The sleeve around a central venous catheter is not a fibrin sleeve, but a stable cellular-collagen tissue covered by endothelium. It is mainly formed by smooth muscle cells migrating from the injured vein wall into the early pericatheter thrombus.

We report a case of clinically significant migration of polytetrafluoroethylene (Teflon) paste particles to the lungs after periurethral injection. These particles were identified by standard and polarized light microscopy. Since the long-term effects in humans are not sufficiently known, we strongly warn against the use of polytetrafluoroethylene paste in children or young adults with a normal life expectancy.

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Lymphocytic airway inflammation is a major risk factor for chronic lung allograft dysfunction, for which there is no established treatment. We investigated whether azithromycin could control lymphocytic airway inflammation and improve allograft function. Fifteen lung transplant recipients demonstrating acute allograft dysfunction due to isolated lymphocytic airway inflammation were prospectively treated with azithromycin for at least 6 months (NCT01109160). Spirometry (FVC, FEV1, FEF25–75, Tiffeneau index) and FeNO were assessed before and up to 12 months after initiation of azithromycin. Radiologic features, local inflammation assessed on airway biopsy (rejection score, IL‐17+ cells/mm2 lamina propria) and broncho‐alveolar lavage fluid (total and differential cell counts, chemokine and cytokine levels); as well as systemic C‐reactive protein levels were compared between baseline and after 3 months of treatment. Airflow improved and FeNO decreased to baseline levels after 1 month of azithromycin and were sustained thereafter. After 3 months of treatment, radiologic abnormalities, submucosal cellular inflammation, lavage protein levels of IL‐1β, IL‐8/CXCL‐8, IP‐10/CXCL‐10, RANTES/CCL5, MIP1‐α/CCL3, MIP‐1β/CCL4, Eotaxin, PDGF‐BB, total cell count, neutrophils and eosinophils, as well as plasma C‐reactive protein levels all significantly decreased compared to baseline (p < 0.05). Administration of azithromycin was associated with suppression of posttransplant lymphocytic airway inflammation and clinical improvement in lung allograft function.

Objective: Intimal hyperplasia is a well-known consequence of arterial injury and arterialization in vein grafts. However, the subacute and chronic vein wall changes which occur after catheterization have not been well studied. In this animal study, intimal hyperplasia in the vein wall after catheterization was examined. Methods: A silicon catheter was placed in the anterior caval vein of 54 rats. After in situ fixation at scheduled intervals (1 day to 6 months), the pathologic changes in the vein wall were studied on semi-serial histology sections by means of light microscopy. Results: Three forms of intimal hyperplasia could be observed: plaque-like, papillary-like and incorporation of the mural part of the sleeve into the underlying vein wall. Although the appearance of each was different, their composition was identical. All were mainly composed of α-actin-positive cells and collagen localized above the internal elastin layer, and covered by endothelium if facing the lumen. The plaque-like and papillary-like forms were mainly localized in the anterior vena cava, while sleeve incorporation mainly occurred in the jugular vein. Plaque-like and papillary-like intimal hyperplasia could be seen together on the same slide, but these two forms were never seen together with sleeve incorporation. Conclusion: Intimal hyperplasia occurs after venous catheterization and is probably caused by chronic injury to the vein wall due to knocking and rubbing movements of the catheter against the wall.