Selective permeability changes in the lungs and airways of sheep after toxic smoke inhalation

The effect of toxic smoke inhalation on selective microvascular sieving of macro-molecules and lymph protein flux was assessed in adult sheep to determine whether the time course of microvascular dysfunction differs between the lung and trachea. Protein flux across the lung increased sixfold 48 h after inhalation of the products of incomplete cotton combustion, whereas tracheal protein flux increased fivefold 8 h after exposure and returned to near base line 48 h after exposure. The lung and trachea selectively retained some sieving to three different protein macromolecules with molecular radii of 36, 54, and 123 A. In the lungs the sieving selectivity for these macromolecules was least 48 h after injury, and in the trachea molecular selectivity was least 8 h after injury. These data suggest that the time course of microvascular injury differs for the trachea and the lung; microvascular changes are detected earlier in the trachea than in the lung. The inhalation injury described thus permits the characterization of the time course of airway and lung microvascular changes.

Download Full-text

Pulmonary edema with smoke inhalation, undetected by indicator-dilution technique

Journal of Applied Physiology ◽

10.1152/jappl.1987.63.3.907 ◽

1987 ◽

Vol 63 (3) ◽

pp. 907-911 ◽

Cited By ~ 17

Author(s):

T. Prien ◽

L. D. Traber ◽

D. N. Herndon ◽

J. C. Stothert ◽

H. J. Lubbesmeyer ◽

...

Keyword(s):

Weight Ratio ◽

Dry Weight ◽

Inhalation Injury ◽

Smoke Inhalation ◽

Lung Edema ◽

Base Line ◽

Gravimetric Analysis ◽

Lung Water ◽

Sheep Model ◽

Injured Lung

Despite experimental evidence for an increase in extravascular lung water (EVLW) after inhalation injury, thermal-dye estimations of EVLW, extravascular thermal volume (EVTV), have repeatedly failed to demonstrate its presence in patients. This situation was evaluated in a sheep model. Under halothane anesthesia one lung was insufflated with cotton smoke and the other with air. EVTV values were 8.4 +/- 0.48 ml/kg at base line and were not elevated at 24 h after smoke inhalation (8.3 +/- 0.45 ml/kg; means +/- SE). Gravimetric analysis 24 h after smoke inhalation showed the development of edema in smoke-exposed lungs. The blood-free wet weight-to-dry weight ratio of the smoke-exposed lungs (5.4 +/- 0.32) was significantly higher compared with the contralateral unsmoked lungs (4.3 +/- 0.15; P less than or equal to 0.05). The thermal-dye technique thus underestimates EVLW. Poor perfusion of the smoke-exposed lungs 24 h after injury was demonstrated indirectly by killing a group of sheep with T-61, an agent that causes a dark red coloration of well-perfused lung areas, as well as directly by measurement of blood flow utilizing a radiolabeled microsphere technique. Thus the inability of the thermal-dye technique to detect the lung edema may be the result of poor perfusion of the injured lung.

Download Full-text

Dose Dependence and Time Course of Smoke Inhalation Injury in a Rabbit Model

Lung ◽

10.1007/pl00007630 ◽

1999 ◽

Vol 177 (2) ◽

pp. 111-122 ◽

Cited By ~ 13

Author(s):

A. Bidani ◽

H. K. Hawkins ◽

C. Z. Wang ◽

T. A. Heming

Keyword(s):

Time Course ◽

Rabbit Model ◽

Dose Dependence ◽

Inhalation Injury ◽

Smoke Inhalation ◽

Smoke Inhalation Injury

Download Full-text

Acute Lung Injury Following Smoke Inhalation: Predictive Value of Sputum Biomarkers and Time Course of Lung Inflammation

10.21236/ada424038 ◽

2004 ◽

Author(s):

Jefferey L. Burgess

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Predictive Value ◽

Lung Inflammation ◽

Time Course ◽

Smoke Inhalation

Download Full-text

A novel large animal model of smoke inhalation-induced acute respiratory distress syndrome

Respiratory Research ◽

10.1186/s12931-021-01788-8 ◽

2021 ◽

Vol 22 (1) ◽

Author(s):

Premila D. Leiphrakpam ◽

Hannah R. Weber ◽

Andrea McCain ◽

Roser Romaguera Matas ◽

Ernesto Martinez Duarte ◽

...

Keyword(s):

Animal Model ◽

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Distress Syndrome ◽

Inhalation Injury ◽

Smoke Inhalation ◽

Large Animal Model ◽

Large Animal ◽

X Ray ◽

Chest X Ray

Abstract Background Acute respiratory distress syndrome (ARDS) is multifactorial and can result from sepsis, trauma, or pneumonia, amongst other primary pathologies. It is one of the major causes of death in critically ill patients with a reported mortality rate up to 45%. The present study focuses on the development of a large animal model of smoke inhalation-induced ARDS in an effort to provide the scientific community with a reliable, reproducible large animal model of isolated toxic inhalation injury-induced ARDS. Methods Animals (n = 21) were exposed to smoke under general anesthesia for 1 to 2 h (median smoke exposure = 0.5 to 1 L of oak wood smoke) after the ultrasound-guided placement of carotid, pulmonary, and femoral artery catheters. Peripheral oxygen saturation (SpO2), vital signs, and ventilator parameters were monitored throughout the procedure. Chest x-ray, carotid, femoral and pulmonary artery blood samples were collected before, during, and after smoke exposure. Animals were euthanized and lung tissue collected for analysis 48 h after smoke inhalation. Results Animals developed ARDS 48 h after smoke inhalation as reflected by a decrease in SpO2 by approximately 31%, PaO2/FiO2 ratio by approximately 208 (50%), and development of bilateral, diffuse infiltrates on chest x-ray. Study animals also demonstrated a significant increase in IL-6 level, lung tissue injury score and wet/dry ratio, as well as changes in other arterial blood gas (ABG) parameters. Conclusions This study reports, for the first time, a novel large animal model of isolated smoke inhalation-induced ARDS without confounding variables such as cutaneous burn injury. Use of this unique model may be of benefit in studying the pathophysiology of inhalation injury or for development of novel therapeutics.

Download Full-text

Bilateral Lobar Lung Transplantation after Smoke Inhalation Injury - A Case Report

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2021.01.2075 ◽

2021 ◽

Vol 40 (4) ◽

pp. S515

Author(s):

E. Olsson ◽

M. Silverborn ◽

U. Smedh ◽

G.C. Riise ◽

J.M. Magnusson ◽

...

Keyword(s):

Case Report ◽

Lung Transplantation ◽

Inhalation Injury ◽

Smoke Inhalation ◽

Smoke Inhalation Injury

Download Full-text

523 Retrospective Outcomes Analysis of Tracheostomy in Paediatric Burn Population

Journal of Burn Care & Research ◽

10.1093/jbcr/irab032.174 ◽

2021 ◽

Vol 42 (Supplement_1) ◽

pp. S108-S109

Author(s):

Nicholas Iglesias ◽

Anesh Prasai ◽

George Golovko ◽

Deepak K Ozhathil ◽

Steven E Wolf

Keyword(s):

Inhalation Injury ◽

Smoke Inhalation ◽

Research Network ◽

Burn Patients ◽

Pulmonary Injury ◽

Smoke Inhalation Injury ◽

Mortality And Morbidity ◽

Laryngeal Injury ◽

Icd 10 ◽

Potential Benefits

Abstract Introduction For decades, controversy has raged regarding the placement of tracheostomy in severe paediatric burns. Numerous variables including extent of smoke inhalation injury, % TBSA burned, age of the patient, and co-morbidities among others complicate reaching consensus. Furthermore, paediatric patients are particularly susceptible to complications including inadvertent loss of airway and long-term swallowing and other anatomic issues. Additionally, previous analysis of the efficacy of tracheostomy in paediatric burn patients appears to be hindered by a lack of nationwide analysis. The aim of this study was to explore the efficacy of tracheostomy in the general paediatric burn patient population. Methods De-identified patient data was obtained from the TriNetX Research Network database. Two cohorts were identified: paediatric burn patients with tracheostomy (cohort A) and paediatric burn patients without tracheostomy (cohort B). Burn patients were identified using the ICD-10 codes T20-T25 & T30-T32. Tracheostomy was identified using the ICD-10 codes 1005887, 1014613, 31600, 31601, 31603, 31604, 31610, and Z93.0. A total of 132 patients were identified in cohort A in 23 HCOs and 83,117 patients were identified in cohort B in 38 HCOs. Infection, hypovolemia, pulmonary injury, laryngeal injury, pneumonia, and death were compared between the cohorts. Results Cohort A had a mean age of 11 (SD=5) and Cohort B had a mean age of 9 (SD=5). Paediatric burn patients with tracheostomy had a higher risk for death, infection, hypovolemia, pulmonary injury, laryngeal injury, and pneumonia when compared to their non-tracheostomy counterparts. The risk ratios for these outcomes were 62.452, 4.713, 9.267, 26.483, 116.163, and 18.154, respectively. Conclusions The analysis of the longitudinal outcomes of pediatric burn patients with tracheostomy as compared to those without tracheostomy demonstrated the tracheostomy cohort suffered much worse mortality and morbidity across several metrics. The potential benefits of tracheostomy placement in pediatric burn patients should be weighed against these outcomes.

Download Full-text

Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00305.2001 ◽

2002 ◽

Vol 283 (5) ◽

pp. L1043-L1050 ◽

Cited By ~ 11

Author(s):

Jiro Katahira ◽

Kazunori Murakami ◽

Frank C. Schmalstieg ◽

Robert Cox ◽

Hal Hawkins ◽

...

Keyword(s):

Leukocyte Adhesion ◽

Experimental Period ◽

Inhalation Injury ◽

Lymph Flow ◽

Smoke Inhalation ◽

Control Group ◽

Fluid Flux ◽

Smoke Inhalation Injury ◽

Lung Lymph ◽

Lung Lymph Flow

We hypothesized that the antibody neutralization of L-selectin would decrease the pulmonary abnormalities characteristic of burn and smoke inhalation injury. Three groups of sheep ( n = 18) were prepared and randomized: the LAM-(1–3) group ( n = 6) was injected intravenously with 1 mg/kg of leukocyte adhesion molecule (LAM)-(1-3) (mouse monoclonal antibody against L-selectin) 1 h after the injury, the control group ( n = 6) was not injured or treated, and the nontreatment group ( n = 6) was injured but not treated. All animals were mechanically ventilated during the 48-h experimental period. The ratio of arterial Po 2 to inspired O2 fraction decreased in the LAM-(1–3) and nontreatment groups. Lung lymph flow and pulmonary microvascular permeability were elevated after injury. This elevation was significantly reduced when LAM-(1–3) was administered 1 h after injury. Nitrate/nitrite (NO x ) amounts in plasma and lung lymph increased significantly after the combined injury. These changes were attenuated by posttreatment with LAM-(1–3). These results suggest that the changes in pulmonary transvascular fluid flux result from injury of lung endothelium by polymorphonuclear leukocytes. In conclusion, posttreatment with the antibody for L-selectin improved lung lymph flow and permeability index. L-selectin appears to be principally involved in the increased pulmonary transvascular fluid flux observed with burn/smoke insult. L-selectin may be a useful target in the treatment of acute lung injury after burn and smoke inhalation.

Download Full-text