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Pain relief in an acute pain situation, besides having a humane value, has an important bearing in the well-being of an individual. Although it may not be possible to achieve total relief in all situations, a serious effort should be made.

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Since the discovery of opioid receptors in 1978, efforts have been made to improve the delivery of analgesic drugs in a more effective way. Thanks to these advances in basic science on the clinical front, the last two decades have witnessed major strides in postoperative analgesia with the creation of acute pain services, the increased use of epidural analgesia, and the introduction of the concept of patient-controlled analgesia.

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The tissue damage produced by surgery is similar to that of acute injury. It causes local and systemic noxious stimuli that initiate nociceptive impulses, relays, and reflexes throughout the nervous system. In addition to the disturbances associated with the conscious interpretation of theses impulses, there are autonomic effects generated that may disrupt the healing and recovery process. The deleterious physiologic side effects of acute pain are well recognized. In the patient who is breathing spontaneously, muscle splinting (seen in conjunction with discomfort of chest or abdominal origin) may result in decreased vital capacity, decreased functional residual capacity, and ultimately decreased alveolar ventilation. Atelectasis is a frequent postoperative complication. Discomfort experienced during coughing may result in retention of secretions and subsequent pneumonia. The sympathetic response to pain may cause increased cardiovascular demands. This may be apparent clinically by signs of tachycardia, increased peripheral resistance, and hypertension; these signs are associated with increased cardiac work and myocardial oxygen consumption. The potential for myocardial ischemia and infarction is obvious. Muscle spasm produced by segmental and suprasegmental reflex motor activity may perpetuate pain. In the chest wall and abdomen, pain and muscle spasm may compromise respiratory function. The gastrointestinal tract similarly is affected by increased sympathetic activity. Pain increases intestinal secretions and smooth muscle sphincter tone and decreases intestinal motility. By similar mechanisms, pain may produce urinary retention. Acute injury also has an impact on the endocrine system, causing sodium and water retention and hyperglycemia. Immobility from acute postoperative pain may predispose the patient to deep vein thrombosis and pulmonary embolism as a result of venostasis and platelet aggregation. In a complex intertwined relationship, psychological alterations may occur concomitantly with the physiologic ones.1

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Numerous guidelines have been published about the management of postoperative pain. First the Agency for Health Care Policy and Research (AHCPR) took the lead in educating caregivers as well as the public. The American Pain Society as well as the American Society of Anesthesia then followed suit, and the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) has published “Standards for Pain Management in Hospital Settings” that were implemented in 2001.2,3

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The guidelines from JCAHO incorporate pain measurements in the bedside chart in addition to tracking the patient’s temperature, blood pressure, heart rate, ...

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