Almost everyone in the SICU had SIRS. Therefore, because of its poor specificity, SIRS was not helpful predicting severe sepsis and septic shock. Patients who developed sepsis or severe sepsis had higher crude mortality and length of stay than those who did not. Studies designed to identify those who develop complications of SIRS would be very useful.

Plasma levels of local anaesthetics following their injection are affected by many factors. Serial plasma levels following injection of lignocaine and prilocaine at various rates in over 500 patients have been measured and this has allowed some of these factors to be assessed and quantified. The vascularity of the site of injection causes major differences in the maximum plasma level. Prilocaine consistently gives lower levels than lignocaine. Adrenaline causes a reduction in the plasma levels of both drugs and the optimal concentration is 1:200,000. Speed of injection is important when giving the drugs intravenously but not epidurally. The concentration of the injected solution does not affect the plasma levels. The weight and age of the patients (all adult females) were unrelated to the mayi'mnm plasma levels.

Plasma levels of lidocaine were measured in 5 normal male volunteers following both intravenous and oral administration of the drug. Each subject received a constant-rate intravenous infusion lasting for 60 minutes and an exponential intravenous infusion which allowed administration of the drug at an ever-decreasing rate having a half-life of 50 minutes.In each case the total dose of lidocaine was 250 mg. The subjects also received a 250 mg. and a 500 mg. oral dose administered in tablet form. The plasma level data were subjected to pharmacokinetic analysis with the use of a two-compartment open model to describe the lidocaine disposition. These calculations suggest that approximately 5 to 7 hours of constant intravenous infusion would be required to approach steady-state plasma levels in human subfects. The plasma level data after oral administration indicate that approximately 35 per cent of the 250 and 500 mg. oral doses reached the systemic circulation. Subfective symptoms typical of lidocaine were noted in some cases after the 500 mg. oral doses. Since these symptoms were noted when the blood levels of lidocaine were lower than those following intravenous administration, it is suggested that they may, in part, be due to a metabolite formed during the first passage of the drug through the liver.

We report a prospective, randomized, controlled clinical trial to evaluate the efficacy of antibiotic-bonded catheters in reducing the incidence of intravascular catheter-related infections. Ninety-three central venous catheters and 85 arterial catheters were studied in the surgical intensive care unit. Study catheters were pretreated with the cationic surfactant tridodecylmethylammonium chloride. The anionic antibiotic, cefazolin, was bonded before insertion of the catheters by immersing them in a 50-mg/mL solution. Fourteen percent of the 81 catheters in the control group were infected, compared with 2% of the 97 antibiotic-bonded catheters. Staphylococcus epidermidis was the most common organism obtained. There was no significant difference in the number of colonized or clinically inflamed catheter insertion sites. None of the 100 antibiotic immersion solutions yielded anything on microbiologic culture. We conclude that antibiotic bonding is an efficient, safe, and cost-effective method of reducing intravascular catheter infection in patients who are in intensive care units.

Fractures of the pisiform are often missed due to improper radiographic evaluation and a tendency to focus on other, more obvious injuries. Delayed diagnosis may result in disabling sequelae. A high index of clinical suspicion and appropriate radiographic examination will establish the correct diagnosis. Ten patients with pisiform fracture are presented. The anatomy, mechanism of injury, clinical presentation, radiographic features, and evaluation of this injury are discussed.

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Forty-seven patients demonstrating prolonged apnoea after suxamethonium have been investigated in a 3-year survey carried out in southeast Scotland. Clinical information, and serum cholinesterase studies using a new substrate, succinyldithiocholine, provide evidence on the aetiology of suxamethonium hypersensitivity. While 13 patients possessed only variant forms of the serum enzyme, the remaining 34 patients appeared to have a catalytically active form of cholinesterase. The causes of prolonged apnoea in the latter group are discussed. The value of screening the relatives of patients with cholinesterase variants is demonstrated by the finding of 26 relatives "at risk" out of 123 screened.

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