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At least 19 recordsLinked to original sources
PubMed1987

Smoke inhalation injury.

Smoke inhalation injury is responsible for more deaths after fire than actual body burns. Many of the effects of heat and chemical burns to the airways are delayed and may not be clinically evident at first. Chest films are often not helpful, and direct laryngoscopic or bronchofibroscopic examination or a ventilation-perfusion scan may be necessary to verify the diagnosis. Treatment depends on the components involved, with chemically induced airway injury being the most complex to manage. Death rates remain high when inhalation injury is combined with severe body burns.

Bronchodilator Agents↗
PubMed1990

The pathophysiology of carbon monoxide poisoning and acute respiratory failure in a sheep model with smoke inhalation injury.

A smoke inhalation model was created in 22 adult male sheep with pine smoke inhalation through an endotracheal tube for 6 min. Arterial blood gases, HbCO, HbO2 and pulmonary compliance (Cdyn) were monitored, and the morphology of the tracheobronchial tree and pulmonary parenchyma were studied by light and electron microscopy. Severe carbon monoxide poisoning with fatal levels of HbCO (greater than 50 percent) was found at the end of smoke inhalation. Acute respiratory distress, progressive hypoxemia, decreased pulmonary compliance and increased P(A-a)O2 and Qs/QT occurred after injury. Tracheobronchial blockade by pseudomembrane cast, pulmonary edema, atelectasis and necrosis of pulmonary epithelia were demonstrated pathologically. The mechanisms of CO poisoning and ARF are discussed.

Acute Disease↗
PubMed1990

Role of sulfidopeptide leukotrienes in synthetic smoke inhalation injury in sheep.

Acute lung injury with smoke inhalation results in significant morbidity and mortality. Previously we have shown that synthetic smoke composed of carbon and acrolein, a common component of smoke, causes delayed-onset noncardiogenic pulmonary edema. To study the possible role of the vasoactive and edemagenic sulfidopeptide leukotrienes (SPLT) in smoke inhalation injury, we measured pulmonary hemodynamics, lung lymph flow, and SPLT and leukotriene (LT) B4 in lung lymph before and after 10 min of synthetic acrolein smoke exposure. After smoke exposure there was a significant rise in pulmonary vascular resistance caused by a rise in pulmonary arterial pressure, a fall in cardiac output, and no change in pulmonary capillary wedge pressure. This was accompanied by an increase in total systemic vascular resistance (P less than 0.05), lung lymph flow (P less than 0.05), and extravascular lung water-to-lung dry weight ratio (P less than 0.05). Both SPLT and LTB4 clearance rose significantly (P less than 0.05), but there was a 10-fold increase in SPLT over LTB4 clearance. In sheep pretreated with FPL55712, a SPLT antagonist, the early rise in pulmonary vascular resistance was attenuated, and the rise in systemic vascular resistance was blocked. This was associated with an attenuated and delayed fall in cardiac output. FPL55712 had no effect on lung lymph flow or extravascular lung water-to-dry weight ratio. SPLT, and especially LTD4, may have a role in increased pulmonary and systemic vascular resistance after smoke inhalation injury but does not appear to affect vascular permeability.

Acrolein↗
PubMed1992

Dynamic balance changes between elastase and antiprotease in the early stages after smoke inhalation injury.

Following the use of a rabbit smoke inhalation injury model established in this institute, there were marked reductions in elastase activities in neutrophils and alveolar macrophages; rapid increases in elastase activity in broncho-alveolar lavage fluid (BALF); reductions of serum trypsin inhibitory capacity; a decrease of Pao2 and an increase of PaCO2, and marked increases of lung water volume. Significant correlations were found between the increased extravascular lung water content and the rising elastase activity in BALF. It seems probable that the imbalance between elastase and antiprotease played an important role in the development of acute lung injury after smoke inhalation.

Animals↗
PubMed1991

Hyperbaric oxygen therapy for acute smoke inhalation injuries.

Hyperbaric oxygen therapy is an important adjunct in the management of respiratory injuries secondary to smoke inhalation, especially when injury is complicated by inhalation of a toxic chemical such as carbon monoxide or cyanide. For carbon monoxide poisoning, such therapy has become a standard of practice. As more information becomes available concerning the ability of hyperbaric oxygen to reduce reperfusion injuries, we anticipate that this therapy will become a standard of practice for managing smoke inhalation injuries and cyanide poisoning as well.

Antidotes↗
PubMed1990

Changes in alveolar macrophage, monocyte, and neutrophil cell profiles after smoke inhalation injury.

Thirty two fire victims with smoke inhalation, with or without burns, and 26 control subjects had bronchoalveolar lavage performed. Cell yields and differential cell counts were assessed. All patients and controls were cigarette smokers. Patients with smoke inhalation (SI) injury generally showed higher total bronchoalveolar lavage (BAL) cell yields, and this was significant on repeat lavage from 12 patients. The increase was almost entirely due to an increase in the proportion of neutrophils in patients with smoke inhalation alone (S) and those with cutaneous burns as well as smoke inhalation (S + B). On sequential lavage of 12 patients with smoke inhalation (SI) the proportion of neutrophils had increased; this was significantly higher than on initial lavage. Using various macrophage markers, the proportions of macrophage subgroups were determined. There was an increase in UCHM1 and RFD9 positive cells in each subgroup: the increase in UCHM1 positive cells was significant in patients with burns as well as smoke inhalation, and the increase in RFD9 positive cells was significant in patients with smoke inhalation alone. Assessment of the role of such cells in the development of acute lung injury (such as adult respiratory distress syndrome) may be important in our understanding of the mechanisms entailed.

Bronchoalveolar Lavage Fluid↗
PubMed1988

Effect of smoke inhalation injury on thromboxane levels and platelet counts.

Thirteen goats with chronic lung lymph fistula suffering from smoke inhalation injury were studied for a 6-h period. All animals were found to have acute respiratory failure after injury, the arterial TXA2 (thromboxane A2) levels had increased by 5 min after injury, they peaked at 2 h, and then subsequently declined. Peripheral platelet counts decreased progressively within 2 h, then gradually recovered but were still lower than baseline values at 6 h after injury. EVLW (extravascular lung water), Q1 (lung lymph flow rate) and L/P (total lymph protein/plasma protein concentration), all increased and peaked at 2 h after injury. A negative linear correlation was observed between the TXA2 levels and the platelet counts. Furthermore, differences between the venous and arterial platelet counts were markedly increased. All these observations suggested that the increased TXA2 triggered the formation of platelet microaggregates which were then trapped in the microvasculatures of viscera such as the lung. This might be one of the causes of the decreased platelet counts in peripheral blood. Both TXA2 levels and platelet counts were closely correlated with EVLW, suggesting that TXA2 may indirectly cause the increased pulmonary microvascular permeability by promoting platelet aggregation and microaggregate formation in the pulmonary microvasculature. This may be one of the reasons for the developing pulmonary oedema in goats following smoke inhalation injury.

Animals↗
PubMed1988

The effect of leukocyte depletion on smoke inhalation injury in sheep.

Leukocytes and the production of oxygen radicals and proteolytic enzymes have been implicated in the pathogenesis of lung injury after smoke inhalation. We investigated the mechanism responsible for this form of pulmonary damage in chronically prepared sheep previously made leukopenic with intra-arterial infusions of nitrogen mustard (mechlorethamine hydrochloride). A control air insufflated group (sham: n = 6), a cotton smoke insufflated group (smoke: n = 12), and a leukopenic cotton smoke insufflation group (smoked + depleted: n = 6) were compared. Although both smoke insufflation groups had equivalent smoke exposure, which was indexed by carboxyhemoglobin, the smoked + depleted group had significant attenuation in the increases in pulmonary artery pressure, pulmonary vascular resistance, and pulmonary lymph flow. The PaO2 to FiO2 ratio (P:F) did not fall to the same extent, nor was there a fall in PaO2. The production of oxygen radicals, which was measured as plasma-conjugated dienes, and the consumption of antiprotease, as measured by alpha 2-macroglobulin levels in lung lymph, were not changed in the smoked + depleted group, whereas it was elevated in the smoked group. We conclude that circulating leukocytes and the release of oxygen radicals and proteolytic enzymes contribute to the lung injury, pulmonary microvascular permeability increase, and pulmonary edema seen after smoke inhalation.

Animals↗
PubMed1990

Smoke inhalation injury and the effect of carbon monoxide in the sheep model.

The role of carbon monoxide (CO) in causing the physiologic and anatomic changes characteristic of smoke inhalation injury was evaluated in 34 sheep. The smoke-exposed group received a dose of smoke known to produce mild inhalation injury. The CO group received a pure gas mixture that contained concentrations of oxygen, carbon dioxide, and CO similar to those in the smoke. Cardiopulmonary function was measured immediately after exposure, and 24 and 72 hours after exposure. The CO group showed a transient increase in cardiac output, but the smoke group showed no such response. The CO group maintained normal PaO2 levels during the 72-hour study period; the smoke group gradually developed hypoxemia. The lungs of the CO exposed animals had no discernible histologic changes; lungs of the smoke group showed progressive inflammatory changes. These results indicate that CO per se is not the primary etiologic agent of smoke inhalation injury.

Animals↗
PubMed1992

Burn edema is accentuated by a moderate smoke inhalation injury in sheep.

We determined the lung and systemic response of a moderate smoke inhalation injury combined with a 15% total body surface third-degree burn compared with a burn alone and inhalation alone. Adult sheep were prepared with chronic lung and bilateral prefemoral soft tissue lymph fistula. The burn was confined to one side. Physiologic parameters, lymph flow (QL), and lymph/plasma protein ratio were monitored. Oxidant changes were measured as lipid peroxidation by circulating and lymph-conjugated dienes and lung tissue malondialdehyde. Animals were resuscitated with lactated Ringer's solution during the 24-hour study period to restore and maintain vascular filling pressures and cardiac index. We found net 24-hour fluid balance for burn-inhalation injuries to be 4.1 +/- 1.2 L compared with burn alone of 2.9 +/- 0.9 L and inhalation alone of 2.4 +/- 0.5 L, a significant difference. Protein-rich burn tissue QL increased by fivefold to sixfold with burn alone compared with more than tenfold with burn-inhalation injury. A twofold increase in both lung and nonburn soft tissue QL was also seen in the combined injury not seen with burn alone. Arterial blood gases decreased only at 12 hours. Plasma conjugated dienes were increased in all groups, whereas burn lymph values were increased only in combined insult. In addition, lung malondialdehyde content at 24 hours was 155 +/- 11 nmol/gm with burn-inhalation injury compared with 62 +/- 8 nmol/L for burn alone, 55 +/- 9 nmol/L in inhalation alone, and 45 +/- 4 nmol/L for controls. However, no alveolar flooding was noted in any group. We conclude that a modest smoke inhalation (carboxyhemoglobin of 25%) added to a 15% total body surface burn markedly increases the degree of burn edema, as well as nonburn soft tissue and lung QL, compared with burn alone, indicating increased plasma to interstitial fluid transport in these tissues as well. Increased burn tissue lipid peroxidation products corresponded with the increased burn fluid losses. The increased lung lipid peroxidation also indicates further lung oxidant activity as well.

Animals↗
PubMed1991

Changes of length of elastic fibers in rabbit lungs after smoke inhalation injury.

Pulmonary morphometry was determined in rabbit lungs after smoke inhalation. Twenty-four hours after injury, changes of the total lung volume (TLV) and the total length of all parenchymal elastic fibers (LT) were measured. Concomitant changes in arterial blood gas levels and pathomorphology of lung tissues were also studied. It was found that alveolar walls were broken and became thinner, and that alveoli were dilated. TLV was markedly increased and LT was markedly decreased as compared to normal lungs (P less than 0.05). These findings suggest that proteinases, especially elastase, released from phagocytes may play an important role in acute lung injury after smoke inhalation.

Animals↗
PubMed1989

[The role of free radicals in smoke inhalation injury in rats].

In this study, lung Schiff Base was used as a measure indicating the lung injury induced by free radicals, and lung water, lung vascular permeability, blood gases levels as well as pulmonary pathomorphological change (IM) as measures denoting extents of lung injury after inhalation injury. Experiment was performed on rats and observed for a period of 12 hr post smoke inhalation. In addition, control studies were also achieved on normal rats, and rats depleted from leukocytes by cyclophosphamide prior to the experiments. The results were: 1. The lung Schiff bases were generally higher than that of the control through the whole observation period and two peaks were demonstrated at 30' and 6 hr (56.2% and 31.4% higher than controls respectively) indicating that free radicals played a significant role on lung damage in smoke inhalation injury. 2. Lung Schiff bases of rats depleted from leukocytes revealed a 33.7% and a 50.3% reduction respectively at 30' and 6 hr after injury. It seems that leukocytes lead a more important position at 6 hr than at 30' after injury. 3. The reduction rates of peripheral leukocytes, lung Schiff bases and lung water content were not identical in rats depleted from leukocyte after inhalation injury. There were 94.3%, 50.3% and 42.6% reduction respectively at 6 hr after injury. Correlations among them were not significant. These data suggest that after smoke inhalation injury leukocyte is not the only source of free radicals and also the free radicals are not the only means which leukocyte rely upon to cause lung injury.

Animals↗
PubMed1990

[Experimental treatment of smoke inhalation injury with anti-lipid peroxidation agents].

The role of oxygen free radicals in the mechanism of lung damage after smoke inhalation injury was investigated. 42 dogs were used and equally divided into control and treated group. In treated group, a comprehensive anti-lipid peroxidation treatment including Ginseng-ophiopgon, hydrocortisone sodium succinate, Vit. C and E were used at 5 min, 6 hr, and 12 hr postinjury. SOD activity in blood, hypoxanthine, xanthine, uric acid, MDA and SCL in plasma, C2H6 and C2H4 in exhaled breath of dogs after smoke inhalation injury were measured. In addition, blood gas analysis and EVLW were determined to evaluate the lung damage. The results demonstrated that the injured dogs suffered from lung edema and acute lung dysfunction. MDA, SCL in plasma and C2H6, C2H4 in exhaled breath increased markedly, reaching their first peaks at 30 min. and second peaks at 24-72 hours postinjury. The values revealing in first peak in treated group were lower than that in control group. The increase of SOD activity, however, was higher in treated group than in control group. Changes of oxygen free radicals and lipid peroxidation were closely related to lung damage and respiratory dysfunction. These data showed that in early postinjury period increase of oxygen free radicals and excessive lipid peroxidation existed in lungs of dogs. And in treated group, anti-lipid peroxidation activity was increased and lipid peroxidation was inhibited. Lung damage was improved obviously. It was believed that the first peak of changes in oxygen free radicals and lipid peroxidation was related to the onset of early pulmonary damage and the stress response, and the second peak to the development of pulmonary infection and lung repaired.

Animals↗
PubMed1992

Oxidants and the pathophysiology of burn and smoke inhalation injury.

A skin burn is a common traumatic injury that results in both local tissue damage and a systemic mediator-induced response. There is evidence of both local and systemic oxidant changes manifested by lipid peroxidation in animal burn models and also in burned man. Both increased xanthine oxidase and neutrophil activation appear to be the oxidant sources. Animal studies have also demonstrated decreased burn edema, and also decreased distant organ dysfunction with the use of antioxidants, suggesting a cause-and-effect relationship, which needs to be tested in man. Smoke inhalation injury, a chemical injury to the airways caused by incomplete products of combustion, is frequently seen in conjunction with a body burn. Lipid peroxidation, both in lung and in distant organs, is also seen with this injury. The combined body burn and smoke inhalation injury lead to a marked increase in mortality rate and also an increase in the degree of generalized oxidant release and lipid peroxidation. Although data in man are limited, the available information, along with that from animal research on burns and smoke inhalation, indicates oxidants may well play a key role, and antioxidants may be of clinical therapeutic use.

Burns↗
PubMed1992

Oxygen consumption early postburn becomes oxygen delivery dependent with the addition of smoke inhalation injury.

We determined the relationship between oxygen delivery, DO2, and oxygen consumption, VO2, in sheep after a moderate smoke inhalation injury and 15% TBSA third-degree burn compared with burn alone and controls. Comparison was made beginning three hours after injury when carboxyhemoglobin levels were back to baseline values. We decreased DO2 between three and eight hours by 25% by either removing blood (controls) or decreasing the resuscitation fluid infusion rate. Lung oxidant, measured as tissue malondialdehyde (MDA) levels, and histologic changes were also assessed. Animals were killed at 24 hours. We found that in controls and animals with a burn alone, a 25% decrease in DO2 was compensated for by an increase in O2 extraction, maintaining VO2 constant. Correlation of DO2 to VO2 was r2 = 0.3, indicating independence of VO2 from DO2. With the combined injury, VO2 decreased in proportion to DO2, since O2 extraction did not increase. The correlation of DO2 to VO2 was r2 = 0.9, indicating delivery-dependent consumption, a pathologic process most likely caused by increased inflammatory mediators from the combined injury. Lung lipid peroxidation was markedly increased in the combined injury, 148 +/- 18 nmol MDA/gram of tissue compared with burn alone, 64 +/- 5 nmol/g, or controls, 45 +/- 4 nmol/g. However, no decrease in arterial O2 tension or increase in lung water was noted, i.e., the sheep did not have ARDS, which is known to impair O2 extraction. We conclude that a pathologic O2 delivery-dependent consumption develops with the combination of burn and inhalation injury, increasing the potential for tissue hypoxemia. This change corresponds with increased lung tissue oxidant change.

Animals↗
PubMed1987

A dose-responsive model of smoke inhalation injury. Severity-related alteration in cardiopulmonary function.

The dose responsiveness of selected physiologic indices was studied in a sheep model of smoke inhalation injury. In this model, graded severity of injury was achieved by changing the contact time with smoke (defined by "unit"), whereas other variables were kept constant. Blood gas and cardiopulmonary indices were measured in 70 sheep, including 12 controls, either 24 or 72 hours after exposure to 3, 6, 9, 12, 15, or 18 units of smoke. A 12-unit dose of smoke was fatal within 72 hours and an 18-unit dose was fatal within 24 hours. The best correlation between smoke dose and response was observed in arterial oxygen tension 24 hours after exposure. At 24 hours, most of the cardiopulmonary indices showed significant change only after a 12-unit exposure. Although the exact shape of the dose-response curve could not be defined, sigmoid or curved linear shape was suggested, reflecting the progressive deterioration.

Animals↗
PubMed1975

The pathophysiology of smoke inhalation injury.

The consequences of near-lethal smoke inhalation in dogs were studied for a 72-hour period following injury. Progressive hypoxemia and decrease in compliance developed. Severe respiratory distress and frank pulmonary edema were not encountered. Respiratory insufficiecy was related more to alterations in ventilation perfusion ratios than to alveolar destruction. These data were related to clinical observations made by others. No deterioration of lung function was seen with crystalloid overload imposed upon smoke inhalation. The presence of bacterial infection in dogs surviving beyond 24 hours appears pathogenically significant.

Animals↗