Multimodal analgesia for outpatients

Pain has been defined by the International Association for the Study of Pain (IASP) as: an unpleasant sensory or emotional experience associated with actual or potential tissue damage or described in terms of such damage. Physiologically pain acts as a homeostatic, protective warning system. Guarding and limited activity are common signs of pain that are indicative of the severity of pain. Severe or persistent (chronic) pain is maladaptive producing pathological responses including persistent hypersensitivity, the spread of pain to uninjured tissues and allodynia. The pain and inflammatory responses or surgical procedures may lead to abnormal behaviours, depression and chronic sickness.

Pain processes and consequences

Pain is normally produced by mechanical, chemical or thermal stimulation of small diameter high-threshold A-delta and C sensory nerve fibres. Chemical mediators of pain and inflammation include histamine, serotonin, bradykinin, leukotrienes, prostaglandins (E2 ), interleukins (IL-1, IL-6), neutrophil-chemotactic peptides, nerve growth factor (NGF) and neuropeptides including substance P. These substances enhance the excitability of sensory nerves and postganglionic sympathetic nerve fibre activity leading to peripheral sensitisation, hyperalgesia and allodynia. Inflammation or nerve damage (neuropathic pain) increases the sensitivity of peripheral terminals of A-delta and C fibres. Current evidence suggests that activation of NMDA receptors, which facilitates calcium entry into cells is an integral component of the wind-up phenomenon and the development of central sensitisation. A similar phenomenon in the hippocampus has been termed long-term potentiation (LTP) and is thought to contribute to pain memory. […]