Rheumatic pain indramayu 29june2013
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Transcript of Rheumatic pain indramayu 29june2013
Rheumatic pain management
In daily practice
Pain GridI II III IV V VI
Acute (Incident Focused) Monophasic Pain
Acute (Diagnostically Focused) Recurrent
Pain
Chronic Malignancy Based Pain
Chronic Progressive Non-Malignancy Based
Pain
Chronic NonProgressive
NonMalignancy Based Pain
Chronic Benign Pain
Examples Examples Examples Examples Examples Examples
Post Operative, Major Trauma, Acute Phase of
Burns, Fractures, Pre- and Post-Procedural Scenarios, Acute Back Pain Syndromes
Sickle Cell Crisis, Acute Flare of Inflammatory Bowel Disease, Acute Flares of Inflammatory
Arthropathies, Hemophilic Arthropathy, Renal
Calculi, Forms of Back Pain, Dysmenorrhea,
Migraine
Self Explanatory based on local spread,
metastatic invasion, pressure or obstruction
A.I.D.S. Progression, Sickle Cell Patients, Hemophilia Patients,
Some Connective Tissue Diseases, Inflammatory
Bowel Disease with Short Gut and ExtraGut
Autoimmune Manifestations
Musculoskeletal Pain Syndromes
(Osteoporosis, spondylolisthesis), TMJ,
Neuropathic Pain Syndromes (Postherpetic
neuralgia, painful polyneuropathy, RSD),
Forms of Back Pain
Pain Associated with a Marked Discrepancy in
Pathologic Findings compared against Strong and Typical Axis I, Axis II
and Premorbid Psychosocial Features
Opioid Advisability Opioid Advisability Opioid Advisability Opioid Advisability Opioid Advisability Opioid Advisability
OK Ok (with cautions) Advised OKRelative
ContraindicationOpioid Avoidance
Courtesy of Craig Pratt, MD (with some changes)
Rheumatic pain
3
Symptoms
■ Joint pain
■ Joint swelling
■ Morning stiffness
■ Fatigue
■ Weight loss
■ Flu-like symptoms
4
The goal of pain management
is
not necessarily pain relief – it is improving a
patient’s quality of life.
Symptomatic Treatments
■ Education/support■ Rest/relaxation■ Joint protection■ Physiotherapy■ Analgesics■ Anti-inflammatory drugs■ Steroids■ Joint injections■ Pain Management Clinics
6
Symptomatic Treatments
■ Education/support■ Rest/relaxation■ Joint protection■ Physiotherapy■ Analgesics■ Anti-inflammatory drugs■ Steroids■ Joint injections■ Pain Management Clinics
7
What are the benefits and risks from NSAIDs?
How do I reduce the GI risks?How do I reduce the CV risks?
Are there specific safety concerns with NSAIDs?
*Note by NSAIDs we mean traditional NSAIDs (e.g. diclofenac, naproxen, ibuprofen); etodolac, meloxicam, or coxibs (e.g. celecoxib,
etoricoxib)
Key questions regarding NSAIDs*
Common Rheumatic problems: Osteoarthritis and Rheumatoid Arthritis
Prevalence of Arthritis in US Adults*
■ 49.9 million (22.2%) with self-reported, physician-diagnosed arthritis†1
■ 21.1 million (9.4%) with arthritis and arthritis-attributable activity limitation1
■ Affects more women than men in every age group2
0
20
40
60
80
100
18–24 25–34 35–44 45–54 55–64 65–74 75–84 85+
Women Men
Age Group, years
* Data sources: 2007-2009 data from the National Health Interview Survey (NHIS). † Includes multiple forms of arthritis.
HCP=health care professional.
1. CDC. MMWR Morb Mortal Wkly Rep. 2010;59(39):1261-1265.2. Graphic adapted from CDC. NHIS Arthritis Surveillance: Arthritis Prevalence in Women and Men.
www.cdc.gov/arthritis/data_statistics/national_nhis.htm. Accessed January 12, 2011.3. CDC. MMWR Morb Mortal Wkly Rep. 2009;58(16):421-426.4. Hootman JM, Helmick CG. Arthritis Rheum. 2006;54(1):226-229.
■ Arthritis and rheumatism leading causes of disability in US3
■ By 2030, a projected 67 million in US will have HCP-diagnosed arthritis4
US
Ad
ult
s (%
)W
ith
Art
hri
tis
US
Ad
ult
s (%
)W
ith
Art
hri
tis
Factors Implicated in the Development of OA
Cartilage breakdown
ObesityObesity
Anatomic abnormalities
Anatomic abnormalities
Microfractures and bony
remodeling
Microfractures and bony
remodeling
Loss of joint stability
Loss of joint stability
TraumaTrauma
AgingAging
Genetic and metabolic diseases
Genetic and metabolic diseases
InflammationInflammation
Immune system activity
Immune system activity
Compromised cartilage
Biophysical changes• Collagen network fracture• Proteoglycan unraveling
Biochemical changes• Inhibitors reduced
• Proteolytic enzymes increased
Abnormal stresses Abnormal cartilage
Mandelbaum B et al. Orthopedics. 2005;28(2 suppl):s207-s214.Adapted with permission from 2002 Medtronic Sofamor Danek, Basic Bone Biology.
EULAR Diagnostic Criteria for Knee OA (2010)
■ Based on review of studies from 1950-2008 and expert consensus
■ Focuses on clinical diagnosis: presence of three symptoms andthree signs correctly diagnoses 99% of cases
SymptomsSymptoms
1 Persistent knee pain √
2 Limited morning stiffness √
3 Reduced function √
SignsSigns
4 Joint crepitus √
5 Restricted movement √
6 Bony enlargement √
EULAR=European League Against Rheumatism.
Zhang W et al. Ann Rheum Dis. 2010;69(3):483-489.
ACR Diagnostic Criteria for Knee OA (1986)
■ Clarified and standardized definition of osteoarthritis Joint symptoms and signs associated with defective integrity of
articular cartilage and changes in underlying joints at bone margin
■ Focuses on clinical examination of knee pain plus:
■ Sensitivity, 95%; specificity, 69%
Presence of 3 of the followingPresence of 3 of the following
1 Age >50 years √
2 Morning stiffness <30 minutes √
3 Joint crepitus on active motion √
4 Bony tenderness √
5 Bony enlargement √
6 No palpable warmth of synovium √
ACR=American College of Rheumatology.
Altman RD et al. Arthritis Rheum. 1986;29(8):1039-1049.
Goals of OA Management:OARSI Recommendations
Reducejoint pain and
stiffness
Reduce physical disability
ImproveHRQoL
Educate patients
Limitprogression of joint damage
Knee and Hip OA: Goals of Treatment
HRQoL=health-related quality of life; OARSI=Osteoarthritis Research Society International.
Zhang W et al. Osteoarthritis Cartilage. 2008;16(2):137-162.
Maintain and improve joint
mobility
Integrated Approach to Treating Patients With OA
NonpharmacologicNonpharmacologic PharmacologicPharmacologic
■ Patient education■ Phone contact (promote self-care)■ Referral to physical therapist■ Aerobic, strengthening, and/or water-based exercise■ Weight reduction■ Walking aids, knee braces■ Proper footwear, insoles■ Thermal modalities■ TENS■ Acupuncture
■ APAP■ Oral NSAIDs■ Topical NSAIDs and capsaicin■ Corticosteroid injections■ Hyaluronate injections■ Glucosamine, chondroitin sulphate, and/or diacerein■ Weak opioids and narcotic analgesics for refractory pain*
SurgicalSurgical
■ Total joint replacement■ Unicompartmental knee replacement■ Osteotomy and other joint preserving surgical procedures
■ Lavage/debridement in knee OA†
■ Joint fusion after failure of joint replacement
* Pain resistant to ordinary treatment. † Controversial.
TENS=transcutaneous electrical nerve stimulation.
Zhang W et al. Osteoarthritis Cartilage. 2008;16(2):137-162.
US Prevalence and Burden ofRheumatoid Arthritis (RA)
■ May affect between 1.3 and 1.5 million adults1,2
Incidence lowest in individuals aged ≤34 yearsIncidence increases progressively with ageOccurs more commonly in women than in men
■ Societal costs3
* Costs in 2005 US dollars.1. Myasoedova E et al. Arthritis Rheum. 2010;62(6):1576-1582.2. Helmick CG et al. Arthritis Rheum. 2008;58(1):15-25.3. Birnbaum H et al. Curr Med Res Opin. 2010;26(1):77-90.
Hand RA
Photos from Towheed TE, Anastassiades TP. Can Fam Phys. 1994;40:1303-1309. Used with permission.
2010 ACR / EULAR Diagnostic Criteria for RA
CriterionCriterion ScoreScore
A Joint Involvement*
1 large joint 0
2-10 large joints 1
1-3 small joints (± large-joint involvement) 2
4-10 small joints (± large-joint involvement) 3
>10 joints (at least 1 small joint) 5
B Serology†
Negative RF and negative ACPA 0
Low-positive RF or low-positive ACPA 2
High-positive RF or high-positive ACPA 3
CAcute-Phase Reactants‡
Normal CRP and normal VHS 0
Abnormal ESR or CRP 1
DDuration of Symptoms§
Less than 6 weeks 0
6 or more weeks 1
Total score ≥6/10 Total score ≥6/10 needed to classify needed to classify
definite RAdefinite RA
Total score ≥6/10 Total score ≥6/10 needed to classify needed to classify
definite RAdefinite RA
* Any swollen or tender joint on examination. Excluded are distal interphalangeal joints, first carpometacarpal joints, and first metatarsophalangeal joints. Large joints = shoulders, elbows, hips, knees, and ankles. Small joints = metacarpophalangeal joints, proximal interphalangeal joints, 2nd through 5th metatarsophalangeal joints, thumb interphalangeal joints, and wrists. The >10 category can include large and small joints, and other joints not listed elsewhere (eg, temporomandibular, acromioclavicular, or sternoclavicular). † Negative: IU values ≤ULN for lab and assay. Low-positive: IU > ULN but ≤3x ULN. High-positive: IU >3x ULN. When only RF-positive or RF-negative is known, positive scored as low-positive. ‡ Normal/abnormal determined by local lab standards. § Patient self-report of duration of signs/symptoms of synovitis in joints clinically involved at time of assessment, regardless of treatment status.
ACPA=anti-citrullinated protein/peptide antibodies; CRP=C-reactive protein; VHS =erythrocyte sedimentation rate; RF=rheumatoid factor.
Aletaha D et al. Arthritis Rheum. 2010;62(9):2569-2581.
* Any swollen or tender joint on examination. Excluded are distal interphalangeal joints, first carpometacarpal joints, and first metatarsophalangeal joints. Large joints = shoulders, elbows, hips, knees, and ankles. Small joints = metacarpophalangeal joints, proximal interphalangeal joints, 2nd through 5th metatarsophalangeal joints, thumb interphalangeal joints, and wrists. The >10 category can include large and small joints, and other joints not listed elsewhere (eg, temporomandibular, acromioclavicular, or sternoclavicular). † Negative: IU values ≤ULN for lab and assay. Low-positive: IU > ULN but ≤3x ULN. High-positive: IU >3x ULN. When only RF-positive or RF-negative is known, positive scored as low-positive. ‡ Normal/abnormal determined by local lab standards. § Patient self-report of duration of signs/symptoms of synovitis in joints clinically involved at time of assessment, regardless of treatment status.
ACPA=anti-citrullinated protein/peptide antibodies; CRP=C-reactive protein; VHS =erythrocyte sedimentation rate; RF=rheumatoid factor.
Aletaha D et al. Arthritis Rheum. 2010;62(9):2569-2581.
Goals of RA Management
Reduce painReduce painPrevent or
control joint damage
Prevent or control joint
damage
Prevent functional
decline
Prevent functional
decline
Maximizepatient
quality of life
Maximizepatient
quality of life
Early and SustainedSuppression of Disease Activity
ACR Subcommittee on Rheumatoid Arthritis Guidelines. Arthritis Rheum. 2002;46(2):328-346.
Treatment Options for Patients With RA1-3
NSAIDsNSAIDs Symptomatic treatment to reduce joint swelling and pain
DMARDs DMARDs (biologic and (biologic and nonbiologic)nonbiologic)
Reduce/prevent joint damage, preserve joint integrity and function Methotrexate, leflunomide, hydroxychloroquine, minocycline,
sulfasalazine Etanercept, infliximab, adalimumab (TNF inhibitors) Rituximab (anti-CD20) Abatacept (cytotoxic T-lymphocyte antigen 4 immunoglobulin) Tocilizumab (anti-interleukin 6 receptor)
GlucocorticoidsGlucocorticoids Short-term use during flare-ups (oral or intramuscular) Local treatment for individual active joints (intra-articular)
SurgerySurgery Carpal tunnel release, synovectomy, resection of metatarsal heads,
total joint arthroplasty, joint fusion
Supportive Supportive StrategiesStrategies
Patient education, cognitive-behavioral interventions Rehabilitation interventions
DMARDs=disease-modifying antirheumatic drugs; TNF=tumor necrosis factor.
1. ACR Subcommittee on Rheumatoid Arthritis Guidelines. Arthritis Rheum. 2002;46(2):328-346.2. Saag KG et al. Arthritis Rheum. 2008;59(6):762-784.3. Smolen JS et al. Lancet. 2007;370(9602):1861-1874.
Distinguishing OA From RA1
CharacteristicCharacteristic OAOA RARA
Prevalence in US adults 27 million2 1.3–1.5 million3,4
Pathophysiologic process Degenerative Autoimmune
Commonly affected jointsHips, knees, spine,
fingersHands, feet
Typically symmetrical involvement
No Yes
Morning stiffness Transient Persistent
Joint swelling Hard tissue Soft tissue
Hand involvement Distal joints Proximal joints
Extraarticular involvement No Yes
Elevated autoimmune markers No Yes
1. Goldman L, Ausiello D. Cecil Textbook of Medicine. 23rd ed. Philadelphia, PA: Saunders Elsevier; 2007. 2. Lawrence RC et al. Arthritis Rheum. 2008;58(1):26-35.3. Helmick CG et al. Arthritis Rheum. 2008;58(1):15-25.4. Myasoedova E et al. Arthritis Rheum. 2010;62(6):1576-1582.
1991: A New Paradigm for COX Biology
GlucocorticoidsGlucocorticoids(block mRNA (block mRNA expression)expression)
Arachidonic AcidArachidonic Acid
COX-1COX-1(Constitutive)(Constitutive)
COX-2COX-2(Cytokine (Cytokine Inducible)Inducible)
StomachStomachIntestineIntestineKidneyKidneyPlateletPlatelet
Inflammatory Site:Inflammatory Site:• MacrophagesMacrophages• SynoviocytesSynoviocytes• Endothelial cells Endothelial cells
NSAIDsNSAIDsx x
McKenna F et al. Scand J Rheumatol 2001;30:11–18.VAS=visual analogue scale.
Less P
ain
Patient’s Assessment of Pain (VAS): Mean change at week 6
Mea
n C
ha
ng
e (m
m)
*p=0.001 vs. placebo
placebo(n=200)
celecoxib100 mg BID(n=199)
diclofenac50 mg TID(n=199)
Coxib vs. diclofenac:6-week Knee OA TrialMcKenna et al. 2001: Patient’s Assessment of Pain
McKenna F et al. Scand J Rheumatol. 2001;30:11-18.
American Pain Society (APS) Pain Measure:Worst Pain in the Past 24 Hours
Mean
Ch
an
ge in
Score p=0.05, active treatment vs.
placebo (days 1-7).
-4.0
-3.5
-3.0
-2.5
-2.0
-1.5
-1.0
-0.5
0.0Baseline Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7
placebo (n=200)
celecoxib 100 mg BID (n=199)
diclofenac 50 mg TID (n=199)
Less P
ain
Coxibs vs. diclofenac:6-week Knee OA TrialMcKenna et al. 2001: American Pain Society – Pain Measure
Gastrointestinal Safety
Risk of upper GI ulcer bleedingLanas A, et al. Gut 2006;55:1731–38
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Ad
justed
RR
Guidelines for Prevention of NSAID-Related Ulcer Complications(ACG Practice Guidelines 2009)
Lanza FL et al. Am J Gastroenterol 2009;104:728-738
Cardiovascular Safety
Primary Endpoint: Cumulative Incidence of Thrombotic CV Events
30
Etoricoxib (320 events)
Diclofenac (323 events)
MonthsNo. of patients at risk*
EtoricoxibDiclofenac
16,81916,483
13,359 10,733 8277 6427 4024 80581538326213790110,14212,800
7.0
6.0
5.0
4.0
3.0
2.0
1.0
06 12 18 24 30 36 420
Cu
mu
lati
ve in
cid
ence
(%
) w
ith
95%
CI
Etoricoxib vs diclofenacHR = 0.95 95% CI = (0.81-1.11)
*Per protocol population.
Boxed Warning for All Prescription NSAIDs
Cardiovascular Risk
NSAIDs may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal. This risk may increase with duration of use. Patients with cardiovascular disease or risk factors for cardiovascular disease may be at greater risk.
[Product] is contraindicated for the treatment of perioperative pain in the setting of coronary artery bypass graft (CABG) surgery.
Gastrointestinal Risk
NSAIDs, including Coxibs, cause an increased risk of serious gastrointestinal adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients are at greater risk for serious gastrointestinal (GI) events.
Cardiovascular Risk
NSAIDs may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal. This risk may increase with duration of use. Patients with cardiovascular disease or risk factors for cardiovascular disease may be at greater risk.
[Product] is contraindicated for the treatment of perioperative pain in the setting of coronary artery bypass graft (CABG) surgery.
Gastrointestinal Risk
NSAIDs, including Coxibs, cause an increased risk of serious gastrointestinal adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients are at greater risk for serious gastrointestinal (GI) events.
So what does this mean for us?
■ BOTH NSAIDs and coxibs are associated to varying degrees with increased CV risk
■ We must consider co-morbidities and concurrent medications that may sway risk
■ Older patients are at increased risk of CV, GI and renal side effects – weigh up risk/benefit
■ Both NSAIDs and coxibs are viable and effective options to treat pain and have manageable side effect profiles
33Arthritic patients with hypertension
NSAIDs: Renal risksMHRA DSU. May 2009
Renal risk
SUMMARY
■ Arthritis Pain is major health problem in our population
■ NSAIDs is scientifically proven to alleviate arthritis pain (OA, RA)
■ In patients with risk of GI tract afflection combine diclofenac with PPI
■ Diclofenac has a well-tolerated safety profille
35
■ NICE advises against use of any NSAID in those taking low-dose aspirin
■ Avoid tNSAIDs and coxibs in those with history of heart failure
■ Avoid tNSAID or coxib in those with GFR <30, use with caution when GFR 30<60
36
Practical Advice
■ Prescribe lowest effective dose for the shortest period of time
■ In chronic pain consider as required dosing and review regularly
■ Advise patient regarding potential side effects and do what you can to minimise risks
■ Monitor BP, renal function and liver function in those on long term
Have an enjoyable learning
Thank you