Septic arthritis, gout and ankylosing spondylitis

The synovial membrane is a thin, highly vascular lining whose normal job is to secrete fluid, not to engulf organisms. It holds few resident macrophages, and synovial fluid is poor in complement and opsonins, the proteins that mark bacteria for destruction. A joint is therefore close to an unprotected space once organisms are inside it. Staphylococcus aureus is well suited to exploit this: its surface adhesins bind directly to cartilage collagen and to fibronectin, so it anchors itself to the very tissue it will destroy. Much of the subsequent damage is inflicted by the host. Neutrophils release proteases and reactive oxygen species, matrix metalloproteinases digest proteoglycan and collagen, and bacterial enzymes such as hyaluronidase break down the lubricating fluid.

Proteoglycan loss begins within roughly twenty-four hours and collagen destruction follows within a day or two. At the same time the effusion distends a capsule that cannot stretch much, so intra-articular pressure rises above capillary pressure and synovial perfusion falls, adding an ischaemic injury to the enzymatic one. Cartilage is avascular, so antibiotics given into a vein reach joint fluid slowly and unevenly. Drainage addresses all three problems simultaneously: it removes organisms, lowers the concentration of enzymes and toxins, and relieves the pressure. It can be done by needle aspiration, by arthroscopic lavage, or by open washout when the hip is involved. Outcomes worsen sharply when treatment is delayed beyond about one to two days, which is why septic arthritis is called an orthopaedic emergency.

The nurse takes blood cultures and joint fluid before the first antibiotic dose whenever that causes no delay, charts temperature, pulse, blood pressure and pain, inspects the skin for the portal of entry, handles the drainage as infected material, and monitors kidney function and drug levels across weeks of therapy.

Purines from food and from the turnover of the body’s own cells are degraded in steps to hypoxanthine, then xanthine, then uric acid; the last two steps are catalysed by the enzyme xanthine oxidase. This is why the two main production-lowering drugs work where they do: allopurinol, and its active metabolite oxypurinol, and febuxostat both inhibit xanthine oxidase, so less uric acid is made. Probenecid works on the other side of the balance by blocking urate reabsorption in the proximal tubule of the kidney, so more urate leaves in the urine; the patient must therefore drink well, and the drug is avoided in people who form uric acid stones.

Pegloticase is a recombinant uricase, an enzyme humans lack, which converts uric acid into allantoin, a far more soluble substance; it is reserved for severe tophaceous gout that has not responded to other treatment. These drugs have a numerical target. Crystals form when serum urate exceeds its saturation point, about 360 micromol/L, equivalent to 6 mg/dL, so treatment aims to hold the level below that figure; once it stays below, tophi slowly dissolve over months. There is a clinical paradox worth knowing: starting or increasing urate-lowering therapy during an acute flare can prolong the attack, so the change is covered by colchicine or an anti-inflammatory drug.

Colchicine itself binds tubulin and prevents neutrophils from assembling the microtubules they need for chemotaxis and degranulation, which is why it works best within twenty-four hours of the onset and why diarrhoea is a common dose-limiting effect. Many ordinary things raise urate: thiazide and loop diuretics, low-dose aspirin, alcohol, fructose-sweetened drinks, obesity and impaired kidney function, so weight reduction, less alcohol and a review of diuretics all lower the level. Finally, a single raised uric acid is not gout: the diagnosis needs crystals in the joint, and the level measured during a flare is often normal.

The primary lesion of ankylosing spondylitis is at the enthesis, the insertion point where a tendon, a ligament or a joint capsule meets bone. In the spine the annulus fibrosus of the disc inserts on the rim of the vertebral body; inflammation there erodes the corner of the vertebra and the healing response fills the defect with new bone. That new bone grows into a syndesmophyte, a fine bony bridge to the next vertebra, and when many levels are involved the spine takes on the appearance described as bamboo. This explains the seemingly contradictory facts about the fused spine. It is stiff because the segments are bridged; but it is also fragile, because the vertebral body itself is often osteoporotic while a rigid spine can no longer absorb force.

A fused spine therefore fractures like a long bone, often through the disc space after only minor trauma, and such a fracture is easily missed on plain radiography: the patient is immobilised and the diagnosis is pursued with computed tomography or magnetic resonance imaging. Extra-articular disease follows the same inflammatory theme. Acute anterior uveitis is the commonest, giving a painful red eye, photophobia and blurred vision that needs urgent ophthalmological review because repeated attacks threaten sight. Later, aortitis can dilate the aortic root and cause aortic regurgitation, and conduction defects, arrhythmia and cardiomyopathy can appear. Cauda equina syndrome with disturbance of bladder, bowel and saddle sensation is rare but is a surgical emergency.

Disease activity and function are followed with standard scores such as the BASDAI and the BASFI together with inflammatory markers, so that treatment can be judged on trend rather than on a single morning. Management rests on daily exercise and posture work, because movement itself reduces pain and helps preserve spinal mobility, then NSAIDs, then tumour necrosis factor inhibitors or interleukin-17 inhibitors when the disease remains active; biologics require screening for latent tuberculosis and hepatitis and continued vigilance for infection. Sulfasalazine helps the peripheral joints more than the spine. Kyphoplasty is used in selected patients to correct a severe forward curve. Smoking worsens the disease and should be addressed at every visit.