Fibrin sheath

Last revised by Dr Rohit Sharma on 22 Sep 2021

Fibrin sheaths are a common complication of central venous catheters in which a proteinaceous film encases the outer wall and endhole of the catheter, which can cause catheter malfunction and thrombosis.

Fibrin sheaths present as catheter malfunction, which may include inability to withdraw blood (ball-valve effect), inability to both withdraw and infuse through the catheter, or low flow rates during hemodialysis. However, fibrin sheaths are also commonly detected incidentally (without catheter dysfunction).

Fibrin sheaths are long fibrous sleeves characterized by layers of eosinophilic material and scattered inflammatory cells 1. These may be complicated by superimposed acute or chronic/organizing thrombus 1.

Fibrin sheaths are a reaction to endothelial injury, either at the site of venipuncture or where the tip contacts and injures the vein wall 2. They can develop at any time: a circumferential fibrin sheath can appear as early as 24 hours and grow to cover the entire catheter within a week 2. The prevalence of fibrin sheaths among dysfunction catheter increases with prolonged dwell time 3.

Catheter venography in the setting of a fibrin sheath most often shows an abnormal flow jet from the catheter endhole, where the contrast stream may be disrupted, turbulent, or refluxed along the length of the catheter under the fibrin sheath before it diffuses in the vein 2. Excessive contrast flow may come from the sidehole(s) 2. Within a looser fibrin sheath, contrast may pool. Within a long and tight fibrin sheath, contrast injected under pressure may reflux all the way back to the venotomy site and into the soft tissues 2.

Fibrin sheaths adherent to a catheter are typically too thin to visualize on CT angiography. However, a fibrin sheath complicated by thrombosis would appear as a filling defect, thin/concentric or thick/nodular, surrounding the distal catheter.

Fibrin sheaths can be retained after catheter removal and appear as a filling defect. Fibrin sheaths may be calcified, which would be best seen on the non-contrast phase 3.

Treatment strategies for catheter dysfunction due to a fibrin sheath include the following 4:

  • mechanical disruption (with a guidewire and/or balloon)
  • thrombolytic infusion (eg, recombinant tissue plasminogen activator over 1-3 hours)
  • fibrin sheath stripping (with a gooseneck snare via transfemoral venous access)
  • over-the-wire catheter exchange
  • pericatheter intravenous filling defect on CTA likely represents thrombosis, whether acute or chronic, which can be with or without a fibrin sheath
  • high density intravenous filling defect on CTA after catheter removal may represent either a retained catheter tip, a retained calcified fibrin sheath, or calcified thrombus 3
    • nodular/irregular and discontinuous morphology favors calcified endogenous material
    • smooth and continuous morphology favors retained catheter tip

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Cases and figures

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