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Rheumatological Emergencies

Rheumatological Emergencies. Dr. Thushani S. Wickramaratne FRCP Consultant Rheumatologist. 46 male , Physical job, alcohol 15 -20 units beer/week known RA, sero positive, mother has PSO on DMARDS, initiated on Golimumab 6/12 ,not effective Urgent review (via nurse help line)

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Rheumatological Emergencies

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  1. Rheumatological Emergencies Dr. Thushani S. Wickramaratne FRCP Consultant Rheumatologist

  2. 46 male , Physical job, alcohol 15 -20 units beer/week • known RA, sero positive, mother has PSO on DMARDS, initiated on Golimumab 6/12 ,not effective • Urgent review (via nurse help line) • Swollen knee –acute, painful -appox 2 weeks, ”going to see GP to get a sick note”

  3. What is the diagnosis? Septic Arthritis? Gout? Trauma? Anything else? PSA

  4. Anything is possible ! Sepsis ! Sepsis! Sepsis!!! SEPTIC UNTIL PROVEN OTHERWISE!

  5. Two broad categories : True Rheumatological Emergencies • Acute arthritis: mono/poly infective, non infective • Acute low backache : Mechanical/osteoporotic/other • Vasculitis: SLE related, GCA, Scleroderma renal crisis Catastrophic antiphospholipid syndrome Medical Emergencies in Patients with Systemic Rheumatic Disease • NSAID induced gastrointestinal bleed • Acute left ventricular failure : cardiovascular diseases • Acute adrenal insufficiency due to sudden steroid withdrawal • Seizures • Fractures/ subluxations • Drugs associated • Cyclophosphamide induced haemorrhagic cystitis immunosuppressive) induced bone marrow suppression • Biologics

  6. Topics covered • Septic Arthritis • Crystal arthropathy • GCA • Acute RA flares

  7. Septic Arthritis Septic arthritis is a medical emergency. 25% Mortality untreated. 50% permanent damage Predisposing factors •   Age >80 years • Diabetes mellitus • Rheumatoid arthritis • Presence of prosthetic joint • Recent joint surgery • Intravenous drug abuse, immuno suppressive therapy • Alcoholism, • Prior intra-articular corticosteroid injection A combinations of independent risk factors will substantially increase risk Patients with RA appear to be especially prone to bacterial arthritis: the risk may also be increased in gout, pseudogout, osteoarthritis, and Patients with RA may have additional predisposing factors, such as prior intraarticular steroid injections, maintenance immunosuppressive medications, and anti-tumor necrosis factor therapy

  8. MECHANISM OF INFECTION  •  Majority : haematogenous .Rarely direct : bite or other trauma • Common predisposing factors for haematogenous dissemination : injection drug use, presence of indwelling catheters, and an underlying immunocompromised state • sign of infective endocarditis :suspect when septic arthritis due to Staphylococcus aureus, enterococci. • bacterial meningitis • SCJ arthritis :subclavian vein catheterization • Hip Septic arthritis: femoral venepuncture or ruptured colonic diverticular disease

  9. Septic arthritis is usually monomicrobial. Polymicrobial infections are less common and usually occur in the setting of penetrating trauma Gonococcal arthritis, Tuberculous / fungal,viral etc. Microbiology 

  10. Management of septic arthritis Joint aspiration :mandatory ASAP Blood cultures : positive in app 50 % Gram stain AFB Crystals Culture Antibiotics Parenteral antibiotics for at least 14 days followed by oral therapy for an additional 14 days. Refer to orthopaedics : washouts etc

  11. “People wish their enemies dead, but I do not; I say give them the gout.” Lady Mary Wortley Montagu (1689 – 1762)

  12. Chronic Gout Comorbidities : consideration of these disorders is critical in the choice of treatment Renal function Cardiovascular disease, including heart failure or poorly controlled hypertension Gastrointestinal disease, including peptic ulcer disease Diabetes mellitus, especially if poorly controlled Drug allergy or intolerance An elevated serum urate level does not confirm gout A normal serum urate does not exclude gout

  13. GENERAL THERAPEUTIC PRINCIPLESAcute Gout  • The goal of therapy in an acute gout attack is prompt and safe termination of pain and disability • Choices are : NSAIDs , colchicine +/- steroids • NSAIDs : are particularly appropriate in younger patients (less than 60 years old) who lack renal, cardiovascular, or active gastrointestinal disease. Most effective when treatment is initiated within 48 hours of the onset of symptoms. Can be discontinued one or two days after clinical signs have completely resolved. the total duration of NSAID therapy for an acute attack is five to seven days. Aspirin is not used for the treatment of acute gout flares because of the paradoxical effects of salicylates on serum urate. • Colchicine : 0.5 mg BD (minimise diarrhoea) Useful when patients are on oral anticoagulants,Avoided in hemodialysispatients with acute gout flares because it is not removed by dialysis, and therefore these patients have a heightened risk of colchicine toxicity. Avoid in pregnancy. • Patients who are unable to take oral medications ,intraarticular or IM injection of glucocorticoids. • End-stage renal disease and transplantation : intraarticular, oral, or parenteral glucocorticoids. Avoid NSAIDS • Acute gout in organ transplant recipients should only be managed by clinicians experienced because of the complexities of management due to reduced uric acid excretion and because of the frequent accompanying use of cyclosporin. Colchicine, NSAIDs, and glucocorticoids can potentially be used, but limits on dosing, frequency, and duration of therapy • Anakinra – Anakinra (100 mg daily, administered subcutaneously) is the preferred IL-1 antagonist • Canakinumab is a fully humanized MaB, long-acting monoclonal antibody that blocks IL-1 : it can be effective for the treatment of acute gout in patients who have a history of multiple flares and who have either refractoriness or contraindication to acute flare treatment with NSAIDs and/or colchicine

  14. urate-lowering therapies • Modification of lifestyle and risk factors • Address CVS risk factors and co-morbidities should be screened for in all patients with gout, reviewed annually and managed appropriately. Smoking, HT, DM, dyslipidaemia, obesity and renal disease • Recurring attacks (⩾2 attacks in 12 months) • Tophi, Chronic gouty arthritis , joint damage, renal impairment, history of urolithiasis; diuretic therapy use; and primary gout starting at a young age • ULT is best delayed until inflammation has settled as ULT is better discussed when the patient is not in pain  • Initial aim of ULT is to reduce and maintain the sUA level at or below a target level of 300 µmol/l (new BSR guidelines) • Allopurinol is the recommended first-line ULT. Initially low dose (50–100 mg daily increments appro every 4 weeks until the sUA target has been achieved.(max dose 900 mg daily) • In patients with RF : smaller increments (50 mg) should be used. maximum dose will be lower, but target urate levels should be the same.

  15. Febuxostat : An alternative XOI allopurinol is not tolerated or whose renal impairment prevents allopurinol dose escalation.Start with a dose of 80 mg daily (max 120 mg) • Uricosuric agents : sulfinpyrazone ,probenecid or benzbromarone(CKD and on named basis) • Losartan and fenofibrate : not as a primary ULT but where treatment for hypertension or dyslipidaemia, respectively, is required( weak uricosuric effect) • Vit C : • A uricosuric agent + xanthine oxidase inhibitor: in patients who do not achieve a therapeutic serum urate target with optimal doses of monotherapy 

  16. GCA GCA : commonest of all vasculitides Visual loss occurs 1/5 preventable by prompt recognition and treatment A patient >50 years of age presenting with the following features should raise suspicion of GCA: Acute headache (usually unilateral in the temporal area) Scalp tenderness. Jaw and tongue claudication Visual symptoms (including diplopia) Constitutional symptoms Polymyalgic symptoms Limb claudication

  17. Examination may show: Features predictive of ischaemic neuro-ophthalmic complications: Jaw claudication Diplopia Temporal artery abnormalities • Abnormal superficial temporal artery: tender, thickened with reduced or absent pulsation • Scalp tenderness • Eye: • Transient or permanent visual loss • Visual field defect • Relative afferent papillary defect • Anterior ischaemic optic neuritis • Central retinal artery occlusion • Upper cranial nerve palsies • Features of large-vessel GCA: vascular bruits and asymmetry of pulses or blood pressure

  18. Laboratory investigations include Full blood count, urea and electrolytes, liver function tests, CRP, ESR,CXR, Urine dip An acute-phase response is the characteristic of GCA (raised ESR, CRP, anaemia,thrombocytosis, raised ALP, polyclonal increase on serum electrophoresis ) Urgent referral for specialist evaluation is suggested for all patients with GCA Temporal artery biopsy (TAB) should be considered whenever a diagnosis of GCA is suspected. This should not delay the prompt institution of high-dose glucocorticosteroid therapy TAB can remain positive for 2–6 weeks after the commencement of treatment (samples should be at least 1 cm in length. Contra lateral biopsy unnecessary) TAB may be negative in some patients – GCA if there is a typical clinical picture and response to glucocorticosteroids Duplex ultrasound : operator dependant : increased diameter of the temporal artery and hypoechoic wall thickening (halo sign) CT/MRI : not useful

  19. Treatment : High-dose glucocorticosteroid therapy should be initiated immediately when clinical suspicion of GCA is raised • Uncomplicated GCA : Prednisolone40–60 mg daily • Evolving visual loss or amaurosis fugax (complicated GCA) : i.v. methylprednisolone (500 mg -1gm) for 3 days before oral glucocorticosteroids • Established visual loss : Prednisolone 60 mg daily : to protect the contralateral eye • And Bone protection +PPI + Aspirin

  20. Tapering regimen : response to treatment, patient wishes, co morbidities, acute phase response • Prednisolone : 40–60 mg continued until symptoms and laboratory abnormalities resolve (at least 3–4 weeks) • then reduce dose by 10 mg every 2 weeks to 20 mg • then by 2.5 mg every 2–4 weeks to 10 mg • then by 1 mg every 1 month (provided no relapse) (Monitoring of therapy should be clinical and supported by the measurement of inflammatory markers ) Relapse : return of symptoms of GCA, ischaemic complications, or polymyalgic symptoms. A rise in ESR/CRP is usually seen with relapse, but relapse can be seen with normal inflammatory markers Treatment escalated ,refer for specialist assessment Recurrent relapse or failure to wean glucocorticosteroid dose requires : consideration of adjuvant therapy, such as MTX or other immunosuppressants. These immunosuppressive agents should be started at the third relapse. Echocardiography, PET and MRI may also be appropriate : aortitis Biological therapies : Tocilizumab: the first interleukin-6-receptor inhibitor –NICE 2018

  21. Acute RA flare • Acute flares of pre-existing arthritis may be precipitated by stress, steroid reduction/withdrawal, pregnancy, infection • Infection needs to be rules out in single joint flare • Acute RA best treated with a short course of corticosteroids oral or IM Depomedrone (120 mg evidence suggested ideal dose) with escalation of DMARD therapy and biological therapies

  22. Questions?

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