Intravenous ketoprofen in postoperative pain treatment after major abdominal surgery.

In recent years considerable attention has been paid to the treatment of postoperative pain, with regard to the favorable effect of adequate analgesia on patient outcome. Multimodal analgesia (e.g., opioids and nonsteroidal anti-inflammatory drugs [NSAIDs] or local anesthetics) is recommended for effective postoperative pain relief. There are few data on the use of NSAIDs in postoperative pain treatment after abdominal surgery. We conducted a randomized, double-blind, placebo-controlled study to assess the analgesic efficacy and safety of ketoprofen after major abdominal surgery. One and nine hours postoperatively patients received 100 mg of ketoprofen i.v. (n = 21) or placebo (n = 22) in addition to a pain-treatment protocol consisting of continuous infusion of tramadol 200 mg and metamizol 5 g over 24 hours with additional 25 mg i.v. tramadol in case of inadequate analgesia. Pain was assessed by numeric rating scale at rest and at deep breath 3, 6, 12, and 24 hours postoperatively and the total dose of tramadol used in the first 24 hours was recorded. Patients in the ketoprofen group had significantly lower pain scores both at rest and at deep breath, at 3 (p < 0.01), 6, and 12 hours (p < 0.05) postoperatively. The 24-hour use of tramadol was significantly lower in the ketoprofen group (p < 0.01), with less nausea and vomiting. There were no bleeding complications or other adverse events related to ketoprofen therapy. The study showed the value of short-term use of ketoprofen to improve the quality of analgesia after major abdominal surgery without significant adverse effects.

[Coagulation tests in septic surgical patients]. / Koagulacijski testovi u sepsi kirurskih bolesnika: kohortna studija.

AIM: To determine whether sequential change in coagulation parameters such as activated partial thromboplastin time (aPTT), prothrombin time (PT), platelets count and fibrinogen level may predict the outcome of patients in sepsis. STUDY DESIGN: Cohort longitudinal study. PATIENTS AND METHODS: Patients with positive two or more clinical criteria for sepsis were eligible for the study. Thirty patients were included, 24 male and 6 female. Eight patients survived, while 22 deceased. Median age of survivors was 66 years (range 23-77), and in non-survivors it was 69 years (range 48-79), p=0.37. In 9 patients malignancy was an underlying disease. APACHE II score was calculated at admittance, median value for survivors was 10 (range 7-15) and for non-survivors it was 26 (range 6-35), p=0.001. Calculated MODS score at the time blood cultures was 2 (range 0-9) for survivor and 6.5 (range 2-13) for non-survivors, p=0.007. Blood cultures were taken at the onset of sepsis, and in 29 patients they were positive. Coagulation parameters were measured at admittance, at the onset of sepsis and 48 hours after the introduction of the specific antimicrobial therapy. RESULTS: Analysis of variance for repeated measurements between survivors and non-survivors has shown that there were no differences in values of coagulation parameters. The only significant difference between these groups of patients was APACHE II and MODS score. In 7 patients with severe thrombocytopenia (<33,000 x 10(9)/L) as a result of irreversible septic shock a clinically visible bleeding was present in only one patient. DISCUSSION: Disseminated intravascular coagulation (DIC) is a clinical-pathological syndrome in which wide-spread intravascular coagulation is induced by procoagulants that are introduced or produced in the blood circulation and overcome the natural anticoagulant mechanisms. DIC causes tissue ischemia from occlusive microthrombi as well as bleeding from both the consumption of platelets and coagulation factors and the anticoagulant effect of products of secondary fibrinolysis. In sepsis, tissue factor which is the most common trigger of DIC can be generated and expressed on membranes of monocytes and endothelial cells during the systemic inflammatory response syndrome (SIRS). The wide-spread generation of thrombi in sepsis induces deposition of fibrin which leads to vessels obstruction and consumption of substantial amounts of haemostatic factors i.e. platelets, fibrinogen, factors V, VIII and others, protein C and antithrombin III (AT III). Intravascular thrombi trigger secretion of tissue plasmin activator (tPA) from endothelial cells which sets of compensatory thrombolysis which may reopen the occluded blood vessels. But byproducts of thrombolysis such as fibrin/fibrinogen degradation products may enhance bleeding by interfering with platelet aggregation, fibrin polymerization and thrombin activity. The typical feature of sepsis is depression of three powerful anticoagulant systems: protein C pathway, AT III pathway and tissue pathway factor inhibitor (TPFI). This sequence of events led us to hypothesize that alterations in coagulation parameters such as PT, aPTT, fibrinogen, platelets count may predict the outcome of disease, as it is well documented that the development of DIC confers prognosis of sepsis. The failure to distinguish survivors from non-survivors by the alteration in the coagulation parameters in this study may be due to a relatively low sample size or to the clinical necessity of an attending physician to substitute the deficient blood or coagulation product. CONCLUSION: The coagulation parameters PT, aPTT, platelet count and fibrinogen level can not serve as predictors of outcome in patients with sepsis. Further studies including more discerning coagulation parameters: AT III, D-dimer, soluble fibrin monomer, thrombin/antithrombin complex, plasmin/antiplasmin complex, fibrinopeptid A, fibrinopeptid B are necessary to evaluate whether these procoagulant and anticoagulant factors may help in predicting outcome and severity of sepsis.