Postoperative Pain Relief

Chapter 7 Postoperative Pain Relief



Carmel F. Martin



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



Treatment options



1. Paracetamol

2. NSAIDs

3. Opiate drugs

4. Local anaesthetic drugs

5. Peripheral nerve blocks


Assessment of pain


The international Association for the Study of Pain defines pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage’.


Pain is a very individual experience, and many factors including previous pain experiences, cultural background, disease or surgical prognosis, coping strategies, fear, anxiety and depression, will interact to produce what the patient then describes as pain. There is, however, often a poor correlation between the patient’s assessment of the pain and that of the nursing or medical staff.



Measurement of pain


In adults, three common methods of self-reported pain measurement are used.


1. Visual analogue scale

2. Verbal numerical rating scale

3. Categorical rating scale.

Each of these methods of measurement is reasonably reliable as long as the endpoints and adjectives employed are carefully selected and standardized.



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.


image

Figure 7.1 Visual analogue scale.


The disadvantages of the VAS system are that it can be more time consuming than other simple scoring methods and some patients may have difficulty understanding or performing this score, especially in the immediate postoperative period.



Verbal numerical rating scale


The verbal numerical rating scale (VNRS) is very similar to the VAS. Patients are asked to imagine that ‘0 equals no pain’ and ‘10 equals the worst pain imaginable’ and then to give a number on this scale that would best represent their pain.



Categorical rating scale


Other systems of pain measurement use different words to rate pain, such as none, mild, moderate, severe, very severe and worst pain imaginable.


At our institution we use the verbal numerical rating scale routinely in all our postoperative patients in the recovery room. Pain should be reassessed regularly during the postoperative period, particularly if the pain is poorly controlled or if the pain stimulus or treatments are changing.



Summary Box 7.1 Treatment options/systemic options



Paracetamol

Parenteral intermittent narcotics by nurses

PCA

NSAIDs

Opiate drugs

Adjunctive agents


Available methods of pain relief



Paracetamol


Paracetamol (acetaminophen) is an acetanilide derivative with the molecular formula C8H9NO2. It is one of the most commonly used drugs worldwide, owing in part to its excellent safety record. Paracetamol has analgesic and antipyretic but not antiinflammatory activity. It is believed to be a centrally acting cyclooxygenase (COX) inhibitor with weak peripheral effects. Current evidence points to multi-site activity in the central nervous system, involving inhibition of prostaglandin synthesis and interaction with both serotonergic and cannabinoid pathways. Paracetamol can be given orally and rectally. An intravenous formulation is now available and has become widely used in the UK as it provides rapid and predictable therapeutic plasma concentrations. Rectal administration is restricted by slow onset time and unpredictable bioavailability and is becoming less popular.



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


The analgesic, antiinflammatory and antipyretic effects of NSAIDs, as well as their most notable side effects, are attributed to inhibiting COX-1 and COX-2 receptors, thereby reducing the production of mediators of the acute inflammatory response. Traditional NSAIDs such as diclofenac, ketorolac or ibuprofen are widely prescribed as analgesics and antiinflammatory agents owing to their inhibition of prostanoid synthesis through blockade of both COX-1 and COX-2 receptors. Unfortunately, these drugs can have the following undesirable adverse effects.



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



Gastrointestinal


Erosions of the gastrointestinal tract (especially the stomach) can develop. They are due to local irritation of the mucosa as well as a decrease in mucus production and mucosal blood flow and increased gastric acid secretion, mediated by a reduction in prostaglandin levels. These problems may be lessened but not avoided altogether if the drugs are given by parenteral or rectal routes. Gastric irritation, dyspepsia and ulceration may develop at any time, but are less likely with short-term treatment. Pre-existing peptic ulcer disease can be exacerbated and indeed may be a contraindication to the use of these drugs.



Renal


The reduction in prostaglandin levels due to NSAID administration may also result in a decrease in renal blood flow and acute renal failure. Pre-existing renal impairment may increase this risk. In the healthy patient renal blood flow is not normally prostaglandin dependent. However, renal blood flow may be altered during anaesthesia.


NSAIDs can also cause sodium, potassium and water retention, which may lead to oedema in some patients.



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



Respiratory


Bronchospasm, related to COX inhibition, can occur in some asthmatic patients. As a consequence, NSAIDs should be used with caution in these people. Up to 20% of adult asthmatics may develop aspirin-induced bronchospasm, and a cross-sensitivity does exist between aspirin and other NSAIDs.



Liver


Abnormalities in liver function tests may occur but are usually transient.



Skin reactions


Skin reaction is the second most common unwanted effect of NSAIDs. Patients may present with a variety of skin conditions ranging from mild rashes, urticaria and photosensitivity, to occasionally more serious and potentially fatal varieties.



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.



Current practice


The new COX-2 inhibitors, despite the sound pharmacological basis for their development, are not ‘miracle’ drugs. They also seem to be associated with adverse effects and, although they may represent a safer alternative to non-selective NSAIDs, their role in postoperative pain management is still not clearly defined. There is also a cost implication as they are considerably more expensive than the older non-selective NSAIDs.

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Sep 8, 2016 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on Postoperative Pain Relief

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