Transition from acute to chronic pain

Abstract

A Feizerfan FRCA G Sheh BHB MBChB FAFRM(RACP) FFPMANZCA Pain is commonly classified into acute and chronic. Acute pain implies a painful condition with a rapid onset or of a short course whereas chronic pain is referred to as a painful condition persisting beyond the normal time of healing. Transition of acute pain to chronic pain is an observed entity associated with enormous burden on the healthcare system. Minimization of this transition has been a challenge for decades. Numerous studies have investigated different factors that increase susceptibility in transition of acute to chronic pain. This article focuses on the basic science and pathophysiological changes during pain processing and clinical modalities aiming to minimize the risk of transition from acute to chronic pain. Pain physiology during acute tissue injury In the periphery Acute tissue insults such as heat, cold, chemical or mechanical injury, cause disturbance in homeosta-sis, and stimulate the pain receptors, called noci-ceptors. Homeostasis can be restored by activation and complex interaction among autonomic, endo-crine, immune, and nervous systems. 1 After an injury, a wide range of inflammatory mediators are released locally either from damaged tissue or by activated mast cells and neutrophils. These media-tors are adenosine-5-triphosphate (ATP), bradyki-nin, prostaglandin E2, sodium (Na þ), hydrogen (H þ), potassium (K þ), histamine, and serotonin. The released substances interact with their corre-sponding receptors located on the peripheral noci-ceptive neurones leading to depolarization of cell membrane and impulse generation within Ad and C fibres. After tissue injury, cyclo-oxygenase-2 enzyme is activated and macrophages release pro-inflammatory substances such as interleukin-1B, interleukin-6, nerve growth factor, and tumour ne-crosis factor-alpha (TNF-a). Peripheral inflamma-tion at the site of tissue injury activates C-fibres, which release substance P, calcitonin gene-related peptide (CGRP), neurokinin A and nitric oxide (NO) in a retrograde fashion called 'neurogenic inflammation'. This amplifies the whole process resulting in an 'inflammatory soup'. The end result is further activation of 'silent' C fibres with a reduction of pain threshold and increased excitability.