Ventilation-Perfusion Imaging in Evaluating Regional Lung Function in Nonpenetrating Injury to the Chest

Background: Blunt chest trauma is frequently present in patients with multiple trauma. In polytraumatized patients thoracic injuries have significant influence on the treatment strategy, not only in the emergency room but also in the intensive care unit. They also affect the decision-making concerning fracture management. The vital role played by blunt chest trauma in the outcome after multiple injuries is highlighted by the fact that polytraumatized patients with severe thoracic trauma have a higher mortality rate than patients with the same injury severity without thoracic trauma. Diagnostics and Injury Severity: Within the broad category of thoracic trauma, there are many different types of injuries. Therefore it is crucial for the treating physician to promptly make the correct diagnosis and to quantify the severity of the injury. This will allow the selection of an appropriate treatment protocol and ensure the best possible outcome for the patient. Scoring Systems: Additionally, various treatment protocols for management can only be evaluated scientifically if the assessment of the trauma severity is standardized. Thus, a reliable CT-independent classification of the severity of thoracic trauma is essential. The "Thoracic Trauma Severity Score" (TTS) is a CT-independent classification of thoracic trauma that is reliable and can be performed quickly in the emergency room. This will allow for adequate treatment of thoracic trauma and the prevention of secondary complications.

show abstract

“…Because of the involved expenditure, this examination is not suitable for the diagnostic purpose in polytraumatized patients [81,82].…”

Section: Ventilation-perfusion Scintigraphymentioning

confidence: 99%

Diagnostics and Scoring in Blunt Chest Trauma

Hildebrand

Griensven

Garapati

et al. 2002

European Journal of Trauma

View full text Add to dashboard Cite

show abstract

“…The pathophysiology of LC includes hypoxemia, hypercarbia, increased work of breathing, and decreased pulmonary volumes in association with ventilation/perfusion mismatching, edema, and segmental lung damage (1, 6, 7). However, little previous work has addressed lung surfactant dysfunction in this clinically important condition.…”

Section: Introductionmentioning

confidence: 99%

Surfactant Dysfunction in Lung Contusion With and Without Superimposed Gastric Aspiration in a Rat Model

Raghavendran¹,

Davidson²,

Knight³

et al. 2008

Shock

View full text Add to dashboard Cite

This study investigates surfactant dysfunction in rats with lung contusion (LC) induced by blunt chest trauma. Rats at 24 h postcontusion had a decreased percent content of large surfactant aggregates in cell-free bronchoalveolar lavage (BAL) and altered large-aggregate composition with decreased phosphatidylcholine (PC), increased lyso-PC, and increased protein compared with uninjured controls. The surface activity of large aggregates on a pulsating bubble surfactometer was also severely impaired at 24 h postcontusion. Decreases in large surfactant aggregate content and surface activity were improved, but still apparent, at 48 and 72 h postcontusion compared with uninjured control rats and returned to normal by 96 h postcontusion. The functional importance of surfactant abnormalities in LC injury was documented in pilot studies showing that exogenous surfactant replacement at 24 h postcontusion improved inflation/deflation lung volumes. Additional experiments investigated a clinically relevant combination of LC plus gastric aspiration (combined acid and small gastric food particles) and found reductions in large surfactant aggregates in BAL similar to those for LC. However, rats given LC + combined acid and small gastric food particles versus LC had more severe surfactant dysfunction based on decreases in surface activity and alterations in large aggregate composition. Combined data for all animal groups had strong statistical correlations between surfactant dysfunction (increased minimum surface tension, decreased large aggregates in BAL, decreased aggregate PC, and increased aggregate lyso-PC) and the severity of inflammatory lung injury (increased total protein, albumin, protein/phospholipid ratio, neutrophils, and erythrocytes in BAL plus increased whole lung myeloperoxidase activity). These results show that surfactant dysfunction is important in the pathophysiology of LC with or without concurrent gastric aspiration and provides a rationale for surfactant replacement therapy in these prevalent clinical conditions.

show abstract

“…The clinical pathophysiology of LC includes hypoxemia, hypercarbia, increased work of breathing, and decreased lung volumes and compliance in association with ventilation-perfusion mismatching, intrapulmonary shunting, edema, and segmental lung damage (1,6,7). As 30% of patients with LC progress to ALI/ ARDS (1), it is important to delineate the factors responsible for the development of progressive respiratory failure.…”

mentioning

confidence: 99%

Role of Macrophage Chemoattractant Protein-1 in Acute Inflammation after Lung Contusion

Suresh

Machado-Aranda

et al. 2012

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Lung contusion (LC), commonly observed in patients with thoracic trauma is a leading risk factor for development of acute lung injury/ acute respiratory distress syndrome. Previously, we have shown that CC chemokine ligand (CCL)-2, a monotactic chemokine abundant in the lungs, is significantly elevated in LC. This study investigated the nature of protection afforded by CCL-2 in acute lung injury/acute respiratory distress syndrome during LC, using rats and CC chemokine receptor (CCR) 2 knockout (CCR2 2/2 ) mice. Rats injected with a polyclonal antibody to CCL-2 showed higher levels of albumin and IL-6 in the bronchoalveolar lavage and myeloperoxidase in the lung tissue after LC. Closed-chest bilateral LC demonstrated CCL-2 localization in alveolar macrophages (AMs) and epithelial cells. Subsequent experiments performed using a murine model of LC showed that the extent of injury, assessed by pulmonary compliance and albumin levels in the bronchoalveolar lavage, was higher in the CCR2 2/2 mice when compared with the wild-type (WT) mice. We also found increased release of IL-1b, IL-6, macrophage inflammatory protein-1, and keratinocyte chemoattractant, lower recruitment of AMs, and higher neutrophil infiltration and phagocytic activity in CCR2 2/2 mice at 24 hours. However, impaired phagocytic activity was observed at 48 hours compared with the WT. Production of CCL-2 and macrophage chemoattractant protein-5 was increased in the absence of CCR2, thus suggesting a negative feedback mechanism of regulation. Isolated AMs in the CCR2 2/2 mice showed a predominant M1 phenotype compared with the predominant M2 phenotype in WT mice. Taken together, the above results show that CCL-2 is functionally important in the down-modulation of injury and inflammation in LC.Keywords: lung contusion; macrophage chemoattractant protein-1; CC chemokine ligand-2; CC chemokine receptor 2; inflammation Thoracic injury is involved in nearly one-third of all acute trauma admissions (1-4), often including clinically significant lung contusion (LC) with subsequent respiratory deficits. LC is an important independent risk factor for the development of acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and ventilator-associated pneumonia in affected patients (1-4), all of which are associated with high mortality and morbidity (5).The clinical pathophysiology of LC includes hypoxemia, hypercarbia, increased work of breathing, and decreased lung volumes and compliance in association with ventilation-perfusion mismatching, intrapulmonary shunting, edema, and segmental lung damage (1, 6, 7). As 30% of patients with LC progress to ALI/ ARDS (1), it is important to delineate the factors responsible for the development of progressive respiratory failure. Several lines of evidence suggest that factors in addition to traumainduced tissue damage may contribute to respiratory failure in LC (1, 3).Macrophage chemoattractant protein (MCP)-1/CC chemokine ligand (CCL)-2 is produced by a number of cells in response to inflammatory stimuli, suc...

show abstract

Ventilation-Perfusion Imaging in Evaluating Regional Lung Function in Nonpenetrating Injury to the Chest

Cited by 17 publications

References 23 publications

Diagnostics and Scoring in Blunt Chest Trauma

Diagnostics and Scoring in Blunt Chest Trauma

Surfactant Dysfunction in Lung Contusion With and Without Superimposed Gastric Aspiration in a Rat Model

Role of Macrophage Chemoattractant Protein-1 in Acute Inflammation after Lung Contusion

Contact Info

Product

Resources

About