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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, ...