Vein pretreatment with magnesium sulfate to prevent pain on injection of propofol is not justified

PURPOSE: Propofol produces anesthesia with rapid recovery. However, it causes pain or discomfort on injection. A number of techniques have been tried for minimizing propofol-induced pain with variable results. We have compared the efficacy of magnesium and lidocaine for the prevention of propofol induced pain. METHODS: Three hundred ASA I and II adults undergoing elective surgery were randomly assigned into three groups of 100 each. Group I received magnesium sulfate 1 g, Group II received lidocaine 2% (40 mg) and Group III received normal saline, all in a volume of 2 mL and accompanied by venous occlusion for one minute. Induction with propofol 2.5 mg.kg(-1) was accomplished following the release of venous occlusion. Pain was assessed on a four-point scale: 0 = no pain, 1 = mild pain, 2 = moderate pain, and 3 = severe pain at the time of pretreatment and propofol injection. Results were analyzed by 'Z' test. A P value of < 0.05 was considered as significant. RESULTS: Pain during i.v. pretreatment with magnesium was 31% as compared to 2% for both the lidocaine and control groups (P < 0.05). Seventy-six percent of patients in the control group had pain during i.v. propofol as compared to 32% and 42% in the magnesium and the lidocaine groups respectively (P < 0.05). Lidocaine and magnesium pretreatment were equally effective in attenuating pain during the propofol injection (P > 0.05). CONCLUSIONS: Intravenous magnesium and lidocaine pretreatment are equally effective in attenuating propofol-induced pain. However, magnesium pretreatment itself causes pain. Therefore, there is no justification in the use of magnesium pretreatment for attenuating pain associated with i.v. propofol.     

Diagnosis of 6 Mercaptopurine Hepatotoxicity Post Liver Transplantation Utilizing Metabolite Assays

Azathioprine and 6-mercaptopurine (6 MP) are commonly used as immunosuppression postsolid organ transplantation. Recently, a better understanding of the metabolism of these drugs has developed. 6 Mercaptopurine is metabolized by thiopurine methyl transferase (TPMT) which is under the control of a common genetic polymorphism. Genetic testing and measurement of levels of 6 MP metabolites allow identification of patients at risk of toxicity. We report two cases of cholestatic hepatocellular injury associated with 6 MP toxicity occurring after orthotopic liver transplantation. Cholestasis developed after the introduction of 6 MP. Patients underwent extensive investigation and 6 MP toxicity was considered only after all other causes had been excluded. Thiopurine methyl transferase alleles identified on genetic testing were normal as were the 6 thioguanine levels. However, 6-methyl mercaptopurine levels were significantly elevated into the toxic range. Cholestasis resolved within a few weeks of drug withdrawal. 6 Mercaptopurine hepatotoxicity can present with a variety of clinical, biochemical and histological manifestations post OLT and should be considered as a cause of liver enzyme elevation. Monitoring of 6 MP metabolite levels in addition to TPMT allele testing is useful to prevent 6 MP toxicity and to help guide therapy.     

Effect of shunt surgery on spleen size, portal pressure and oesophageal varices in patients with non-cirrhotic portal hypertension

Shunt surgery is considered to be the treatment of choice in patients with non-cirrhotic portal hypertension. There is little data on the effect of side-to-side lieno-renal (SSLR) shunt on oesophageal variceal size, splenic size and splenic pulp pressure (SPP) in patients with non-cirrhotic portal hypertension. We evaluated pre- and postoperatively endoscopic grading of varices, splenic size and SPP for predicting shunt patency in 86 patients with non-cirrhotic portal hypertension: 56 with extrahepatic portal venous obstruction (EHPVO) and 30 with non-cirrhotic portal fibrosis (NCPF). The EHPVO patients with patent shunts (n= 47) showed significant reduction in SPP (pre-operative 43.56±7.9 vs postoperative 29.96±7.7 cm of saline), splenic size (6.5±2.8 vs 4.00±2.6 cm below costal margin) and varices grades (2.96±0.5 vs 0.92±0.8). Patients with blocked shunt (n= 9) did not show significant reduction in SPP and varices grades. However, there was reduction in spleen size (8.6±3.0 vs 6.3±4.3). In the NCPF group, 28 had patent shunts and showed significant reduction in SPP (46.3±13.5 vs 33.8±7.6 cm of saline), splenic size (9.1±3.3 vs 6.8±4.6 cm below costal margin) and varices grades (2.8±0.7 vs 1.05±0.96). As only two patients with NCPF had blocked shunts, no statistical comparison between patients with patent and patients with blocked shunts could be done. In conclusion, following SSLR, there is a significant reduction in SPP and varices grades in patients with patent shunts. Endoscopic grading of varices can be used to predict shunt patency. However, spleen size is not a good criteria for predicting shunt patency.