These data suggest that, in addition to underlying clinical conditions, some invasive procedures can be independent risk factors for nosocomial infection in ICU.
Intravenous administration of low dose ketamine before induction and maintenance with propofol preserves hemodynamic stability without changing the duration and the quality of recovery compared with propofol alone.
Malposition of the chest tube is an important aetiological factor of Horner's syndrome, and it is reversible if the tube position is corrected urgently.
The mechanisms of injury of, and methods of treating patients with, carbon monoxide (CO) poisoning are poorly understood. Besides the hypoxic degenerative effects of CO, reoxygenation injury may play an important role. Amifostine (Ami), which is most often used in radiotherapy for its tissue protective characteristics, may offer benefits. In this study, investigators evaluated the effectiveness of various treatments in a CO-poisoned rat model. A total of 36 Wistar rats were randomly assigned to 1 of 6 groups (n=6 each), including control and poisoned groups exposed to CO at 2000 ppm (v/v) for 1 h, followed by various 1-h treatments: group C (control), group COair (ambient air), group CO-NBO (normobaric 100% oxygen), group CO-HBO (hyperbaric oxygen with 3 atmospheres absolute [3 ATA]), group CO-NBO-Ami (normobaric oxygen with intraperitoneal [i.p.] injection of amifostine 250 mg/kg body weight [bw]), and group CO-70O (70% O2 and 5% CO2 with dexamethasone 10 mg/kg bw, i.p.). Blood gas analysis, carboxyhemoglobin determination, brain tissue lipid peroxidation, and glutathione peroxidase (GSHPx), superoxide dismutase (SOD), lactate dehydrogenase (LDH), and creatine kinase (CK) activities were evaluated. Carboxyhemoglobin concentration in the air-treated group was 44+/-2%; it decreased to the control level with all oxygen treatments. Brain tissue GSH-Px and SOD measurements did not change. The activity of LDH in group CO-HBO and the activities of LDH and CK in group CO-70O were similar to those of group C. Lipid peroxides were high in ambient air and normobaric oxygen, but HBO, amifostine with oxygen, or 70% O2 reduced these to control levels (P<.05).
Pain intensity may be high in the postoperative period after spinal vertebral surgery. The aim of the study was to compare the effectiveness and cost of patient controlled analgesia (PCA) with tramadol versus low dose tramadol-paracetamol on postoperative pain. A total of 60 patients were randomly divided into two groups. One group received 1.5 mg/kg tramadol (Group T) while the other group received 0.75 mg/kg tramadol plus 1 g of paracetamol (Group P) intravenously via a PCA device immediately after surgery and the patients were transferred to a recovery room, Tramadol was continuously infused at a rate of 0.5 mL/h in both groups, at a dose of 10 mg/mL in Group T and 5 mg/mL in Group P. The bolus and infusion programs were adjusted to administer a 1 mL bolus dose of tramadol with a lock time of 10 minutes. In Group P, 1 g of paracetamol was injected intravenously every 6 hours. The four-point nausea scale, numeric rating scale for pain assessment, Ramsey sedation scale, blood pressure, heart rate, respiration rate, peripheral oxygen saturation values and side effects were recorded at 0, 15 and 30 minutes, and at 1, 2, 4, 6, 12, 18 and 24 hours. The time to reach an Aldrete score of 9 was also recorded. A cost analysis for both groups was performed. In Group P, the numeric rating scale scores were significantly lower than that in Group T at 0 and 15 minutes. The number of side effects, additional analgesic requirement and the total dose of tramadol were lower in Group P than in Group T. However, the total cost of postoperative analgesics was significantly higher in Group P than in Group T (p < 0.001). We conclude that PCA using tramadol-paracetamol could be used safely for postoperative pain relief after spinal vertebral surgery, although at a higher cost than with tramadol alone.
It is important to be rigorous in investigating the etiology of low-back pain. Meralgia paresthetica can mimic low-back pain because of the similarity of the symptoms. It can be treated by conservative or ablative therapeutic interventions; however, conservative methods should be considered primarily.
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