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Desaturating Patient with Long Bone Fractures
Published in Kajal Jain, Nidhi Bhatia, Acute Trauma Care in Developing Countries, 2023
Devendra Kumar Chouhan, Narendra Chouhan
According to the current understanding, FES is classified into three phases:Mechanical phase – The fat globules enter into circulation at the time of injury and can embolize in the lung and other vital organs.Latent phase – Circulation distress occurs because of droplets.Chemical phase – The free fatty acid induces a chemical influence in the lung parenchyma. Inflammatory cells infiltrate focally, resulting in tissue oedema, epithelium damage and bronchial obstruction. Finally, tissue fibrosis occurs because of focal inflammation and collagen deposition and smooth muscle action leading to narrowing of the vessel lumen and vessel wall thickening. This results in a ventilation–perfusion mismatch.
Injuries in Children
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Pulmonary contusions are the most common thoracic injuries in children and, owing to the child’s chest wall elasticity, may occur in the absence of an overlying rib fracture. Contusion may manifest as an area of consolidation on a radiograph, but radiographic signs may lag behind clinical signs. The resultant ventilation–perfusion mismatch will decrease compliance, cause hypoventilation and lead to hypoxia. The clinical course will therefore depend on the extent of the injury, and mechanical ventilation may be necessary in up to 35% of children with pulmonary contusion. Fluid restriction, supplemental oxygen, pain control and the avoidance of prolonged immobilization or general anaesthetic all contribute to the management of this condition.
The Chest
Published in Kenneth D Boffard, Manual of Definitive Surgical Trauma Care: Incorporating Definitive Anaesthetic Trauma Care, 2019
The pulmonary contusion is an entity in development. The initial chest x-ray will not show the complete full-blown contusion in the stable patient; CT scan is the modality of choice. The contusion will very often be accompanied by a flail chest. The contusion is a complex of intra-parenchymal bleeding, oedema, and alveolar collapse owing to reduced surfactant production. This leads to ventilation–perfusion mismatch, shunting, and decreased compliance. Treatment consists of a ventilation strategy where one should realize that the ventilation stressors are primarily exerted on the healthier lung. Low volume, high PEEP, permissive hypercapnia, and maintaining a minimum oxygen saturation in order to avoid high oxygen concentrations, may be needed. If oxygenation to the required level is not achieved, extracorporeal membrane oxygenation (ECMO) can be considered, to bridge the time needed to reduce swelling and blood in the alveoli (see also Section 17.3).
Pharmacological management of adult patients with acute respiratory distress syndrome
Published in Expert Opinion on Pharmacotherapy, 2020
Maria Gabriella Matera, Paola Rogliani, Andrea Bianco, Mario Cazzola
Pulmonary injury or infections trigger an overwhelming inflammatory response (cytokine storm). The acute-response cytokines tumor necrosis factor and interleukin (IL)-1β and the chemotactic cytokines IL-8 and monocyte chemoattractant protein-1 appear early after infection and are followed by a substantial and constant increase in IL-6 [8]. They induce migration to, and accumulation of leukocytes in the lungs and their activation. This gives rise to the release of reactive oxygen species (ROS) and proteases that induce substantial damage to the capillary endothelium and alveolar epithelium with consequent disruption of the normal barrier that protects against alveolar edema [9,10]. The inflammatory exudate disrupts surfactant structure and function, leading to alveolar collapse and a dramatic reduction in ventilation/perfusion matching. The ventilation/perfusion mismatch can lead to acute pulmonary hypertension, which in severe cases can cause right heart failure. Furthermore, uncontrolled activation of coagulation and suppression of fibrinolysis appear [9,10]. Within a few days, the pathological picture evolves toward a proliferative phase with resolution of pulmonary edema and regeneration of damaged tissue. However, in several patients it progresses to a fibrotic stage with irreversible changes of lung architecture that seems to be correlated to protracted mechanical ventilation and is associated with an increase in mortality [9].
Prime the Line! A Case Report of Air Embolism from a Peripheral IV Line in the Field
Published in Prehospital Emergency Care, 2020
Tiffany M. Abramson, Stephen Sanko, Saman Kashani, Marc Eckstein
Symptoms vary based on the amount of air and the rate at which it enters the vascular system (3). Larger, more rapid infusions of air cause a greater degree of symptomatology. Small VAEs are often asymptomatic as the bubbles are filtered and broken up in the capillary beds of the lungs (5). However, moderate amounts of air can result in respiratory symptoms as a result of pulmonary vasoconstriction, and ventilation-perfusion mismatch (3, 5). When larger volume VAEs enter the right ventricle, there is risk of complete outflow obstruction resulting in decreased cardiac output, hypotension, ischemia and compete cardiovascular collapse resulting in death (3). Additionally, reports of systemic inflammatory response syndrome (SIRS) have been associated with air embolisms as the turbulent flow secondary to the air embolism increases platelet aggregation and release of platelet activator resulting in an inflammatory cascade (2, 8).
Personalized pharmacological therapy for ARDS: a light at the end of the tunnel
Published in Expert Opinion on Investigational Drugs, 2020
Pedro Leme Silva, Paolo Pelosi, Patricia R. M. Rocco
Alveolar macrophages participate by orchestrating the inflammatory process, recruiting neutrophils and circulating macrophages to the site of lung damage [14]. The presence of neutrophils either adhered to endothelial adhesion molecules or within the alveolar space may release proteases, reactive oxygen species, cytokines, eicosanoids, and phospholipids, thus perpetuating leukocyte recruitment as well as damage to alveolar epithelial and endothelial cells. Type II epithelial cell damage reduces surfactant production and disrupts normal fluid transport, impairing edema resolution. In addition, the presence of protein-rich edematous fluid impairs surfactant function, thus increasing surface tension, promoting alveolar collapse, and reducing lung compliance. Endothelial cell injury results in a further increase in vascular permeability and interstitial/alveolar edema. Moreover, platelets contribute to pulmonary vascular changes, formation of microthrombi, and altered vasomotor tone, yielding pulmonary arterial hypertension and right ventricular dysfunction. In this scenario, ventilation-perfusion mismatch impairs oxygenation and increases carbon dioxide, thus increasing minute ventilation and alveolar dead space [15].