Basics of Acute Postoperative Pain

Acute pain is an important fear for most patients and influences their recovery and overall experience. Poorly treated, it could lead to undesirable effects and patient dissatisfaction. Hence, it is important to understand, assess and treat acute pain effectively. Pain management has been transferred from intraoperative into per operative period throughout the emergence of modern anesthesiology. Pain management in postoperative period is one of the most essential components of sufficient post-surgical patients care. The objective of this review is to define and demonstrate the risks and different sequelae of acute post operative pain.

Acute pain perception begins with activation of specific sensory nerves, termed nociceptors. These are unencapsulated free nerve endings that are present in the skin, deep somatic tissue and viscera. Providing the stimulus is suitably intense, high threshold nociceptors will still activate in the absence of actual tissue damage. Nociceptors are probably activated by mechanical distortion of the nerve leading to an increase in H+ and K+ concentration. Nociceptors can be divided into two main classes; A-delta and C fibers. The main properties of these fibers are summarized in the Multiple tracts and centers exist within the central nervous systems which are responsible for the transmission, modulation and perception of noxious stimuli. It is important to realize that these areas should not be considered as fixed or functioning in isolation. Rather, they are subject to change from both descending and ascending pathways and can alter or expand their connections to interact with adjacent nerves.
[8] Cell bodies of afferent nerves lie in the DRG with fibers synapsing in the dorsal horn of the spinal cord. The output from the dorsal horn is however dependent on other neuronal input to the synapse. Afferent neurons may divide prior to entering the cord and send branches cephalic or caudal in the longitudinal tract of Lissauer before synapsing with dorsal horn neurons. The result of this being that a single C-fiber afferent may be responsible for innervating dorsal horn neurons at multiple spinal levels.
[9] The gray matter of the spinal cord can be divided into ten physiologically and histological distinct layers known as rexed lamina. Laminae 1 to 6 and 10 are the sites that sensory nerves synapse with dorsal horn cells and are important in pain transmission. Laminas 7-9 are involved with motor function.

Physiology of Pain
The ability of the somatosensory system to detect noxious and potentially tissue-damaging stimuli is an important protective mechanism that involves multiple interacting peripheral and central mechanisms. The detection of noxious stimuli requires activation of peripheral sensory organs (nociceptors) and transduction into action potentials for conduction to the central nervous system. Nociceptors are stimulated by chemical, thermal or mechanical damage and trigger the nociceptive impulses.
[11] Nociceptive primary afferents are widely distributed throughout the body (skin, muscle, joints, viscera, meninges) and comprise both lightly myelinated A-delta fibers (diameter 2-5 mm) and slow-conducting unmyelinated C-fibers (diameter <2 mm). These fibers enter the dorsal horn of the spinal cord and synapse at different sites (Aδ at laminae II and V, C at laminae II). The substantia gelatinosa (lamina II) integrates these inputs and second-order neurons form the ascending spinothalamic and spinoreticular pathways on the contralateral side, figure (2).
[12] The larger AB fibres conducting "touch" and descending pathways stimulate inhibitory interneurons within the substantia gelatinosa and inhibit C fibre nociceptive inputs. This is the basis of the gate theory of pain. Pain may be modified by altering the neural pathway from its origin at the nociceptor to its interpretation within the central nervous system by various agents. Psychological factors that influence the experience of pain include the processes of attention, other cognitive processes (e.g. memory/learning, thought processing, beliefs and mood), behavioral responses, and interactions with the person's environment. [13]

Assessment and Measurement of Acute Pain
Pain should be assessed within a biopsychosocial model that recognizes that physiological, psychological and environmental factors influence the overall pain experience. The assessment of acute pain should include a thorough general medical history and physical examination, a specific 'pain history' and an evaluation of associated functional impairment along with any side effects of treatment. In acute pain management, assessment must be undertaken at appropriately frequent intervals. [14] Sometimes associated factors such as hyperalgesia, the stress response (e.g. plasma cortisol concentrations), behavioral responses (e.g. facial expression), functional impairment (e.g. coughing, ambulation) or physiological responses (e.g. changes in heart rate) may provide additional information. [15] The assessment of acute pain should include a thorough general medical history and physical examination, a specific 'pain history' and an evaluation of associated functional impairment. In acute pain management, assessment must be undertaken at appropriately frequent intervals. At these times, evaluation of pain intensity, functional impact, and side effects of treatment must be undertaken and recorded using tools and scales that are consistent, valid and reliable. [16]  The well-known visual analogue scale (VAS) and numeric rating scale (NRS) for assessment of pain intensity agree well and are equally sensitive in assessing acute pain after surgery, and they are both superior to a four-point verbal categorical rating scale (VRS). They may be used for worst, least, or average pain over the last 24 h, or during the last week. [17] Assessment of pain immediately after surgery can be more difficult and lead to greater inter patient variability in pain scores because of transient anesthetic-

Adverse Physiological and Psychological Aspects of Pain
Clinically significant injury such as surgeries responses can lead to a range of physiological effects which may lead to adverse clinical effects. Patients at greatest risk of adverse outcomes from unrelieved acute pain include very young or elderly patients, those with concurrent medical illnesses and those undergoing major surgery. [18] Sustained acute nociceptive input, as occurs after surgery can also have a major influence on psychological function, which may in turn alter pain perception. Failure to relieve acute pain may result in increasing anxiety, inability to sleep, demoralization, a feeling of helplessness, loss of control, inability to think and interact with others -in the most extreme situations, where patients can no longer communicate, effectively they have lost their autonomy. [19] Aggressive perioperative pain prevention can yield both short-term and long-term benefits as unrelieved pain affects patient recovery, prolongs hospital stays, increases hospital morbidity, and adds to the burden of growing healthcare costs. In total, there are many important reasons for aggressive acute pain management. [20] Postoperative pain is considered a form of acute pain secondary to surgical trauma and is associated with an inflammatory reaction and subsequent pathway of afferent neuronal signals. Acute postoperative pain is associated with autonomic, endocrine-metabolic, physiological, and behavioral responses summarized in following table (2) [21]   Acute surgical pain causes a global sympathetic response capable of increasing heart rate, peripheral vascular resistance, blood pressure, and subsequently cardiac output. This sympathetic cascade can increase the oxygen demand of the myocardium and potentiate myocardial ischemia, especially in patients with preexisting coronary artery disease. [22] Acute pain has also been found to decrease limb blood flow by directing blood away from skin and viscera and toward vital organs. This decrease in extremity blood flow may impair wound healing and increase muscle spasm. Postoperative pain may also reduce patient mobility, promoting venous stasis. Increases in fibrinogen and platelet activation related to surgical trauma will increase blood coagulability. These factors together increase the risk of venous thromboembolism. [23] Data suggest that "the use of epidural anesthesia in the perioperative period results in less platelet activation and significantly better fibrinolytic function" thereby resulting in significant protection against Thromboembolic complications. This protection also may be related to the systemic effect of local anesthetics, which have been shown to have an antithrombotic effect. [24] Perioperative cardiovascular adverse events may result in considerably prolonged postoperative stay. Cardiovascular events warranting unanticipated hospital admissions are infrequent. Cardiovascular events occur with higher frequency among patients with preexisting cardiovascular diseases (e. g. hypertension, congestive heart failure). Increasing age is also associated with higher incidence of cardiovascular conditions among elderly patients. [25] 6. Pain Management 6.1 Non-pharmacological methods of pain relief  Preoperative explanation and education  Relaxation therapy  Hypnosis  Cold or heat  Splinting of wounds  Transcutaneous electrical nerve stimulation (TENS). intermittently or continuously, and infuses IV opioids or non-opioids. The use of intravenous opiates is still limited because of side effects such as respiratory depression. [27] Pre-emptive Analgesia:

Pharmacological and interventional methods of pain relief
The administration of analgesia before surgery (preemptively) may be effective in reducing the postoperative pain from surgery by preventing the peripheral and central sensitization caused initially by surgical incision and later by inflammatory injury. There are studies that support the effectiveness of preemptive analgesia. However, other studies concluded that there was a lack of evidence for preemptive treatment with NSAlD's, intravenous opioids, and ketamine, peripheral local anesthetics, and caudal analgesia. [28] The effectiveness of preemptive analgesia is likely to remain a controversial issue for some time. Despite this, the preoperative administration of non opioid analgesia, such as NSAlDs, ketamine, and local anesthetics, prior to surgical incision is an important component in reducing postoperative pain scores and analgesic requirements in the first 24 hours after discharge. [29] Regional anesthesia and analgesia can be used to significantly reduce postoperative pain scores and spare the use of systemic opioids. Regional anesthesia can be performed at the neuraxis (epidural and intrathecal), the nerve root (paravertebral), and the peripheral nerve (transversus abdominis plane) level. Local anesthetic deposition at these sites will selectively block nerve conduction and result in different analgesic and side effect profiles. [30] 7. Conclusion Acute postoperative pain is multifactorial with complicated Pathophysiology, but careful history and good assessment lead to ideal selection of treatment plane either medications or interventions according to operation performed. Interventional methods are favorable due to many reasons; avoiding chronic pain and decreased side effects of systematic medications as opioids.