Mechanism of thrombosis caused by sclerotherapy of esophageal varices using sodium tetradecyl sulphate

Surg Endosc. 1992 Jan-Feb;6(1):4-9. doi: 10.1007/BF00591179.

Abstract

The mechanism of thrombosis following intravariceal injection of sodium tetradecyl sulphate (S.T.D.) was investigated with respect to effects on the vascular endothelium, the coagulation cascade, and platelet function. Using an umbilical cord model designed to simulate blood flow over the endothelium, it was found that S.T.D. is a potent toxin for endothelial cells in that brief exposure to even low concentrations of the agent were effective in stripping endothelium over a considerable distance, exposing highly thrombogenic endothelium in the process. Effects on coagulation and platelet function were found to be dependent on concentration. Diluted S.T.D. induced a hypercoagulable state, possibly in consequence of a selective inhibition of the physiological anticoagulant, protein C, and promoted platelet aggregation. Higher concentrations inactivated the coagulation cascade and lysed platelets completely. These results suggest that intravariceal infusion of S.T.D. at considerable dilution may be at least as effective in inducing thrombosis as standard dosage, and possibly more so.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Coagulation / drug effects
  • Blood Platelets / drug effects
  • Endothelium, Vascular / drug effects
  • Esophageal and Gastric Varices / therapy*
  • Humans
  • Microscopy, Electron, Scanning
  • Platelet Aggregation / drug effects
  • Sclerosing Solutions / therapeutic use*
  • Sodium Tetradecyl Sulfate / therapeutic use*
  • Umbilical Veins / drug effects

Substances

  • Sclerosing Solutions
  • Sodium Tetradecyl Sulfate