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.
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 past few decades have witnessed major strides in postoperative analgesia with the creation of acute pain services, the increased use of regional and epidural techniques, and the introduction of the concept of multimodal approach.
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 these 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 a 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 (GI) 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
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 and the American Society of Anesthesia then followed suit, and the Joint Commission on Accreditation of Healthcare Organizations (JCAHO; now The Joint Commission) published “Standards for Pain Management in Hospital Settings,” which were implemented in 2001.2,3 In 2012, the American Society of Anesthesia published its updated guidelines on acute pain management.4
The guidelines from The Joint Commission incorporate pain measurements in the bedside chart in addition to tracking the patient’s temperature, blood pressure, heart rate, and respiratory rate, thus making pain rating the fifth vital sign.
However, a simple numerical assessment of pain on the visual analog scale or verbal rating scale does not differentiate between pain at rest and pain with movement or incident pain, which is usually more challenging to manage.
Also, to effectively adjust the analgesic regimen, one needs to track sedation and other possible adverse effects associated with the administration of analgesics such as nausea and vomiting, respiratory depression, and cognitive impairment.
The importance of good postoperative analgesia and its impact on favorable postsurgical outcomes are undeniable. Pain in the postoperative period may contribute to adverse outcomes, including thromboembolic and pulmonary complications.
Many factors influence our perception of postoperative pain. Determinants of the intensity, quality, and duration of postoperative pain include:
The site, nature, and duration of the operation, including the type of incision and the amount of intraoperative trauma
The physiologic and psychological makeup of the patient
The preoperative psychological, physical, and pharmacologic preparation of the patient
The presence of serious related complications
The anesthetic management
The quality of postoperative care. Some of the ineffectiveness of current medical analgesic therapy can be attributed to inadequate understanding by nurses of the pharmacology of narcotics.
Inadequate understanding by physicians of the nature of pain also has been demonstrated. A structured interview of 37 medical inpatients showed that 32% had severe distress despite a narcotic analgesic regimen; an additional 41% declared themselves to be in moderate distress. As part of the study, a questionnaire survey of 102 staff physicians showed an underestimation of effective dose ranges, an overestimation of the duration of action, and an exaggerated concern with the addictive potential of meperidine in a therapeutic dosing range. It is thought that the development of addiction in patients with no previous addictive history is rare. Children, perhaps the most dependent group in the hospital population, also bear the burden of postoperative suffering. As a reaction to discomfort, many children withdraw and vegetate. This may be misinterpreted as coping with the pain. Many immature patients fear injection, deny pain, and are unable to realize that a short-term discomfort may grant a longer period of analgesia.5,6 Postoperative pain management is still undermanaged, and the reason is multifactorial, although there is increased awareness, and more studies are being performed in this area.7
In summary, few major factors contribute to the inadequacy of traditional analgesic therapy. Foremost is the incomplete comprehension by medical personnel of analgesic pharmacodynamics. This lack of knowledge coupled with overconcern about respiratory depression and addiction liability leads to the administration of inadequate doses. Second is the inadequate use of interventional techniques (regional and neuraxial) along with systemic analgesics in the postoperative period. There are system deficiencies of structured pain management, such as protocols for assessment and management and education of caregivers. Logistics and the cost of administering pain management protocols in resource-deficient countries are common reasons. Another barrier to adequate analgesia is a common hospital community attitude that stoicism is a virtue. A suffering patient may sense such an attitude and, rather than attacking this formidable barrier, refrain from requesting appropriate medication.8
The perioperative physiologic changes that occur after surgery affect all organ systems.
Approximately 5% of the worldwide surgical population will develop some type of perioperative cardiac morbidity. An imbalance between myocardial oxygen supply and demand contributes to this. Uncontrolled pain causes an increase in sympathetic tone and a resetting of baroreceptors that cause an increase in heart rate and blood pressure. This in turn translates into increased work for the myocardium. In the presence of coronary artery disease, this predisposes the myocardium to ischemia and arrhythmias. Stress per se is also arrhythmogenic in a nonischemic myocardium.
Neural outflow also causes redistribution of blood to and within various organs. Besides the increase in catecholamines and sympathetic neural outflow, there is a reflex decrease in parasympathetic outflow caused by pain. This imbalance in the autonomic nervous system alters baroreceptor settings. Although individual randomized controlled trials might seem equivocal on whether postoperative pain management might affect perioperative outcomes, two meta-analyses suggest that thoracic epidural analgesia might be associated with an improvement in perioperative cardiac outcomes.9,10
Pulmonary dysfunction is commonly seen after thoracic and upper abdominal surgery. It is a significant problem affecting up to 10% patients undergoing elective abdominal surgery. The pathophysiology is multifactorial and includes disruption of normal respiratory muscle activity; reflex inhibition of diaphragmatic function; and reflex increased spinal arc activity, causing increased intercostal and abdominal muscle tone and pain. All of these factors cause voluntary inhibition of respiratory activity, which manifests clinically as a decrease in functional residual capacity and tidal volume. Preexisting pulmonary disease or respiratory depression caused by opioids may compound these problems. Multiple meta-analyses suggest that postoperative pain management may decrease the risk of postoperative pulmonary complications.9,11,12
Any injury provokes a neurohumoral response involving the hypothalamic–pituitary–adrenal axis, activation of sympathetic nervous system, and an increase in glucagon secretion.1 Surgery leads to a similar reproducible response, which causes hyperglycemia, increased lipolysis, lipid oxidation, accelerated protein breakdown, and nitrogen loss.2,3
These responses begin during surgery and may last for many days, especially after major abdominal or thoracic surgery. The stress response peaks in the postoperative period.4 Clinically, this presents as hypertension, tachycardia, arrhythmias, myocardial ischemia, protein catabolism, immune system suppression, and impaired renal excretory function. Suppression of the stress response is possible but not complete. The intensity of the stress response depends on the site of surgery (extremities vs. thoracic or abdominal), pain control modality, (neuraxial vs. systemic), medication used (local anesthetic vs. opioid), and initiation and maintenance of treatment (intraoperative vs. postoperative). Studies have shown that stress response and morbidity in the first 24 hours are lower in patients receiving epidural analgesia with local anesthetics with or without opioids.13,14
A combination of surgery and anesthesia in addition to pain produces a decrease in gastric motility, especially in the colon. Whereas the stomach and small intestines recover within 12 to 24 hours after abdominal surgery, the colon recovers in 48 to 72 hours. The pathophysiology of postoperative ileus and decreased GI motility is multifactorial. It includes neurogenic (spinal, supraspinal, adrenergic) pathways, local inflammatory responses that initiate neurogenic inhibitory pathways, and pharmacologic mechanisms. Analgesic agents differ in their effects on GI motility.15 Epidural opioids inhibit GI motility less than systemic opioids.16
A large amount of clinical evidence shows suppression of both humoral and cellular mechanisms of the immune system after trauma and surgery. These mechanisms include a decrease in responsiveness to antigen and mitogen, delayed hypersensitivity, natural killer cell activity, and antibody response.17 The exact causative mechanism is not known. Increased release of glucocorticoids is seen as one of the reasons, but other stress response hormones may also cause immune modulation.18
The incidence of fatal pulmonary embolism in the absence of thromboembolic prophylaxis is about 0.1% to 0.8% after general surgery, 0.3% to 0.7% after elective hip surgery, and 4% to 7% after emergency hip surgery. Surgery causes activation of the coagulation cascade, increased platelet activity, and decreased fibrinolytic activity, leading to increased coagulability. It is believed that intraoperative neuraxial anesthesia may attenuate perioperative hypercoagulability and increased extremity blood flow, both of which may contribute to a decrease in perioperative coagulation-related complications. However, it is unclear if postoperative analgesia continues to provide the same benefits as those conferred by intraoperative neuraxial anesthesia. It has been found to produce less platelet activity and improved fibrinolysis, which may be related to the systemic effects of local anesthetics.19
Postoperatively, 10% to 50% of patients develop transient cognitive impairment, which is worse on the second day, but they usually recover within 1 week. Elderly patients may take up to 3 months to recover baseline cognitive function. Exact mechanisms are not clear, and there are no conclusive data to suggest a particular choice of anesthetic technique. Delirium occurs in about 10% of patients undergoing noncardiac surgery after age 50 years. Electrolyte abnormality, sleep apnea, history of alcohol abuse, and benzodiazepines and meperidine intake are risk factors for delirium. Studies have found that high levels of postoperative pain can cause delirium, and vice versa, delirium can impair cognition and cause exacerbation of pain.
A surgical incision cuts through a variety of tissues, including nerve endings, and activates specific nociceptors (pain receptors) as well as free nerve endings. It is associated with the release of inflammatory mediators such as bradykinin, serotonin, and histamine, contributing to peripheral sensitization. Clinically, this phenomenon is manifested by hyperalgesia, which is an amplification of noxious pain signals. These painful signals are transmitted to the dorsal horn of the spinal cord in an amplified fashion and are increased in duration.
The nociceptor information is transmitted to the cord via the A-δ (myelinated) fibers and the C (unmyelinated) fibers. When peripheral sensitization occurs, painful information can also be carried by A-α and A-β fibers. This is manifested by allodynia, a pain state in which non-noxious stimuli are transformed and expressed as painful. Signals entering the central nervous system from the periphery are increased in amplitude and duration. This is the phenomenon of “wind up” or central sensitization.20
Analgesic techniques, to be effective, need to counteract these activations of nociceptors at the periphery as well as centrally, thus the need for a multimodal or “balanced” analgesia. Multimodal technique of using more than one group of analgesics or technique provides additive or synergistic effects while minimizing individual side effects.21
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