◽  
Vol 36 (4) ◽  
pp. 130-140
Author(s):  
Megan K. Phelps ◽  
Logan M. Olson ◽  
Megan A. Van Berkel Patel ◽  
Molly J. Thompson ◽  
Claire V. Murphy

Objective: To review the clinical effects of nebulized heparin and N-acetylcysteine (NAC) in patients with smoke inhalation injury (IHI) and provide recommendations for use. Data Sources: A search of PubMed, MEDLINE, and Scopus databases was completed from database inception through April 15, 2020, using terms: heparin, acetylcysteine, smoke inhalation injury, and burn injury. Study Selection and Data Extraction: All studies pertaining to efficacy and safety of nebulized heparin and/or NAC for IHI in adult patients were evaluated. Reference lists were reviewed for additional publications. Nonhuman studies, non-English, and case report publications were excluded. Data Synthesis: Eight studies were included. Four demonstrated positive outcomes, 3 demonstrated no benefit or possible harm, and 1 assessed safety. Supporting trials treated patients within 48 hours of injury with 10 000 units of nebulized heparin with NAC for 7 days or until extubation. Two trials with negative findings treated patients within 72 hours, or unspecified, with 5000 units of nebulized heparin with NAC for 7 days, while the third used 25 000 units within 36 hours but was grossly underpowered for analysis. Clinical findings include reduced duration of mechanical ventilation and improved lung function with possible increase risk of pneumonia and no evidence of increased bleeding risk. Conclusions: Nebulized heparin may improve oxygenation and reduce duration of mechanical ventilation in IHI. If nebulized heparin is used, 10 000 units every 4 hours alternating with NAC and albuterol at 4-hour intervals is recommended. Sterile technique should be emphasized. Monitoring for bronchospasm or new-onset pneumonia should be considered.


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