Gout

Surgery itself provokes flares - Post-operative status, acute medical illness, trauma, fasting, dehydration, and alcohol or dietary swings all precipitate attacks, and around 60% of patients have a second attack within a year. Warn the patient and the ward team, and don't reflexively blame a new hot joint on positioning.

A polyarticular flare mimics sepsis - Multiple hot joints with fever, malaise, and elevated WBC, ESR, and CRP can produce a systemic inflammatory response that masquerades as sepsis. Arthrocentesis with compensated polarized light microscopy settles it: needle-shaped, negatively birefringent crystals. Septic fluid instead runs a WBC over 50,000/mL with a positive Gram stain.

Renal function drives the plan - Renal insufficiency reduces urate excretion, and gout clusters with chronic kidney disease, hypertension, diabetes, obesity, heart failure, and prior myocardial infarction. Get a recent creatinine and eGFR before you commit to an analgesic or a fluid plan.

NSAIDs often unavailable - Contraindications are active gastric or duodenal ulcer, uncontrolled hypertension or heart failure, NSAID allergy, and creatinine clearance under 60 mL/min/1.73 m². That removes the usual multimodal workhorse in precisely the patients who have gout.

Aspirin does not treat it - Aspirin is not used for a flare because of the paradoxical salicylate effect: doses under 2 to 3 g/day cause renal uric acid retention while higher doses are uricosuric. Low-dose aspirin is itself a listed cause of hyperuricemia, alongside diuretics and cyclosporine.

Colchicine has a narrow margin - It is eliminated hepatically and needs dose reduction with hepatic or renal impairment. ABCB1 (P-glycoprotein) inhibitors such as cyclosporine and clarithromycin can tip it into toxicity, and colchicine neuromyopathy can appear weeks after cyclosporine is started. Adverse effects run to myotoxicity and myelosuppression — leukopenia, thrombocytopenia, aplastic anemia — so a CBC is worth having. IV colchicine is strongly advised against; deaths have been reported.

Allopurinol plus azathioprine - Allopurinol potentiates the cytolytic and immunosuppressive effects of azathioprine and 6-mercaptopurine, which are partly metabolized by xanthine oxidase, and the combination should be avoided. Febuxostat is likewise contraindicated with azathioprine, 6-mercaptopurine, and theophylline. Surface it if the patient also carries a transplant or IBD regimen. Allopurinol also destabilizes warfarin control, so the INR needs watching.

Steroids as the fallback - When NSAIDs and colchicine are out, prednisone or prednisolone 30 to 40 mg daily is the standard flare dose and is the agent of choice in renal insufficiency; intra-articular injection covers a single joint. Expect hyperglycemia, fluid retention, higher blood pressure, and mood changes, and note that steroids raise the risk of impaired wound healing in post-operative patients.

Don't start urate-lowering therapy now - Initiating allopurinol or febuxostat precipitates flares, which is why it is begun at low dose with colchicine prophylaxis for three to six months. The perioperative window is the wrong time to start or titrate it; continue what is already established instead.

Tophi, positioning, and valves - Tophi collect in joints, ears, finger pads, tendons, and bursae and produce destructive, deforming arthritis with extensive bone loss, so pad and position deformed joints deliberately and expect fragile overlying skin that can ulcerate. Tophaceous deposits have also been reported on heart valves and in the cornea.

Pegloticase carries a boxed warning - Reserved for refractory gout and infused every two weeks. Current FDA labeling (DailyMed, resolved live) carries a boxed warning for anaphylaxis and infusion reactions: 6.5% anaphylaxis and 26% infusion reactions with pegloticase alone, falling to 1% and 4% when it is co-administered with methotrexate, and most reactions appear within two hours. Patients are premedicated with an antihistamine and a corticosteroid. G6PD deficiency is a labeled contraindication because of life-threatening hemolysis and methemoglobinemia, and the label requires screening at-risk patients beforehand — particularly those of African, Mediterranean, or Southern Asian ancestry. Remember the methemoglobinemia when the saturation will not track.

Gout is inflammatory arthritis driven by deposition of monosodium urate (MSU) crystals in joints, tendons, and bursae. Humans lack uricase, so urate is the end product of purine metabolism, and above roughly 6.8 mg/dL — the approximate limit of urate solubility — it comes out of solution. The glomerulus filters nearly all urate, so the body pool is managed by renal excretion and anything that impairs clearance raises it.

A flare comes on abruptly, peaks within 12 to 24 hours, and is usually monoarticular in the lower extremity, most often the first metatarsophalangeal joint. What makes it a perioperative problem is that the things surgery does — the operation itself, trauma, fasting, dehydration, diuretics, and starting urate-lowering therapy — are exactly the shifts in extracellular urate that set off an attack.