Randomized clinical trial on acute effects of i.v. iron sucrose during haemodialysis

Aim: Haemodialysis induces endothelial dysfunction by oxidation and inflammation. Intravenous iron administration during haemodialysis could worsen endothelial dysfunction. The aim of this study was to ascertain if iron produces endothelial dysfunction and the possible neutralizing effect of N‐acetylcysteine when infused before iron. The oxidative and inflammatory effects of iron during haemodialysis were also assessed. Methods: Forty patients undergoing haemodialysis were studied in a randomized and cross‐over design with and without N‐acetylcysteine infused before iron sucrose (50 or 100 mg). Plasma Von Willebrand factor (vWF), soluble intercellular adhesion molecule‐1 (sICAM‐1) levels, malondialdehyde, total antioxidant capacity, CD11b/CD18 expression in monocytes, interleukin (IL)‐8 in monocytes and plasma IL‐8 were studied at baseline and during haemodialysis. Results: Haemodialysis produced significant (P < 0.001) increase in plasma vWF, sICAM‐1, malondialdehyde, IL‐8 and CD11b/CD18 expression in monocytes, as well as decrease in total antioxidant capacity. Iron induced significant increase in plasma malondialdehyde and IL‐8 in monocytes, but had no effect on total antioxidant capacity, CD11b/CD18 expression, plasma IL‐8, vWF and sICAM‐1. The addition of N‐acetylcysteine to 50 mg of iron produced a significant (P = 0.040) decrease in malondialdehyde. Conclusion: Standard (100 mg) and low (50 mg) doses of iron during haemodialysis had no effects on endothelium. Iron only had minor effects on inflammation and produced an increase in oxidative stress, which was neutralized by N‐acetylcysteine at low iron dose. Haemodialysis caused a significant increase in oxidative stress, inflammation and endothelial dysfunction markers.     

Respiratory depression following epidural morphine in an infant of three months of age

Epidural administration of combinations of opioids and a local anaesthetic provides prompt and effective analgesia and is increasingly used in paediatric anaesthesia. However, respiratory depression by rostral spread of opioid in the CSF is by far the greatest concern after epidural morphine. An infant of three months of age underwent portoenterostomy (Kasai's operation) for extrahepatic biliary duct atresia. A median approach at the L₃–L₄ epidural interspace was used and a dose of 1 ml·kg^–1 of 0.125% bupivacaine with adrenaline 1:400 000 mixed with 50 μg·kg^–1 morphine was injected using a 19 gauge Tuohy needle. Six h after epidural morphine, the infant developed respiratory depression with an increase in drowsiness, miosis and decreased respiratory rate. Low arterial saturation ( S pO₂) was detected by pulse oximetry and confirmed by blood gas analysis. An intravenous bolus of 5 μg·kg^–1 naloxone followed by a 3-h infusion of 2 μg·kg^–1·h^–1 resulted in complete reversal of signs and symptoms of respiratory depression. Epidural opioids should be limited to paediatric patients admitted to specialized recovery units for the first postoperative day.