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A Case of Acute Opioid Overdose

Pain is a unique universal experience. Painful experiences span an extensive spectrum of intensity, ranging from mild discomfort to debilitating and excruciating agony. Apart from the physical dimension, pain is also a subjective experience (Hawthorn & Redmond, 1998, p. 1-3). According to the International Association for the Study of Pain (IASP) Subcommittee on Taxonomy, pain refers to “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Brannon & Feist, 2009, p. 165).

Pain can either be categorized as nociceptive (acute) or non-nociceptive (chronic, non-malignant, and benign) pain. Nociceptive pain occurs as a normal bodily reaction to painful stimulus transmitted through nociceptive pathways. This reaction is the process of transmission of pain from the site of tissue injury to the central nervous system. Acute pain can be treated much easily because it responds to a wide range of analgesics. Nociceptive pain can further be divided into visceral and somatic pain. The experience of somatic pain is concentrated in superficial structures, fascia, and muscles.

Often described as achy or dull, acute pain is highly localized and is in consonance with the underlying lesions. On the contrary, visceral pain occurs in hollow organs. Visceral

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pain is deep, cramp-like, squeezing, and poorly localized. Common examples of visceral pain include myocardial infarction and intestinal contractions. One important distinction between visceral and somatic pain is that the latter is strongly related to autonomic sensations and visceral pain is often felt at sites remote from the exact site of tissue injury (Brooker & Nicol 2003, p. 120).

The Physiological Processes Involved in Acute Pain Sensory receptors are discriminatorily sensitive to potentially noxious or noxious stimuli prevalent in the connective tissues, abdominal, thoracic, and visceral viscera, muscles, bones, and skin. The free nerve endings of sensory receptors (nociceptors) involved in the transduction of noxious stimuli initiate the conduction of electrical discharges from the site of tissue injury to the spinal cord through A-fibers (A and A) and C-fibers.

The 2. 5 m thick A fibers are thinly myelinated hence they can only conduct action potentials at a speed of 5 m/s or less. When these fibers are activated; a sharp, stinging pain sensation is induced. Contrarily, C fibers are about 0. 3 ? m thick and unmyelinated. These fibers conduct action potentials at a speed of 2 m/s or less. When C fibers are activated by noxious stimuli, a vaguely localized burning or dull pain is developed (Doyle 2005, p.  289; Brooker & Nicol 2003, p. 113).

The stimulation of nociceptive pain is determined by a well defined threshold below which pain cannot be perceived. The perception threshold is relatively constant in all individuals contrary to popular thought. The difference in pain perception between individuals can be explained by the differences in the maximum amount of pain stimulation that an individual can tolerate; hence the pain tolerance threshold (Brooker & Nicol 2003, p. 112).

Several theories have been postulated to explain the processes of pain perception. The common one is the ‘gate control theory’. The gate control theory provides a more extensive biopsychsocial rationale for understanding the perception of pain. It examines not only the physical sensations involved in pain perception, but also the influence of psychosocial factors and their importance in pain treatment and management (Kahneman et al 2003, p. 159).

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