Obstructive sleep apnoea (OSA) is defined as episodes of obstructive apnoeas and hypopnoeas during sleep with daytime somnolence. The gold standard in diagnostic tool patients with these symptoms is polisomnography. The goals of this study were to determine the frequency of OSA symptoms and the prevalence of OSA in patients undergoing operation. Patients were asked questions pertaining to symptoms of sleep apnoea. The patients who had two major symptoms or one major and two minor symptoms were invited to undergo a sleep study. Patients were diagnosed as OSA when they had apnoea-hypopnoea index higher than five. Forty-one patients with two major or one major and two minor symptoms of 433 patients were referred to the sleep laboratory. The most frequent major symptom was snoring, and the most frequent minor symptom was morning tiredness. In this connection, 18 (43.9%) patients accepted to be studied in the sleep laboratory (14 with two major, 4 with one major and two minor symptoms). Obstructive sleep apnoea was finally diagnosed in 14 patients or 3.2% of the initial entire population. Thirteen of them had two major symptoms, and only one of the 14 had one major and two minor symptoms. Six of the OSA patients were women. High percentage of OSA focus attention on anaesthesiology concerns of OSA. The exact management of each sleep apnoea patient with regard to intubation, extubation and pain control requires judgement and is a function of many anaesthesia, medical and surgical considerations. Therefore, we suggest that all patients should be asked for OSA symptoms, and patients with two major OSA symptoms must be evaluated with polisomnography.

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Cardiopulmonary bypass (CPB) contributes to the secretion of anti-inflammatory cytokines that mediate the inflammatory response observed during open heart surgery. In addition to many factors, type of anesthesia management affects immune response and central nervous system in cardiac surgery. The aim of this study was to assess the effect of propofol versus desflurane anesthesia on systemic immune modulation and central nervous system on patients undergoing coronary artery bypass grafting. Forty patients undergoing elective coronary artery bypass graft surgery with CPB were included in this prospective randomized study. Patients were allocated to receive propofol (n = 20) or desflurane (n = 20) for maintenance of anesthesia. The blood samples for IL-6, IL-8, TNF-α, and S100β were drawn just prior to the operation before the induction of anesthesia, second before cardiopulmonary bypass, third after CPB, fourth 4 h postoperatively at the ICU. Major finding in our study is that S100β levels were lower in propofol group when compared to desflurane anesthesia. And also immune reaction was less in patients exposed to desflurane anesthesia when compared to propofol anesthesia as indicated by lower plasma concentrations of IL-8 and IL-6. Propofol is more preferable in terms of S100β for anesthetic management for CABG.

TENS was more effective than placebo TENS or control treatments in decreasing pain and limiting opioid and nonopioid medication intake during the first 24-hour period following MS.

The aim of this experimental study was to investigate the possible protective effect of dexmedetomidine (DEX) on traumatic spinal cord injury (SCI). Twentytwo New Zealand rabbits were divided into three groups: sham (no drug or operation, n = 6), Control [SCI ? single dose of 1 mL saline intraperitoneally (i.p), after trauma; n = 8] and DEX (SCI ? 1 lg/kg dexmedetomidine in 1 mL, i.p, after trauma, n = 8). Laminectomy was performed at T10 and balloon angioplasty catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated by an independent observer according to the Tarlov scoring system. Blood, cerebrospinal fluid (CSF), tissue samples from spinal cord were taken for biochemical and histopathological evaluations. After 4 h of SCI, all animals in control or DEX treated groups became paraparesic. On the other hand, 24 h after SCI, partial improvements were observed in both control and DEX treated groups. Traumatic SCI leads to increase in the lipid peroxidation and decreases enzymatic or nonenzymatic endogenous antioxidative defense systems. Again, SCI leads to apoptosis in spinal cord. DEX treatment slightly prevented lipid peroxidation and augmented endogenous antioxidative defense systems in CSF or spinal cord tissue, but failed to prevent apoptosis or neurodeficit after traumatic SCI. Therefore, it could be suggested that treatment with dexmedetomidine does not produce beneficial results in SCI.