[Risk assessment in pain therapy]. / Risikoabschätzung in der Schmerztherapie.

Analgesic therapy is not without risk. However, the risk of most analgesic interventions is minor compared to the risk of the inadequate treatment of pain and insufficient treatment may lead to chronic pain.A correct diagnosis should be the basis of any specific treatment of pain disorders. Only a diagnosis which implicates a multi-disciplinary assessment and which considers both the pathoanatomical, functional and biopsychosocial dysfunctions can lead to an adequate therapeutic intervention. Furthermore, therapeutic planning should include the personal needs of the patient and should have realistic aims.Pharmacological treatment is guided by the WHO pain ladder. The risks of the relevant substance groups must be considered. NSAIDs (non-steroidal anti-inflammatory drugs) which are included in all steps of the WHO pain ladder carry specific risks for the gastrointestinal, cardiovascular and renal systems and are contraindicated in many patients in need of analgesic therapy, e.g. in many elderly patients. Opioids which are recommended at steps 2 and 3 of the WHO pain ladder have less organ toxicity but they are still used reluctantly. Coanalgetics, especially antidepressants bear specific risks and the discussion on suicide rates under antidepressant medication is ongoing.Invasive methods such as the intrathecal application of analgesics are valuable procedures if the indication is correct and the treating physician has sufficient experience. Pain therapy is essential and the risks of the procedures are manageable. Considering the current knowledge on the mechanisms of pain sensitisation, the lack of adequate pain control can lead to chronic pain with severe consequences for the patient.

Selected blood coagulation parameters during extracorporeal circulation.

We investigated selected coagulation parameters in 13 patients who had undergone open heart surgery with extracorporeal circulation (ECC). During ECC factor XIIa increased considerably to 38%. This may lead to intravascular coagulation, which is however inhibited during ECC by the administered heparin. The C1-inhibitor activity decreased to 12% during ECC, this decrease was considerably greater and lasted longer than the decrease of the C1-inhibitor concentration, which declined to 59%. The levels of the other coagulation factors I, II, V, VII, X, XII, antithrombin III, alpha 2-antiplasmin and platelets decreased to 50-60%. The latter was predominantly due to hemodilution at the beginning of ECC. We assume that the critical period for the coagulation system in ECC appears when ECC is discontinued. At this point we have a high factor XIIa level and a low C1-inhibitor activity so that intravascular coagulation (DIC) may occur because then the inhibitory effect of heparin is neutralized by protamine.