Lita Dr Emergency Clinical Rheum a to Logic
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Transcript of Lita Dr Emergency Clinical Rheum a to Logic
RHEUMATOLOGY EMERGENCY IN CLINICAL PRACTICE
LITA DIAH R, DIV. REUMATOLOGI, DEPT PENY DALAM,
RSUD DR SOETOMO SURABAYA
Why?
Approximately 10% to 25% of patients with rheumatologic disorders visiting emergency department require hospital admission one third of the hospitalized patients need intensive care
RA, scleroderma, SLE, 75% ( ICU). 50% ofadmissions infections, 25% - 35% exacerbationof the rheumatologic disorder.
Causes of Life Threatening
. Exacerbation (flare-up) Infections resulting from immunosuppressionAdverse effects of drugs used to treat autoimmune Malignancy resulting from prolonged use of cytotoxic
drugsAcute serious illnesses that are unrelated to the
rheumatic disease
ICU admission
The acute problems leading to ICU admission :gastrointestinal bleeding, cardiac conditions,Pneumoniasepsis interstitial lung disease seizurescerebral hemorrhagePancreatitispulmonaryembolismcerebral infarction
Classification of RheumatologicalEmergencies
rheumatological emergencies can be divided into 2 broadcategories :A. True Rheumatological Emergencies1. Acute low backache2. Acute gout3. Acute arthritis4. Lupus flare5. Systemic necrotizing vasculitides6. Scleroderma renal crisis7. Catastrophic antiphospholipid syndrome8. Erythema nodosum
Classification of RheumatologicalEmergencies
B. Medical Emergencies in Patients withSystemic Rheumatic Disease
– NSAID induced gastrointestinal bleed– Acute left ventricular failure (LVF) in lupus nephritis with hypertension– Intracranial bleed in lupus nephritis with HT– Tuberculous meningitis in SLE– Acute adrenal insufficiency due to sudden steroid withdrawal– Seizures in SLE- Cyclophosphamide induced haemorrhagic cystitis- Drug (immunosuppressive) induced bone marrow suppression, etc.
ACUTE ARTHRITIS
A Acute Monoarthritis– Septic arthritis– Gout– TraumaB Acute Oligo/Poly Arthritis– Reactive arthritis/Reiter syndrome– Viral arthritis– Rheumatic fever– HIV– Disseminated gonococcal infection
ACUTE MONOARTHRITIS
Acute monoarthritis should be considered amedical emergency. The condition warrantsimmediate joint aspiration. Synovial fluid shouldbe aspirated to rule out pus in the joint and crystal identification should be performed
Total and differential WBC counts, culture,Gram’s stain, ZN (Ziehl Neelsen’s) stain andcrystal identification should be performed onall fluids.
Acute gout
Acute gout is one the commonest rheumatologicalemergencies. usually a male, acute pain in one of the lower limb joints. monoarthritis(single joint) or oligoarthritis (2-4 joints).Polyarticular is very rare The diagnosis is made on clinical grounds.Confirmation is by crystal identification aftersynoviocentesis. Serum uric acid levels may benormal. Joint aspiration is mandatory
Gout
Aspiration findingsNegatively birefringent sodium urate crystals
Gout
Why in ED?First time attackMultiple attacks pain
Establish your dxTreat arthritis acutely
NSAIDs x 5-10 d (sx resolution)Colchicine (poorly tolerated)Corticosteroids Bed rest
Pyogenic Arthritis
Intrarticular infectionNongonococcal, gonococcal, and viral
NongonococcalAbnormal host (joint damage, IVDA, endocarditis)Acute monoarthritis of weight bearing joint or wristLarge effusionsCausative organism found elsewhere on body
Non gonococcal Arthritis
S. aureus most commonGram – increasing frequency
E. Coli, Pseudomonas
5-10% mortalityFever / chillsJoint aspirate> 50K wbc / µL, > 90% PMNs
Non gonococcal arthritis
Joint aspiration Joint drainage Surgical arthrotomy for septic hips/shoulders, if osteomyelitis co-exists with septicarthroscopic drainage.Antibiotics need to be given for 2 weeks
parenterally followed by 2-6 weeks of oral therapy.
Gonococcal Arthritis
Disseminated Gonococcal diseaseEpidemiology
Otherwise normal hostMost common urban pyogenic arthritis 2-3 x more common in females (esp menses / preg)Rare at age > 40Often identifiable source (cervicitis, urethritis, pharyngitis, proctitis)
Gonococcal Arthritis
1-4 day migratory polyarthralgiasWrists, knees, elbows, ankles60% develop tenosynovitis40% develop purulent monoarthritis (usually knee)Characteristic asymptomatic skin rash (most pts)
Joint AspirationBlood culturesSwab everywhere
Joint Aspiration
Enter the joint while aspirating
Joint Aspiration
Withdraw as much fluid as possible
Systemic Lupus Erythematosus
Inflammatory Autoimmune SyndromeClinical manifestations from
Trapping of antigen-antigody complexes in capillaries of visceral structuresAutoantibody mediated host cell destruction
Lupus flaremay be precipitated by stress,exposure to sunlight, steroid reduction,pregnancy, infection etc,.
SLE
Why in ED?Ocular
ConjunctivitisBlindness
PulmonaryPleurisyPleural effusionBronchopneumoniaPneumonitis
SLE
Why in EDCardiac
CHFMyocarditsHypertension
Cardiac arrhythmiasVerrucous endocarditis
Valvular incompetenceEmboli
PericarditisMI (Late, 2° chronic steroids)
SLE
Why in EDMesenteric vasculitis
Aneurysms in medium size vesselsAbdominal pain / abdominal anginaIleusPeritonitisPerforation
SLE
Why in EDNeurologic complications
PsychosisOrganic brain syndromeSeizuresPeripheral / cranial neuropathyTransverse myelitisStroke
SLE
Why in EDGlomerulonephritis
MesangialFocal proliferativeDiffuse proliferativeMembranous
Interstitial nephritis
SLE
Why in EDMiscellaneous
Arterial / Venous thrombosisHashimoto’s thyroiditisHemolytic anemiaThrombocytopenia purpuraArthritic pain
SLE
ruled out in febrile lupus patient. A low TLC and normal CRP lupus activity while leukocytosis and raised CRPsuggest infection.
Institution of aggressive therapy beginning with highdose of glucocorticosteroids Infections must be carefully excluded before instituting orincreasing GCS therapy. Consideration of co-morbid disease hypertension, DM, osteoporosis
Management
Initial therapy high dose daily GCS (1-1.5mg/kg) given in divided doses or IV methyl prednisolonepulses (500-1000 mg/d for 3 days) followed by oralprednisolone.Combining with cytotoxic drug is superior to GCS alonein controlling acute severe SLENew therapies for aggressive SLE : intravenousgammaglobulinsB-lymphocyte depletion by rituximab are showing promisingresults in SLE.
Emergent Rheumatologic Complications
Airway obstructionRelapsing poychondritis
Cartilage inflammation / breakdownAirway involved in 50%
RACricoarytenoid dysfunctionCan freeze in closed position
Emergent Rheumatologic Complications
Ventilatory failureDermatomyositis / polymyositis
Muscle failure late in disease
Pleursy / Pleural effusionsRA / SLE
Pulmonary hemorrhageGoodpasture’s, SLE, hpersensitivity vasculitis, SLE, Wegener’s granulomatosis
Emergent Rheumatologic Complications
Pulmonary FibrosisAnkylosing spondolitis, scleroderma, RA
Interstitial pneumonitisMyositis
Admit to r/o infectionImmunosuppress
Emergent Rheumatologic Complications
CardiacPericarditis
RA, JRA, SLE (with other flare sxs)Atherosclerosis
SLEMI
PAN, KawasakiPancarditis
Acute Rheumatic Fever
Emergent Rheumatologic Complications
CardiacValvular heart disease
Seronegative spondyloarthropathiesRelapsing polychondritis
Emergent Rheumatologic Complications
Adrenal InsufficiencyAny rheumatic dz pt on chronic steroidsNo harm in stress doseIf unclear (nonspecific sxs, steroids in past 18 mo)
Cortisol levelDexamethasone
Emergent Rheumatologic Complications
High Morbidity ComplicationsC-spine / Spinal Cord
RA, ankylosing spondylitisTransverse myelitis
SLE
Anterior spinal artery syndrome
Emergent Rheumatologic Complications
High Morbidity ComplicationsBlindness
TASjogren’s Syndrome
RAIndependently
Red Eye in RAEpiscleritis—Painless, self limitedScleritis—Ocular tenderness, blindness, rupture
Emergent Rheumatologic Complications
High Morbidity ComplicationsHypertension
PAN, SLE, RAScleroderma
Was leading cause of deathACEI changed this
Drug induced nephrotoxicity
Emergent Rheumatologic Complications
High Morbidity ComplicationsRenal Disease
GlomerulonephritisSLEWegener’s
Renal vein thrombosisATIII deficiency in SLE / nephrotic syndrome
Microangiopathic disease Diffuse scleroderma—rapidly progressive
Emergent Rheumatologic Complications
High Morbidity ComplicationsRhabdomyolisis
Acute polymyositisMetabolic muscle disease
Management
laboratory testsCRP, ferritin,ANA , CAM, and cytokines .Complement. Serum CRP and PCT used to differentiat exacerbation and infection. Procalcitonin are greatly elevated in acute bacterial and fungal infection butnormal or only mildly elevated in viral inf and flaresCT scan, bronchoscopy, culture sample
Management
Aggressive Corticosteroids.but not effective scleroderma, Kawasaki,HSP, Still’s dis cytotoxic drug ,necrotizing vasculitis, Wegener’s granulomatosis,Goodpasture’s, NL, severe polymyositis,Plasmapheresis NPSLE, hemophagocytic syndrome,Goodpasture’s syndrome,,JRA, TTP, catastrophic APS IvIg dermatomyositis, Kawasaki, ITP, severe NLACE inh :scleroderma renal crisis
Prognosis
Simplified Acute Physiology Score II (SAPS II) scores, poor health status before admission, and cs treatment : poorICU outcome .Thong et al: duration of rheumatic disease ,high doses of CS or immunosuppressiv ~ poor outcome .Mortality is high ;renal failure , coma , ARDS,infectionoverall ICU mortality rate in patients systemic rheumatic diseases 30% to 60% (APACHE) II or SAPS II scores
Terima Kasih