CRYSTAL ARTHROPATHIES AND THE ANKLE

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CRYSTAL ARTHROPATHIES AND THE ANKLE



Neil McGill





Introduction


Gout is the commonest inflammatory arthropathy in men over the age of 40 years and is a cause of severe joint pain. Clinicians in all areas of medicine can expect to be confronted with a patient with acute gout who requires prompt effective therapy. Septic arthritis can present in the same manner and needs prompt but very different, therapy. The correct approach to assessment and diagnosis should allow the disorders that cause acute monarthritis to be differentiated promptly so that the correct therapy is used. Gout is often accompanied by a range of other health problems such as obesity, hypertension, hyperlipidaemia (elevated serum lipids) and alcohol excess. Although it may have been gout that led to the patient–doctor interaction, recognition and effective management of these other health problems may bring rewards greater than simply controlling gout.


Effective management for gout is available in the vast majority of cases. Achieving good compliance in the long term is the major practical problem and success in that aspect is based on the patient obtaining sufficient information to understand the need for lifelong therapy.


The calcium crystal associated arthropathies that occur with sufficient frequency to warrant consideration in this text can be divided into calcium pyrophosphate dihydrate (CPPD) and basic calcium phosphate (BCP) associated arthropathies. The presence of CPPD deposition in a person less than 55 years of age should prompt consideration of underlying causes such as haemochromatosis. Calcium crystal associated arthropathies can masquerade as other disorders and thus the correct identification is helpful in avoiding unnecessary treatment.


This chapter will review the principles of investigation of acute monarthritis, joint aspiration technique (using the ankle as an example), risks of hyperuricaemia, production and handling of uric acid in normal and disordered circumstances, and principles of the treatment of gout. Calcium crystal associated disorders will also be briefly reviewed with an emphasis on aspects with direct clinical relevance.



Differential diagnosis of acute monarthritis of the ankle


As discussed in Chapter 1, an acutely painful swollen joint can be explained by bacterial infection, crystal-induced inflammation (gout or pseudogout), trauma, haemarthrosis (bleeding into the joint) and occasionally by disorders such as rheumatoid arthritis, psoriatic arthritis or reactive arthritis. The postoperative period is a time of increased risk for acute crystal-induced arthritis, particularly gout. Invasive procedures also have the potential to cause bacteraemia that could lead to septic arthritis, although the risk of that occurring at the time of a sterile procedure such as arthroscopy is very low. One could consider the possibility of trauma (e.g. while anaesthetized) but for trauma to produce a red, swollen, warm joint, the injury needs to be substantial. Thus, the most likely diagnoses are crystal-induced arthritis or sepsis. They both typically produce an abrupt onset of marked joint inflammation.



Joint aspiration to allow examination of the synovial fluid is the best way of establishing the diagnosis. It should be performed promptly using correct aseptic technique and the fluid obtained should be promptly examined and processed for culture. Aspiration will require knowledge of the anatomy of the ankle region.



Essential anatomy



The ankle joints


The ankle region comprises three joints:



Involvement of any of these three joints will cause ‘ankle’ pain. The tibiotalar joint is a true hinge joint whose movement is almost entirely limited to plantar flexion (downwards) and dorsiflexion (upwards). The fibula articulates on the lateral side of the tibia but does not bear weight. The subtalar joint allows the foot to be inverted or everted. The midtarsal joints, including the talonavicular joint, allow forefoot supination and pronation.



Articular capsule, ligaments and tendons


The articular capsule is lax on the anterior aspect but tightly bound on both sides by strong medial and lateral ligaments. All the tendons crossing the ankle joint lie superficial to the articular capsule and are partly enclosed in synovial sheaths (Fig. 7.1B). Disorders of the peroneal tendons (inferoposterior to the lateral malleolus), the tibialis posterior tendon (inferoposterior to the medial malleolus), the tendons that run anterior to the ankle joint (such as tibialis anterior, extensor hallucis longus and extensor digitorum longus) or the Achilles tendon also cause ‘ankle’ pain. Which structure is responsible for the patient’s pain can often be determined by testing specific movements and the patient’s ability to resist movement in specific directions. The tibialis posterior muscle helps to maintain the ankle in a position of inversion, and the peroneal muscles help to maintain eversion.




Investigations and diagnosis



Aspiration and synovial fluid analysis


An anterior approach to the ankle is usually used. The joint line should be carefully palpated with the help of passive movement of the joint (if the patient actively moves the ankle, then tendon movement obscures the joint line). The point at which the needle enters the skin is approximately 1 cm proximal to the tip of the medial malleolus. The needle is directed posteriorly.


Joint aspiration is usually performed as a clean (not sterile) procedure. Thus, palpation of the joint line and marking the site with an indentation of the skin needs to be performed prior to cleaning the skin. The solution used to clean the skin (e.g. iodine) should be allowed to dry. Gloves are worn to protect the person performing the aspiration against blood-borne viral infection. Unless the person performing the aspiration is very experienced and can confidently place the needle in the joint space at the first attempt, local anaesthetic should be used to anaesthetize the skin and periarticular structures. The needle route should avoid the major tendons anterior to the ankle and the dorsalis pedis artery. If joint fluid is not obtained on the first attempt, then the needle should be slightly repositioned.


The synovial fluid obtained should be examined promptly; including macroscopic appearance, cell count, Gram stain, culture and microscopic examination for crystals. In Chapter 1 we described the characteristics of synovial fluid in normal and abnormal joints. Here, we will consider only those aspects of synovial fluid analysis that apply to crystal identification. Examination for crystals requires only a tiny amount of synovial fluid (even an apparently ‘dry’ tap may yield enough) but the examination should be performed immediately. Polarized microscopy allows the identification of urate crystals (strongly negatively birefringent needle-shaped crystals) and CPPD crystals (weakly positively birefringent rod-shaped or rhomboidal crystals) as shown in Fig. 7.2. The technique is not difficult but the experience of the observer and the adequacy of the microscope (e.g. rotating stage) can make a major difference to accuracy. CPPD crystals are often missed, and thus a repeat examination of a fresh specimen may be appropriate if the diagnosis appears likely, but no crystals are seen initially.




Other investigations


Other investigations can provide useful supplementary information but cannot replace synovial fluid examination. X-rays can detect or help to exclude pre-existing joint or bone disorders, chondrocalcinosis (CPPD deposition in cartilage) and bone trauma. It is sensible to assess laboratory parameters of inflammation, such as white cell count and ESR, for comparison with future results but they assist little in the differentiation of septic from gouty arthritis. The serum uric acid level is of little help in the setting of possible acute gout. A normal level does not exclude gout and an elevated level does not confirm gout. However, the uric acid level is very important in the long-term management of gout.




Pathophysiology of gouty arthritis


Acute gout is caused by the interaction between the inflammatory system (particularly neutrophils) and crystals of monosodium urate monohydrate (urate). Urate crystals form in and around joints and have a predilection for the cooler areas of peripheral joints (because of the decreased solubility of urate at lower temperatures). Although the inflammatory episode comes on abruptly, the formation of urate crystals probably occurs slowly over weeks to months (there remains some doubt as to the maximum speed of urate crystal formation in vivo). Urate crystals can only form in a supersaturated solution of sodium urate, which approximately equates to a uric acid concentration above 0.42 mmol/L (7.0 mg/dL). Thus the attack of acute gout is the culmination of a sequence of events:


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Jul 3, 2016 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on CRYSTAL ARTHROPATHIES AND THE ANKLE

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