Venous air embolism (VAE) is an iatrogenic process involving the entrapment of air into the venous system causing acute occlusion of pulmonary arterial circulation resulting in sudden cardiovascular collapse. We report a case of VAE resulting in acute lung injury following removal of a vascular catheter.CASE PRESENTATIONS: 38 years old woman with history of multiple sclerosis admitted for plasmapheresis treatment. She underwent placement of a right intra-jugular 15-cm Schon XL vascular catheter. She received 3 cycles of plasmapheresis, and the catheter was removed while she was in the supine position. Shortly after that, she reported sudden severe chest pain, shortness of breath, dizziness and near fainting. She was in severe distress, tachycardic and hypotensive that responded to fluids. Arterial PO2 was 39mm Hg on room air. Chest x-ray was normal. Echocardiography revealed dilated right ventricle (RV). She was placed on 100% oxygen; put in supine position, started on IV hydration and catheter site was securely covered. She continued to be tachypneic, her WBC count increased to 66200 and hematocrit to 51.1 mg/dl. Repeated chest x-ray revealed bilateral vascular congestion and large bilateral pleural effusion. Her clinical picture was consistent with non-cardiogenic pulmonary edema from capillary leak syndrome secondary to gas embolism. She improved with supportive measures; and her laboratory values, radiographic and echocardiographic abnormalities normalized. She was discharged 7 days later.
VAE is known to occur during catheter insertion however, it could also happen during catheter removal due to pressure gradient difference between the atmosphere and the venous system. Fatal air embolus volumes causing circulatory collapse are estimated to be 3-8 ml/Kg. Predictors of severity of VAE include volume of air embolus, rate of entry, duration of air entrapment, pre-existing medical conditions and body position. RV outflow obstruction with air causing severe gas exchange abnormalities, right heart strain, paradoxical embolism and may lead to circulatory arrest. The presence of air in the RV causes RBC and platelets aggregation with formation of fibrin and microthrombi, which later embolize to the distal pulmonary capillary bed. That causes local endothelial damage and complement cascade activation with the release of different inflammatory and cytotoxic mediators. The end result of this process in the lung is capillary leak syndrome with extravascular fluid shift precipitating a picture of non-cardiogenic pulmonary edema. Diagnosis relies on the recognition of the clinical picture in the proper setting. Transesophageal echocardiography is a sensitive method for detection of the embolus in the heart chambers. Treatment is supportive. High concentration of inspired oxygen reduces the gas embolus volume by displacing the nitrogen out of the air bubbles. Supine position is recommended over the trendelenberg left lateral position. Increasing the central venous pressure is achieved by IV fluid administration to prevent further air entry. Hyperbaric oxygen treatment is useful in particular with CNS involvement. Our patient had the clinical picture of acute lung injury and capillary leak syndrome with evidence of non-cardiogenic pulmonary edema. Leukocytosis and elevated hematocrit are due to severe hypoxemia, stress and fluid shift. All of these changes normalized with supportive care and restoration of normal oxygenation, circulation and adequate tissue perfusion.CONCLUSIONS: VAE is a catastrophic complication of vascular catheter removal. It causes an acute circulatory compromise with end organ damage. Acute lung injury with capillary leak syndrome resulting in non-cardiogenic pulmonary edema and extravascular fluid shift could occur as a result of this complication. Prevention of further air entry and the institution of other supportive measures are critical in the management of these patients.
M. Shibli, None.