1/20/14

Tendon rupture atrophy

Tendon rupture atrophy - These are probably minimized by careful attention to technique, i.e. withdraw the needle a little if an unusual amount of resistance is encountered and use a peppering technique at the enthesis with the smallest effective dose and volume of steroid7'1 . The whole issue of steroid-associated tendon rupture is controversial disputed8 0 , anecdotal- in humans - is not well supported in the literature although it is widely accepted that the repeated injection of steroids into load-bearing tendons carries the risk of tendon rupture8 1.

The current climate of opinion among consultants in locomotor specialties is equivocal about steroid injection around the Achilles tendon. If this is being contemplated it is advisable to image the tendon first (by MRI or ultrasound) to confirm that it is a peritendinitis with no tendinopathy (degenerative change with or without tears in the body of the tendon). Low-dose peritendinous steroid injections appear to be safe1 6 1 . The patient should rest from provocative activity for 6-8 weeks7 5 (consider putting the keen athlete into a walking cast), and return to it gradually after a graduated programme of stretching and strengthening. In rabbits, local injections of corticosteroid, both within the tendon substance and into the retrocalcaneal bursa, adversely affect the biomechanical properties of Achilles tendons. Additionally, tendons from rabbits that have received bilateral injections of corticosteroid demonstrate significantly worse biomechanical properties than tendons from those that have received unilateral injections of corticosteroid. Bilateral injections of corticosteroids should be avoided because they might impart a systemic effect in conjunction with the local effect, further weakening the tendon1 4 3 . Surgery for chronic Achilles tendinopathy has a complication rate of around 10% and should not be assumed to be a trouble-free treatment option1 6 8 .
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Steroid arthropathy

Steroid arthropathy - This is a well known and much feared complication of local injection treatment- it is also largely a myth6 9 . There is evidence that in many instances injected steroids can be chondroprotective rather than destructive3 1 , 4 3 , but the information from animal models about whether steroids damage or protect joints is contradictory7 0 , 1 8 4 . There is good evidence linking prolonged highdose oral steroid usage with osteonecrosis, but almost all the reports linking injected steroids with accelerated non-septic joint destruction are anecdotal, and mainly relate to joints receiving huge numbers of injections6 9 . A reasonable
guide7 1 is to give injections into the major joints in the lower limbs at no less than 3-month intervals, although this advice is based on consensus rather than evidence7 2 1 8 5 . Reports of Charcot-like accelerated joint destruction after corticosteroid injection in human hip osteoarthritis (OA) might reflect the
disease itself rather than the treatment3 1 , 7 3 . Currently, no evidence supports the promotion of disease progression by steroid injections1 6 4 , 1 9 2 . Repeat injections into the knee joint every 3 months seem to be safe over 2 years1 6 5 .
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Soft tissue calcification

Soft tissue calcification - Corticosteroid injections into osteoarthritic interphalangeal joints of the hand can result in calcification or joint fusion, possibly because of pericapsular leakage of steroids due to raised intra-articular pressure6 8 . No deleterious effects have been ascribed to this calcification.
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Steroid chalk or paste

Steroid chalk or paste - This might be found on the surface of previously injected tendons and joints during surgery. Suspension flocculation, resulting from the mixture of steroid with a local anaesthetic containing preservative, might be responsible. The clinical significance of these deposits is uncertain3 1 .



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Bleeding or bruising

Bleeding or bruising - These can occur at the injection site, especially in patients taking warfarin, aspirin or NSAIDs with significant antiplatelet activity, e.g. naproxen.
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Subcutaneous atrophy and/or skin depigmentation

Subcutaneous atrophy and/or skin depigmentation - This is more likely to occur when superficial lesions are injected, especially in dark-skinned patients5 3 , 6 6 . Take care not to allow injected drugs to reflux back through the needle tract - pressure around the needle with cotton wool when withdrawing can help. In thin dark-skinned women especially, it might be preferable to use hydrocortisone for superficial lesions. These patients must always be advised of the possibility of this side-effect, and the fact recorded in the notes. Local atrophy appears within 1-4 months of injection and characteristically proceeds to resolution 6-24 months later, but may take longer
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Postinjection flare of pain

Postinjection flare of pain - The quoted figures are from about 2% to 10%6 3 , 6 4 , but this is well in excess of our own experience. When it does happen it is usually after a soft-tissue injection, and rarely follows joint injection6 4 . It appears to be caused by rapid intracellular ingestion of the microcrystalline steroid ester and must always be distinguished from sepsis2 8 , 3 1 , 3 6 , 2 6 0 . There appear to be more frequent postinjection flares with methylprednisolone but this might have more to do with the preservative in the drug than with the steroid itself5 7 . An early increase in joint stiffness following intra-articular corticosteroids is consistent with a transient synovitis1 7 9 . Multidose bottles of lidocaine (Xylocaine) contain parabens as a preservative. Many steroids will precipitate when added to parabens and this precipitate might be responsible for some cases of postinjection flare of pain and 'steroid chalk' (see below). Parabens might also be responsible for some allergic reactions to local injections. The use of multidose bottles increases the risk of cross-infection and should be avoided2 2 0 . Single-dose vials of lidocaine do not contain parabens.
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Local Side Effects of Injection

Local Side Effects of Injection - Most local side-effects occur when too large a dose, in too large a volume, is injected too often. Subcutaneous placement of the steroid and using a bolus technique at the entheses of tendons must be avoided.


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Potential Side Effect of Injection

Potential Side Effect of Injection - Side-effects from injection therapy with corticosteroids and/or local anaesthetics are uncommon and, when they do occur, are usually mild and transient6 4 . Nonetheless, it is incumbent upon the clinician practising injection therapy to be aware of the presentation and management of all the potential minor and more serious side-effects associated with this treatment5 . Consider carefully before giving corticosteroid injections to pregnant or breastfeeding women; this treatment is often recommended for carpal tunnel syndrome and de Quervain's tenovaginitis6 2 , 2 3 9 . There is no evidence that the woman or her baby will be harmed1 8 1 - indeed, Cortisol levels rise in pregnancy - but pregnancy and childbirth are highly emotive and if the mother has a difficult delivery or a baby with an abnormality she might try to blame the injection. Detailed discussion of the benefits and potential adverse effects
of injection therapy should be carefully documented.

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Prilocaine and procaine

Prilocaine and procaine - Prilocaine has low toxicity similar to lidocaine but is not as commonly used. Procaine is now also seldom used; it is as potent as lidocaine but with shorter duration of action.

Lidocaine (under the brand name Xylocaine) and Marcain are also manufactured with added epinephrine (adrenaline) (which causes vasoconstriction when used for skin anaesthesia, and so prolongs the local anaesthetic effect). Do not inject these drugs into joints or soft-tissue lesions. Xylocaine is clearly marked in red that it has epinephrine added. Recommended maximum doses are given in Table 2. In practice, however, we suggest that much lower maximum doses are used
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Marcain (bupivacaine)

Marcain (bupivacaine) - Marcain has a slow onset of action (about 30 minutes for the full effect) but the duration of block can be 8 hours or more. It is the principal drug for spinal anaesthesia in the UK. We do not use it for routine outpatient injections because the delayed onset of action precludes the immediate diagnostic effect available with lidocaine, and if there is an adverse effect it will take a long time to dissipate. There is no evidence of any long-term benefit from using bupivacaine instead of lidocaine9 4 . Compared to placebo, the effect of intraarticular bupivacaine wears off in less than 24 hours2 2 8 .
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Lidocaine hydrochloride (lignocaine hydrochloride)

Lidocaine hydrochloride (lignocaine hydrochloride) - The most widely used local anaesthetic, lidocaine hydrochloride acts more rapidly and is more stable than other local anaesthetics. The effect occurs within seconds and duration of block is about half an hour; this is the local anaesthetic we prefer.
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Rationale for Using Local Anaesthetics

• Analgesic: although the effect is temporary, it can make the overall procedure less unpleasant for the patient, break the pain cycle (by reducing nociceptive input to the 'gate' in the dorsal horn of the spinal cord), and increase the confidence of the patient in the clinician, the diagnosis and the treatment. In one study, pain inhibition was better with bupivacaine than lidocaine during the first 6 hours, because of its longer half-life; in later evaluations no differences in outcomes were observed9 3 . In another study, bupivacaine was superior to lidocaine at 2 weeks, but not at 3 and 12 months9 4 . Some practitioners inject
a mixture of short- and long-acting local anaesthetic to obtain both the immediate diagnostic effect plus more prolonged pain relief

• Diagnostic: pain relief following an injection confirms the diagnosis and correct placement of the solution9 2 . Sometimes even the most experienced practitioner will be unsure exactly which tissue is at fault; in this situation, inject a small amount of local anaesthetic into the most likely tissue, wait a few minutes, and re-examine. If the pain is relieved then the source of the problem has been identified and further treatment can be accurately directed; if not, further testing should follow until sure of the cause of the pain

• Dilution: the internal surface area of joints and bursae is surprisingly large, due to the highly convoluted synovial lining with its many villae, so increased volume of the injected solution helps to spread the steroid around this surface

• Distension: a beneficial volume effect in joints and bursae might be the stretching of the capsule or bursa with physical disruption of adhesions9 5 , 9 6 , 1 7 8 , 2 1 7 . Distension is not required at entheses, so use the smallest volume that is practicable; distension in tendons by bolus injection of a relatively large volume of solution may physically disrupt the tendon fibres and compress the relatively poor arterial supply. It can also give rise to distension pain
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Local Anaesthetics

Local Anaesthetics - These membrane-stabilizing drugs act by causing a reversible block to conduction along nerve fibres. The smaller nerve fibres are more sensitive, so that a differential block can occur where the small fibres carrying pain and autonomic impulses are blocked, sparing coarse touch and movement9 1 . Following most regional anaesthetic procedures, maximum arterial plasma concentrations of local anaesthetic develop within about 10-25 minutes9 1 . This has implications for outpatient practice if significant volumes of the drug are injected.


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Hydrocortisone

Hydrocortisone - • Hydrocortistab: 25 mg/ml ery dilute Very soluble - this has the shortest duration of action of the steroids mentioned here5 2 . We recommend its use particularly for superficial injections in thin, dark-skinned females, where there may be risk of depigmentation or local fat atrophy3 3 . Twenty mg of Hydrocortistab is equipotent to 4mg of triamcinolone or methylprednisolone.
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Methylprednisolone acetate

Methylprednisolone acetate - • Depo-Medrone: 40 mg/ml concentrated This drug may cause more postinjection pain than triamcinalone acetonide5 1 . It is also available premixed with local anaesthetic as Depo-Medrone (40 mg/ml) and with lidocaine (10 mg/ml) in 1-ml and 2-ml vials, which we do not recommend because it is a fixed-dose combination and therefore difficult to adjust.
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Triamcinolone acetonide

Triamcinolone acetonide - Throughout the book we recommend Kenalog for ease of administration. This drug can be used in very small quantities and so is ideal for small joints and tendons where distension can increase pain. Adcortyl, however, is useful where larger volume is required as in larger joints and bursae. The duration of action of the drug is approximately 3 weeks2 6 2 . Triamcinolone hexacetonide (Lederspan) was the least soluble and longestlasting injectable drug
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Rationale For Using corticosteroids

We know surprisingly little about the precise pharmacological effects of corticosteroids when they are injected directly into joints and soft tissues3 4 , 2 0 6.
Local steroid injections are thought to work by:

• Suppressing inflammation in inflammatory systemic diseases such as rheumatoid or psoriatic arthritis, gout, etc2 8 , 3 1 , 3 4 - 3 6 , 1 9 4 , 2 1 8

• Suppressing inflammatory flares in degenerative joint disease3 1 , 3 2 , 3 7 - 4 0 . The classic distinction between osteoarthrosis and osteoarthritis is not helpful, and there are no reliable clinical features to tell us how much 'osis' (wear and tear) and how much 'itis' (inflammation) is contributing to a particular
symptomatic joint4". Often, the only way to find out is to treat it

• Breaking up the inflammatory damage-repair-damage cycle, which is postulated to set up a continuous low-grade inflammatory response, inhibiting tissue repair and sound scar formation, while forming adverse adhesions4 1 , 4 2 . There is little direct evidence to support this, however

• Possibly a direct chondroprotective effect on cartilage metabolism or other effects not related to anti-inflammatory activity of the steroids, e.g. promotion
of articular surfactant production3 2 , 4 3 , 4 4 , 2 0 6 , 2 1 6 , 2 2 4 - 2 2 6 , 2 41

Inflammation is a complex cascade of molecular and cellular events that is often poorly understood by the clinicians who treat it3 1 6 , 3 1 7 . The precise
role of inflammation in 'tendinitis' is the subject of considerable debate, and many authors prefer the terms 'tendinosis' or 'tendinopathy' to describe the pathological changes4 5 - 4 8 . The pain might not be due to inflammation (tendinitis) or structural disruption of the tendon fibres (tendinosis), but to the stimulation of nociceptors by chemicals released from the damaged tendon4 9 . Corticosteroids (and possibly local anaesthetics) might affect
the release of noxious chemicals and/or the long-term behaviour of local nociceptors.
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Corticosteroids

Corticosteroids - The commonly used injectable corticosteroids are synthetic analogues of the adrenal glucocorticoid hormone Cortisol (hydrocortisone), which is secreted by the innermost layer (zona reticularis) of the adrenal cortex. Cortisol has many important actions, including effects on protein and glucose metabolism, but it also has anti-inflammatory activity, which is mediated by effects on polymorph and macrophage migration and suppression of the immunological response of lymphocytes2 6 , 2 7 , 1 9 7. When they were first administered systemically in the 1940s steroid drugs were hailed as the new 'universal panacea', but it soon became apparent that major side-effects greatly limited their systemic use2 8 . In 1951, Hollander, in the USA, reported the first use of local hydrocortisone injections for arthritic joints2'. Virtually insoluble steroid suspensions are used because intraarticular soluble steroids will rapidly clear into the systemic circulation.

The suspensions work by minute quantities of the active drug dissolving off the surface of the crystals when in contact with the inflamed tissue28. In joints, the steroid is taken up by the synovial cells before being gradually absorbed into the blood and cleared1 , 3 1 , 2 6 1 , 2 6 2. Corticosteroids exert their many effects on the cells involved in the immune and inflammatory responses primarily by modulating the transcription of a large number of genes. They act directly on nuclear steroid receptors to control the rate of synthesis of mRNA3 2 . However, they also influence the mechanisms by which proteins are synthesized, and thereby affect the production of a wide range of proinflammatory mediators including cytokines" and other important
enzymes.
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