Chapter 7 Postoperative Pain Relief
Introduction and background
The goal of postoperative pain relief is to achieve optimal analgesia, facilitating a quick return to normal activities with minimal side effects. In addition, the effective treatment of acute postoperative pain may reduce the incidence of chronic pain after surgery. Acute postoperative pain differs from chronic or cancer pain because it is more transitory and there may be an affective component relating to anxiety about the outcome of the surgical procedure and concern for suboptimal analgesia. Studies have shown that for patients awaiting surgery the possibility of severe acute postoperative pain is a major concern.1 In addition, uncontrolled postoperative pain can lead to delayed recovery from surgery, pulmonary dysfunction and hypoxia, together with restriction of mobility and subsequent increased risk of thromboembolism. Surveys in the UK, the USA and Europe have identified an unacceptable prevalence of poor pain control after surgery.2,3 However, in recent years the introduction of acute pain management services in hospitals has promoted improvements in postoperative pain.4 In addition, the use of ‘multimodal’ or ‘balanced’ analgesia – a combination of opiates, non-steroidal antiinflammatory drugs (NSAIDs), local anaesthetics and other adjuvants have been recommended to manage postoperative pain. Recently, White and Power reviewed the evidence for such pain management. They showed that multimodal analgesia improves the efficacy of pain relief, decreases the risk of side effects and is an evidence-based, established effective strategy for postoperative pain management.5,6
Measurement of pain
In adults, three common methods of self-reported pain measurement are used.
Visual analogue scale
The visual analogue scale (VAS) uses a 10 cm line with endpoint descriptors such as ‘no pain’ marked at the left end of the line and ‘worst pain imaginable’ marked at the right end (Fig. 7.1). Patients are asked to mark a point on the line that best represents their pain. The distance from ‘no pain’ to the patient’s mark is then measured and this equals the VAS score.
Available methods of pain relief
Paracetamol
Oral paracetamol
Paracetamol is well absorbed from the proximal small bowel and is not subject to significant first-pass metabolism in the liver, with oral bioavailability estimated at between 63% and 89% in adults. Because paracetamol does not cause gastric irritation, is relatively non-toxic in therapeutic doses and has minimal side effects, it should be considered as the basic building block of most postoperative analgesic regimens. Paracetamol is considered an effective and well-tolerated agent in the management of mild to moderate pain and, as it has none of the renal or cardiovascular side effects that characterize antiinflammatory drugs, it can be used in both NSAID and opioid-sparing roles. Studies have shown that paracetamol combined with patient-controlled analgesia (PCA) morphine induces a significant morphine-sparing effect of the order of 20% in the first 24 h.7 However, this is not associated with a reduction in morphine-related side effects. Combining paracetamol with NSAIDs appears to result in a synergistic interaction but so far there is only limited evidence that this interaction is advantageous in the clinical setting.
Parental paracetamol
An intravenous formulation of paracetamol is now available in the UK which facilitates its administration in patients under anaesthesia (or who cannot swallow) before the end of surgery, with the aim of reducing opioid-induced sedation and respiratory depression in the recovery room. The recommended dose of paracetamol is 15 mg/kg, with a maximum daily dose of 60 mg/kg. Peak plasma concentration (Cmax) is achieved approximately 25 min after a 1 g intravenous infusion compared to 45 min after 1 g orally. Clinically this difference has been shown to lead to a quicker onset of analgesia. Several recent studies have looked at the use of an initial loading dose of paracetamol of 2 g to improve early postoperative analgesia, with conflicting results.8 In our practice we routinely give a 1 g dose of i.v. paracetamol at the start of surgery.
Non-steroidal antiinflammatory drugs
Postoperative analgesia comparable with that of opioids has been demonstrated with NSAIDs. An opioid-sparing effect of the order of 30–50% has also been observed with NSAIDs, as well as a reduction in opioid-induced nausea, vomiting and respiratory depression. This reduction in opioid requirement and side effects may benefit the patient by producing increased postoperative analgesia and potentially reducing hospital stay.9
Summary Box 7.2 Side effects of NSAIDs
| Gastrointestinal | Gastric erosions |
| Renal | Decreased renal blood flow |
| Acute renal failure | |
| Haematological | Prolonged bleeding time |
| Respiratory | Bronchospasm |
| Others | Skin rashes |
Adverse effects/complications
Haematological
Aggregation of platelets depends on a balance between prostacyclin (from endothelial cells) and thromboxane A2 (from platelets). The former is a vasodilator and inhibits platelet aggregation; the latter is a vasoconstrictor which stimulates platelet aggregation. NSAIDs inhibit the synthesis of both these factors and the net balance will determine the tendency to bleed. NSAIDs also inhibit platelet COX, although the effect lasts only as long as the drug remains in the blood (five half-lives). An increase in operative bleeding has been reported as a result of the use of NSAIDs and surgeons should be aware of this risk. A meta-analysis of several randomized controlled trials showed a higher risk of postoperative bleeding after tonsillectomy with the postoperative use of NSAIDs.10 However, others have disagreed with this analysis, citing poor surgical technique and that in some patients the bleeding occurred at a time when the drug had been eliminated from the body.11
Cox-2 inhibitors
In an effort to minimize the potential for bleeding at the surgical site and to reduce the incidence of serious gastrointestinal adverse effects and renal dysfunction associated with traditional NSAIDs, selective COX-2 inhibitors, also named ‘coxibs’, such as rofecoxib and celecoxib, were developed . Other novel COX-2 inhibitors with improved biochemical selectivity recently developed include etoricoxib, valdecoxib, parecoxib and lumiracoxib. These ‘coxibs’ have similar analgesic efficacy to that of NSAIDs, with reduced risk of bleeding and less gastrointestinal toxicity. However, large outcome and epidemiological studies suggest that while COX-2 inhibitors do confer improved gastrointestinal safety, they are not devoid of gastrointestinal effects during long-term use. Two of these drugs have already been withdrawn because of safety concerns: rofecoxib because of cardiovascular problems and valdecoxib because of serious subcutaneous adverse reactions.12
Concerns have also been raised regarding the increased incidence of thrombotic complications (leading to myocardial infarction and stroke) associated with selective COX-2 compounds.13 COX-2 inhibition with coxibs may increase the risk of vascular thrombus formation by upsetting the balance between pro- and anti-platelet aggregation effects: thromboxane A2 synthesis is primarily a COX-1-induced effect, and prostaglandin I2 synthesis a COX-2 effect.
