Good Practice in Postoperative and Procedural Pain Management ...

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Table 6.5.1NSAIDDosemgÆkg )1IntervalhoursMaximum daily dosemgÆkg )1 Æday )1Licensedfrom ageIbuprofen 5–10 6–8 30 3 monthsDiclofenac 1 8 3 6 monthsKetorolac a 0.5 6 2Naproxen 7.5 12 15Piroxicam a 0.5 24 0.5 N/RKetoprofen a 1 6 4a High incidence of GI complications. Not licensed for acutepain.6.5.2 NSAID toxicity and side effectsBecause of their mechanism of action, NSAIDs havethe potential to cause adverse effects at therapeuticplasma levels.l Hypersensitivity reactionsl NSAIDs reduce platelet aggregation and prolongbleeding time. Therefore, they are usually contraindicatedin children with coagulation disorders or inthose who are receiving anticoagulant therapy.l NSAIDs can inhibit prostaglandin-mediated renalfunction, and this effect is greater in the presence ofrenal disease and dehydration. Ibuprofen has beenshown to reduce the glomerular filtration rate inneonates by 20%. NSAIDs should not be administeredconcurrently with nephrotoxic agents. Renaltoxicity is low in healthy children.l NSAIDs can cause gastric irritation and bleeding.They are therefore relatively contraindicated in childrenwith a history of peptic ulcer disease. Ibuprofenhas the lowest potential for gastric irritation. The riskof adverse GI effects is low when NSAID use is limitedto 1–3 days in the postoperative period; it may be furtherreduced by co-prescription of proton pump inhibitors,for example, omeprazole and H2 antagonists inpatients at higher risk. Piroxicam, ketorolac, and ketoprofenare known to be especially likely to cause GI sideeffects particularly in the elderly. In the UK, piroxicamis no longer licensed for acute indications and is subjectto special prescribing and monitoring restrictions.l Owing to excess leukotriene production, NSAIDshave the potential to exacerbate asthma in a predisposedsubset of asthmatics. It is estimated that 2% ofasthmatic children are susceptible to aspirin-inducedbronchospasm and 5% of this subgroup are likely tobe cross-sensitive to other NSAIDs, that is, 1:1000.The incidence of asthma in children is increasing, andit is important that children who are not sensitive arenot denied the benefits of NSAIDs. History of previousuneventful NSAID exposure should be establishedin asthmatic children whenever possible.Studies have provided some reassuring data regardingthe safety of short-term use of ibuprofen and diclofenacin asthmatic children. NSAIDs should be avoidedin children with severe acute asthma.l NSAIDs should be used with caution in childrenwith severe eczema, multiple allergies, and in thosewith nasal polyps. NSAIDs should be avoided in liverfailurel Animal studies using high doses of Ketorolac demonstrateddelayed bone fusion. This has led to concernthat the use of NSAIDs in children may delay bonehealing following fracture or surgery. This has notbeen supported by human studies, and the analgesicbenefits of short-term NSAID use outweigh the hypotheticalrisk of delayed bone healing: see section 5.8.l NSAIDs are not currently recommended for analgesiain neonates due to concerns that they mayadversely affect cerebral and pulmonary blood flowregulation.Of the NSAIDs currently available, ibuprofen has thefewest side effects and the greatest evidence to supportits safe use in children. In a large community-basedstudy in children with fever, the risk of hospitalizationfor GI bleeding, renal failure, and anaphylaxis was nogreater for children given ibuprofen than those givenparacetamol (15).6.6 ParacetamolParacetamol is a weak analgesic (16,17). On its own, itcan be used to treat mild pain; in combination withNSAIDs or a weak opioid such as codeine, it can beused to treat moderate pain. Studies have demonstratedan opioid sparing effect when it is administeredpostoperatively.6.6.1 Paracetamol preparations, doses, androutesParacetamol is available for oral administration insyrup, tablet, and dispersible forms. Following oraladministration, maximum serum concentrations arereached in 30–60 min. As the mechanism of action iscentral, there is a further delay before maximum analgesiais achieved. Suppositories are available; however,there is wide variation in the bioavailability of paracetamolfollowing rectal administration. Studies have demonstratedthe need for higher loading doses (of the76 ª 2012 Blackwell Publishing Ltd, Pediatric Anesthesia, 22 (Suppl. 1), 1–79
Table 6.6.1 Paracetamol dosing guide – oral and rectal administrationAgeRouteLoadingdoseMaintenancedoseMaximum Duration atInterval daily dose maximum(mgÆkg )1 ) (mgÆkg )1 ) (h) (mgÆkg )1 ) dose (h)28–32 Oral 20 10–15 8–12 30 48weeks Rectal 20 15 12PCA32–52 Oral 20 10–15 6–8 60 48weeks Rectal 30 20 8PCA>3 Oral 20 15 4 90 48months Rectal 40 20 6PCA, postconceptual age.Table 6.6.2 IV Paracetamol dosing guideWeight (kg) Dose Interval (h) Maximum daily dose50 1 g 4–6 4 gorder of 40 mgÆkg )1 ) to achieve target plasma concentrationsof 10 mgÆl )1 following rectal administration.The time to reach maximum serum concentration followingrectal administration varies between 1 and 2.5 h.Rectal administration of drugs is contraindicated inneutropenic patients because of the risk of causing sepsis.Recently, an intravenous preparation of paracetamolhas become available. Initial experience with IVparacetamol is that the higher effect site concentrationachieved following intravenous administration is associatedwith higher analgesic potency. When administeredIV, it should be given as an infusion over 15 min.There are several published dosage regimens for paracetamol(perhaps indicating that the optimum regimenis still to be determined). The regimen used willdepend on the age of the child, the route of administration,and the duration of treatment. The clearancein neonates is reduced and the volume of distributionis increased. The dose of paracetamol therefore needsto be reduced in neonates – see Table 1. Bioavailabilityfollowing rectal administration is higher in the neonate.The current recommendations stated in the BNFcare shown in Tables 6.6.1 and 6.6.2.is limited by the potential for hepatotoxicity that canoccur following overdose (exceeding 150 mgÆkg )1 ).Multiple doses may lead to accumulation in childrenwho are malnourished or dehydrated. The mechanismof toxicity in overdosage is the production of N-acetylp-benzoquinoneimine(NABQI). The amount of NAB-QI produced following therapeutic doses of paracetamolis completely detoxified by conjugation withglutathione. In overdosage, glutathione stores becomedepleted allowing NABQI to accumulate and damagehepatocytes. Acetylcysteine and methionine replenishstores of glutathione and are therefore used in thetreatment of toxicity.6.7 Nitrous oxide (N 2 O)6.7.1 Preparations, dosage, and administrationNitrous oxide is supplied compressed in metal cylinderslabeled and marked according to national standards(18). It is a weak anesthetic with analgesicproperties rapidly absorbed on inhalation. The blood/gas partition coefficient is low, and most of the inhaledN 2 O is rapidly eliminated unchanged through thelungs. Premixed cylinders with 50% N 2 O in oxygenare available, but it is also occasionally administeredat inspired concentrations up to 70% with oxygen.Nitrous oxide inhalation using a self-administrationwith a face mask or mouthpiece and ‘demand valve’system is widely used for analgesia during proceduressuch as dressing changes, venepuncture, as an aid topostoperative physiotherapy, and for acute pain inemergency situations, see section 4.0. It is also used indentistry. The system is only suitable for children ableto understand and operate the valve, generally thoseover 5 years of age. Heathcare workers must be specificallytrained in the safe and correct technique ofadministration of N 2 O.Nitrous oxide is given using a self-administrationdemand flow system operated by the patient unaidedsuch that sedation leads to cessation of inhalation.Analgesia is usually achieved after 3 or 4 breaths.Recovery is rapid once the gas is discontinued.Continuous flow techniques of administration, wherethe facemask is held by a healthcare worker ratherthan the patient, is capable of producing deep sedationand unconsciousness, and therefore the use of thismethod is not included in this guideline.6.6.2 Paracetamol toxicity and side effectsWhen the maximum daily dose of paracetamol isobserved, it is well tolerated. The maximum daily dose6.7.2 Side effects and toxicityNitrous oxide potentiates the CNS depressant effectsof other sedative agents. There is a risk of increasedª 2012 Blackwell Publishing Ltd, Pediatric Anesthesia, 22 (Suppl. 1), 1–79 77
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PediatricAnesthesiaVolume 22 Supple
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doi: 10.1111/j.1460-9592.2012.3838.
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1.6 Contact informationCorresponden
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RecommendationsChildren’s self-re
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Topical anesthetic preparations, fo
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2.7.6 Laparoscopic surgeryGood prac
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In order to assess pain, effective
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Postoperative painl NCCPC-PV (Non-C
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68 Broome ME, Richtsmeier A, Maikle
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however, reductions in the response
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increased success rate (i.e., less
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Newer preparations such as liposoma
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Good practice pointLubricant contai
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Page 30 and 31: 12 Bellieni C, Bagnoli F, Perrone S
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Page 34 and 35: 172 van Twillert B, Bremer M, Faber
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Page 38 and 39: when compared with LA alone and sal
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Page 42 and 43: Analgesia Table 5.5.1 Sub-umbilical
Page 44 and 45: was more effective with less motor
Page 46 and 47: with using landmark techniques (205
Page 48 and 49: Good practice pointWound infiltrati
Page 50 and 51: Analgesia Table 5.6.4 Urological Su
Page 52 and 53: (298). Ketorolac did not influence
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Page 58 and 59: 14 Grainger J, Saravanappa N. Local
Page 60 and 61: day-stay unit. Int J Paediatr Dent
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Page 64 and 65: 245 Morton NS, O’Brien K. Analges
Page 66 and 67: 321 Taenzer AH, Clark C, Taenzer AH
Page 68 and 69: Section 6.0AnalgesiaContents6.1 Ana
Page 70 and 71: enhance systemic absorption. Lidoca
Page 73 and 74: undergoes hepatic biotransformation
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