Desaturation during Onyx embolization.

Editor—The Onyx Liquid Embolic System (Onyx; Micro Therapeutics, Inc., Irvine, CA, USA) is a new non-adhesive liquid embolic agent and is currently being used at our institution in the embolization of cerebral vascular lesions. The disadvantage of Onyx is that it is dissolved in dimethyl sulphoxide (DMSO). Systemic toxicity, such as pulmonary oedema, bronchospasm, bradyarrhythmia, and even cardiac arrest, has been a major concern because of the action potential reducing effects of DMSO. There are reports regarding the use of Onyx in the treatment of arteriovenous malformations (AVMs) and dural arteriovenous fistulas (DAVFs) from the operative point of view, but there is little on the anaesthetic experience. – 6 This is the first study in a large number of patients undergoing embolization on the effect of Onyx injection on the anaesthetic management and oxygenation. This retrospective study included 69 patients, 10–73 yr old treated with Onyx embolization for AVMs and DAVFs during 1 yr (January–December 2008). None of these patients had any significant cardiac, pulmonary medical history, orcurrent problems. General anaesthesia was induced with propofol 2 mg kg, fentanyl 2 mg kg, and cisatracurium 0.15 mg kg and maintained with remifentanil and sevoflurane or propofol in 50% O2/N2O mixture. Ventilation was maintained to achieve end-tidal ECO2 : 4.0–4.7 pKa. Changes in haemodynamic parameter variables by more than 20% from the pre-induction baseline values were considered significant. Immediately after extubation, all patients received supplemental oxygen, 5 litre min, by a facemask. In total, 23 patients had desaturation intraoperatively: 17 by 1–3% and six by 4–8% from baseline. All the episodes of desaturation happened 3–7 min after the initiation of infusion of DMSO, lasted for about 10 min and then SpO2 returned to baseline without any clinical intervention. No significant haemodynamic changes were observed that could be attributable to DMSO infusion. In a patient with a giant AVM, we observed severe desaturation (SpO2 : 89%, PaO2 : 8.1 kPa) 10 min after extubation, accompanied by tachypnoea. Over the course of 20 min, the patient’s oxygen saturation gradually improved to 97% (PaO2 : 10.3 kPa) and 20 min later the patient met discharge criteria from the postanaesthesia care unit. Figure 1 presents graphically the SpO2 changes. In most cases, desaturation was clinically insignificant. In one case of severe desaturation, the patient did not develop acute respiratory distress syndrome (ARDS) or pulmonary oedema. It is known that most of the DMSO metabolites are eliminated through the kidneys, but some of the early elimination occurs via the skin or lungs. This may cause a relative decrease in the partial pressure of oxygen in the alveoli in the intraoperative and postoperative period. Other potential causes of desaturation include diffusion difficulties at the level of alveolar-capillary membrane such as intrapulmonary shunt, ventilation/perfusion mismatching, or even