Recently, lipid-free propofol with thiomersal as a preservative (Cleofol 1%®, Themis Pharmaceuticals, Mumbai, India) has become available in India. Venous thrombosis of the upper limb was caused by this agent in a patient requiring radiofrequency lesioning for trigeminal neuralgia. A 55-year-old, well-controlled (metoprolol) hypertensive woman was administered lipid-free propofol (Cleofol) 1.5 mg.kg−1 through a 20 G intravenous cannula positioned in the left forearm. The patient complained of severe pain in the forearm and arm at the time of injection, which subsided after flushing the cannula with normal saline. Two subsequent injections of propofol during lesioning also caused severe pain. Following the fourth bolus of propofol injected during lesioning, the patient woke up with excruciating pain in the limb. The superficial veins of the left forearm became prominent, tender, cord-like and the peripheral blood oxygen saturation (Spo2) monitored from the left index finger decreased to 78–80% (compared with 96–98% on the right side). The left forearm and hand were swollen, dusky blue and cold. There was a retrograde flow of blood into the intravenous giving set. The intravenous infusion in the left forearm was discontinued and a new line started on the right hand. Efforts to flush the cannula in the left forearm were unsuccessful, but on aspiration, a 5 cm blood clot was removed. Heparin 10 000 IU was injected as a bolus and an intravenous infusion of 5% dextrose with nitroglycerine at a rate of 5–8 μg.min−1 was started. Nifedipine 5 mg was administered orally. The Spo2 in the affected limb improved to 93–96% and the pain decreased over a period of 20 min. A similar episode of pain and cyanosis of the limb occurred 30 min after the first episode. Doppler examination revealed a block of the brachial vein at the left antecubital fossa and compression of the brachial artery by grossly engorged brachial veins. A second dose of heparin 10 000 IU was administered followed by 1000 IU.h−1 for the next 24 h. The patient's symptoms were relieved 20 min after the second episode. The oedema of the left upper limb resolved over a period of 48 h. The signs and symptoms in our patient were caused by thrombosis of the deep brachial veins. The reduction in Spo2 in the affected limb was probably related to the compression of brachial artery by engorged brachial veins and also by oedema due to deep venous obstruction. Pain, vascular changes [1] and thrombophlebitis [2] have been reported after administration of propofol formulations without soya bean oil. Tissue necrosis following extravasation of propofol has also been reported [3]. Activation of the kallikrein–kinin system in plasma with subsequent generation of bradykinin that acts locally to dilate the vein and increase its permeability has been reported [4]. This may explain the escape of the drug, leading to damage to the surrounding tissues, tissue oedema and subsequent arterial compromise. This report poses serious questions about the safety of lipid-free propofol.