Most patients anticipated some degree of postoperative pain as an associated feature of surgery and a consequence of performing a surgical incision. However, with better anesthesia and analgesia, many patients have now come to expect less pain than previous generations endured. This in itself is an important consideration, as anticipation of the extent of the pain may modify the actual perception of pain, and additionally, patient “satisfaction” with medical/surgical treatment may be heavily contingent upon their prior expectation of the intensity of pain they might suffer when agreeing during “informed consent” to a procedure. Realistically, however, some pain is usually expected, by most patients, with most surgical procedures. In effect, with much improved analgesia (thankfully), we also inadvertently “raise the bar” of patient and community expectation for “pain-free” surgical and anesthetic care. Despite the enormous advances in anesthesia and analgesia over the last 50 years, some postoperative pain is still experienced by many patients, and the overall aim is therefore to make the patient as comfortable and as least distressed by the pain, as possible. Indeed, the so-called “breakthrough” pain is important for the surgical diagnosis of postoperative complications, such as vascular compartment syndrome in a limb or following an undetected gastrointestinal perforation or an anastomotic leak. Not infrequently, pain precedes surgery, especially with acute surgical conditions or following trauma, and so the postoperative pain potentially arising from surgery is often a mix of preoperative pain, any intraoperative pain, and the postoperative pain induced by surgical intervention. Indeed, for many patients in pain prior to surgery, postoperative pain is a lesser and a much preferable option. Postoperative pain as a pathophysiological response is therefore important but must be managed appropriately to reduce the amount of distress and discomfort to acceptable levels for the patient and in a safe manner. This chapter focuses on some of the underlying mechanisms, types of pain experienced by patients, pain associated with complication following surgery, and its possible management.

The nociceptor relays information on thermal, mechanical, and chemical noxious stimuli via slower unmyelinated (C) fibers and small, lightly myelinated (A-delta) fibers to the dorsal horn of the spinal cord at the respective corresponding segmental level or rostrally and caudally passing through Lissauer’s tract. Modulation of this signal at the dorsal horn involves both inhibitory and excitatory mechanisms through local and supraspinal inputs, before transmission to supraspinal structures involved in the perception of pain (Siddall and Cousins 2009). The discovery of transduction mechanisms for heat/capsaicin (TRPV₁) and for chemical stimuli (ASIC) has been a major advance that opens up new avenues for peripheral blockade of acute pain (see Siddall and Cousins 2009).

There is now considerable evidence that psychological factors account for a significant proportion of the variance in pain response. In addition, unrelieved pain leads to psychological changes, with increased anxiety, sleep disturbances, low morale, loss of control, and inability to think and interact (Cousins et al. 2004; Katz and Melzack 2009). Anxiety is the psychological variable which is most reliably related to high levels of pain. Circumstances associated with acute postoperative pain are probably some of the most potent in aggravating such fears. Fear of the unknown is also a major component of the general anxiety which patients experience. Hospitalization itself produces many threats, including possible disability, loss of life, coping with a new situation, loss of normal freedom, and separation from one’s family and normal routine (Johnson 1980; Katz and Melzack 2009).

The effects of situational or environmental variables have been shown to be important, as exemplified by the powerful effect of anxiety and perceived control over the situation (Peck 1986). Some patients may interpret the use of sophisticated monitoring equipment as implying that their situation is one of the imminent disasters (Cousins 1970). The anxiety experienced by family members is often transferred directly to the patient and serves to reinforce or reactivate his or her own fears. Another important area of investigation has been the interaction between individual and situational variables, such as the interaction between coping style and the control the patient has over the situation (Andrew 1970).

Placebo and expectation effects can sometimes play a very powerful role. One aspect of these effects is the patient’s confidence and belief that the healthcare professional will be able to provide pain relief, and clearly such a placebo response is augmented by a positive doctor–patient or nurse–patient relationship (Dimatteo and Di Nicola 1982).

Studies suggest that the initial relief experienced in a new situation may be an important determinant of future relief, because the patient’s expectations may be conditioned at that time. On the other hand, inadequate relief may condition a negative expectation, which could adversely affect later pain control. This indicates the importance of providing adequate pain control as quickly as possible and conveying the expectation that the pain control procedures will continue to provide effective pain relief (Voudoris and Peck 1985; Katz and Melzack 2009).

Neuropathic pain is pain initiated or caused by a primary lesion (or dysfunction) in the nervous system (Merskey and Bogduk 1994). In the postsurgery or posttrauma patient, neuropathic pain may have an early onset within the first 24 h; this is contrary to classic teaching. There may also be a delayed onset of the order of 10 days. Numerous physiological and structural changes occur following nerve injuries and have been summarized in several review articles (Siddal and Cousins 2008; Woolf and Manion 1999). Experimental evidence concerning the mediators involved in nerve injury and central sensitization is numerous. Injured sensory neurons undergo Wallerian degeneration with myelin sheath disruption, invasion by immune cells, and distal degeneration of the axon before regeneration can occur. Many changes have been implicated including neuroma formation, increased or novel expression of sodium channel subtypes leading to ectopic pacemaker-like activity, upregulation of voltage-gated channel expression, and neuro-immune interactions both peripherally and centrally. These afferent barrages, alterations in inhibitory and anatomical changes, lead to marked changes in the dorsal horn neurons that may lead to persistent central sensitization. Recognition of neuropathic pain and early aggressive treatment are therefore paramount to prevent long-term problems. Features suggestive of neuropathic pain are:
(Adapted from Acute Pain Management: scientific evidence NHMRC 1999)

Despite these features neuropathic pain remains a significant diagnostic challenge. There is no single diagnostic test for neuropathic pain. Nerve conduction velocity tests and electromyography provide information about large myelinated fibers, but not about the small nociceptive afferents. Quantitative sensory testing is a psychophysical test that informs about large and small fiber function through subjective appreciation of detection thresholds to touch, pain, thermal, and vibration stimuli. Its use is limited in daily clinical practice due to the specialized equipment and training needed. Many neuropathic assessment tools have been validated for the discrimination of neuropathic pain. The S-LANSS (Leeds Assessment of Neuropathic Symptoms and Signs pain scale) score is a simple and valid seven-item self-reporting tool with sensitivity of 74 % and specificity of 76 % (Table 7.1). While these tools can aid in diagnosis, the “gold standard” at present is clinical history and examination.