2. Objectives Define crystal deposition disease Describe the etiology, epidemiology, signs and symptoms, diagnosis and treatment of acute gout Discuss the prevention of gout Discuss the complications of gout Describe the etiology, epidemiology, signs and symptoms, diagnosis and treatment of chronic gout Describe the etiology, epidemiology, signs and symptoms, diagnosis and treatment of pseudogout
3. Objectives Compare and contrast bursitis, tendinitis and other periarticular disorders Discuss the etiology, epidemiology, risk factors, clinical presentation and treatment of periarticular disorders by joint or location
5. Gout Essentials of diagnosis Acute onset, usually nocturnal and monoarticular, often 1st MTP joint Identification of urate crystals in joint fluid or tophi is diagnostic Postinflammatory desquamation and pruritus Hyperuricemia in most cases Dramatic response to NSAIDs or colchicine Tophi formation with chronic gout
7. General Considerations Often familial Hyperuricemia due to overproduction or underexcretion of uric acid Characterized by recurring acute arthritis early and chronic deforming arthritis later Common in Pacific Islanders May be secondary to acquired hyperuricemia
8. Risks for Acute Attacks Alcohol ingestion Changes in diet (NPO due to abdominal surgery) Rapid fluctuations in serum urate levels
9. Epidemiology 90% of gout patients are men Usually age > 30 Postmenopausal women 5-10% of patients will also have uric acid kidney stones
10. Origin of Hyperuricemia Primary – idiopathic; increased production or purine or decreased renal clearance of uric acid Secondary Myeloproliferative disorders Lymphoproliferative disorders Carcinoma and sarcoma Chronic hemolytic anemias Cytotoxic drugs Psoriasis
11. Origin of Hyperuricemia Secondary Intrinsic kidney disease Functional impairment of tubular transport Drug-induced (thiazides) Hyperlacticacidemia (EtOH, lactic acidosis) Hyperketoacidemia (DKA, starvation) Diabetes insipidus Bartter’s Syndome
12. Characteristics Tophus Nodular deposit of monosodium urate monohydrate crystals with associated foreign body reaction Cartilage, subcutaneous, periarticular, tendon, bone, kidneys Relationship between hyperuricemia and gouty arthritis is unclear
13. Signs and Symptoms Attack has sudden onset, usually nocturnal Can occur after alcohol excess or change in medication Sometimes there is not an apparent cause Most common in MTP joint of great toe (“podagra”)
14. Signs and Symptoms Can develop in the periarticular soft tissues (i.e., the arch of the foot) Involved joints are swollen and exquisitely tender Overlying skin is tense, warm and dusky red Fever is common
15. Signs and Symptoms Local desquamation and pruritus during recovery is characteristic but not always present Tophi usually seen only after several acute attacks Tophi may be on ears, hands, feet, olecranon and prepatellar bursas Can evolve into chronic, deforming polyarthritis
16. Laboratory Findings Serum uric acid is elevated ( > 7.5 mg/dL) in 95% of patients Sed rate and WBC’s may be elevated during an acute attack Examination of tophi or joint fluid under polarized light shows sodium urate crystals – needle-like and negatively birefringent
18. Imaging Studies Early in the disease, x-rays are normal Later, “rat bite” lesions may develop Rat bite lesions adjacent to a soft-tissue tophus are diagnostic of gout
19. Imaging Studies “Rat bite” is a punched out lesion with an overhanging rim of cortical bone
20. Differential Diagnosis Acute gout Cellulitis Acute infectious arthritis Pseudogout Chronic gout Chronic RA Chronic lead intoxication
21. Treatment of Acute Attack NSAIDs – treatment of choice for acute gout Traditionally, indomethacin 25-50 mg PO q 8 hours until attack resolves (usually 5 – 10 days) Contraindications are active PUD, impaired renal function, allergy to NSAIDs Can use Cox II inhibitors instead
22. Treatment of Acute Attack Corticosteroids – oral, IV or injected into joint Reserved for patients unable to take NSAIDs Analgesics – NOT aspirin Bed rest until attack has been resolved for 24 hours Early ambulation can trigger a recurrence
23. Treatment Between Attacks Focused on minimizing urate deposition in the tissues Dietary changes Low-purine diet (avoiding meats, seafood, gravies, yeast, alcohol, beans, peas, lentils, oatmeal, spinach, asparagus, cauliflower and mushrooms) Weight loss Reduction of EtOH consumption Increased fluids
24. Treatment Between Attacks Avoidance of hyperuricemic medications Thiazide and loop diuretics Low doses of aspirin Niacin Colchicine – for frequent attacks; used for prophylaxis at 0.6 mg PO bid
25. Treatment Between Attacks Reduction of serum uric acid Gout not controlled by colchicine prophylaxis No need to treat asymptomatic hyperuricemia Two classes of agents can be used Uricosuric agents – undersecretors; less than 800 mg/d in 24-hour urine Allopurinol – overproducers; more than 800 mg/d in 24-hour urine
26. Treatment Between Attacks Uricosuric drugs Block tubular reabsorption of filtered urate Can be given with colchicine Probenecid 0.5 g daily to start; gradually increase to 1-2 g daily Sulfinpyrazone 50-100 mg bid to start; gradually increase to 200-400 mg bid
27. Treatment Between Attacks Uricosuric drugs Patients need to maintain good urinary output (2000 mL or more) Aspirin > 3 g daily is uricosuric Allopurinol – lowers plasma urate levels and facilitates tophus mobilization Used in overproducers and tophaceous gout
28. Treatment Between Attacks Allopurinol Can be used in patients who do not respond to uricosuric agents Most frequent adverse event is the precipitation of an acute gout attack Hypersensitivity rash in 2% of patients can progress to toxic epidermal necrolysis Initial dose is 100 mg/d, increased weekly depending on response
29. Treatment Between Attacks Allopurinol drug interactions With ampicillin causes a rash in 20% of patients Increases the half-life of probenecid, but probenecid increases excretion of allopurinol Potentiates azathioprine, so need to reduce dose of azathioprine by 75% before starting allopurinol, and use only if necessary
30. Chronic Tophaceous Gout Tophaceous deposits can be shrunk with allopurinol therapy Need to maintain serum uric acid level under 5 mg/dL May require use of allopurinol and an uricosuric agent Surgical excision of large tophi
32. Prognosis Without treatment, an acute attack can last from a few days to several weeks Intervals between attacks shorten as the disease progresses Chronic gout occurs after several inadequately treated attacks Younger patient = more progression
33. Pseudogout Chondrocalcinosis is the presence of calcium-containing salts in articular cartilage Pseudogout is its clinical correlate Usually patients > 60 years Acute, recurrent arthritis of large joints Most common in knees and wrists
34. Pseudogout May be familial Commonly associated with metabolic disorders – hemochromatosis, hyper-parathyroidism, ochronosis, DM, hypothyroidism, Wilson’s disease, and gout Often develops 24-48 hours after surgery, like gout
35. Pseudogout Diagnosed by identification of calcium pyrophosphate crystals in joint aspirate Crystals are rhomboid shaped, blue when parallel and yellow when perpendicular Xrays show calcification of cartilaginous structures and signs of DJD
37. Pseudogout Does not improve with colchicine Treatment is directed at primary disease, if present NSAIDs may help treat the acute episodes Colchicine may help with prophylaxis Resistant cases may be treated with steroid injections
39. General Considerations Can cause pain that may be confused with arthritis True cause of pain can often be determined at the bedside with careful examination Presence and localization of swelling is helpful to determine cause Tendinitis causes little swelling
40. General Considerations Examination done by direct palpation, passive and active ROM, and isometric loading against resistance With synovitis, palpation causes generalized tenderness over entire synovial surface Bursitis tenderness is localized to the bursa
41. General Considerations With tendinitis, active ROM or isometric loading is best to elicit pain Rarely tender with passive ROM unless it stretches the inflamed tendon
42. Shoulder Most common causes of shoulder pain Subacromial bursitis Rotator cuff Tendinitis Biceps tendinitis
43. Shoulder Rotator cuff problems Most common cause of shoulder pain Usually caused by overuse of the arm in an overhead position Acute impingement may be caused by a fall on the arm or shoulder Pain on active abduction of the shoulder
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45. Rotator Cuff Tendintis Supraspinatus most commonly affected Caused by injury or overuse of arm with elevation and forward flexion Begins with edema and hemorrhage of the rotator cuff, which evolves to fibrotic thickening and rotator cuff degeneration with tendon tears and bone spurs
46. Rotator Cuff Tendintis Patients complain of dull aching in shoulder that impairs sleep Severe pain with active abduction overhead Tender over lateral aspect of humeral head below acromion Passive forward flexion to 90 degrees impinges the inflamed rotator cuff and confirms the diagnosis
47. Rotator Cuff Tendinitis Treatment NSAIDS Steroid Injections Physical Therapy Surgical decompression if refractory to conservative treatment
48. Bicipital Tendinitis Involves the long head of the biceps as it traverses the bicipital groove Anterior shoulder pain radiating down biceps into forearm Painful and limited abduction and external rotation of the arm Tender to direct palpation of the biciptial groove Pain along tendon by resisting supination of forearm with elbow at 90 degrees
50. Bicipital Tendinitis Treatment NSAIDs Rupture may develop which results in “Popeye” bulge in belly of biceps muscle after retraction of the long head of the biceps (May be painless in elderly) In Elderly surgery not indicated In Young patients Ortho referral for surgical correction
51. Subacromial Bursitis Largest and most frequently inflamed shoulder bursa Pain in the lateral aspect of the shoulder Often accompanies rotator cuff tendinitis Differs from rotator cuff tendinitis by presence of pain on direct palpation beneath the acromion process Full passive ROM Pain increased with active resisted abduction
53. Subacromial Bursitis Treatment NSAIDs Prevent aggravating movements Steroid Injection Ortho referral for refractory or recurrent
54. Adhesive Capsulitis AKA “frozen shoulder” Loss of full passive and active ROM in all directions May follow bursitis or tendinitis Prolonged immobilization of shoulder May be associated with DM, TB, cervical spine disease, upper extremity injuries, CAD, and chronic pulmonary disease
55. Adhesive Capsulitis Treatment Refer to Ortho Arthrography confirms diagnosis Steroid Injections NSAIDs Physical Therapy Manipulation under anesthesia Difficult to treat once established
56. Elbow Most common causes of elbow pain are epicondylitis and olecranon bursitis Epicondylitis Medial – golfer’s elbow Lateral – tennis elbow Both are overuse syndromes
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59. Lateral Epicondylitis Treatment NSAIDs Rest Ultrasound Ionophoresis Steroid Injection Avoid activity x 1 month Forearm band Improvement takes several months Occasionally Surgical release required
60. Medial Epicondylitis Less common than lateral epicondylitis Work related repetitive activities also with swimming & baseball Reproduce pain with resisting wrist flexion and pronation with elbow extended
61. Medial Epicondylitis Treatment NSAIDs Rest Ultrasound Ionophoresis Steroid Injection No activity x 1 month Physical Therapy Occasional Surgical release if sx > 1 yr
65. DeQuervain’s Tenosynovitis Tenosynovitis of the extensor pollicis brevis and abductor pollicis longus tendons. Overuse condition, generally due to radial deviation Pain on grasping with their thumb, such as with pinching. Dx is clinical. + Finkelstein’s test Tx- Rest, splint, NSAIDs, cortisone injection, surgery for failure of conservative treatment.
66. Carpal Tunnel Syndrome Compression of the median nerve in the carpal tunnel. Most often chronic but may be acute Presents with parasthsia along the median nerve distribution with symptoms often occurring at night. May reveal thenar atrophy. Dx- + tinnels sign, + Phalen’s test, PNCV/EMG to confirm Tx- Cock up wrist splint at night, Vit B6, cortisone injection. Most require surgical release of the carpal ligament to prevent permanent nerve damage.
68. Wrist and Hand Trigger finger Painful clicking in the affected finger during active use Locking sensation when extending the flexed finger Caused by thickening of the A1 retinacular pulley in the palm, causing entrapment of the tendon within the tendon sheath
70. Hip Hip has 3 main bursae Most clinically significant is the trochanteric bursa Trochanteric bursitis Hip pain Tender to direct palpation Full passive ROM
72. Knee Prepatellar bursitis Swelling and tenderness limited to prepatellar area Palpation along medial and lateral knee is unremarkable May need to R/O Infection & Gout Pes anserine bursitis Pain along the medial aspect of the knee below the medial tibial plateau Swelling uncommon Tenderness to palpation of the bursa
76. Knee Patellar tendinitis Overuse of the patellar tendon Anterior knee pain exacerbated by use of the quadriceps muscles (jumping) Tenderness to palpation localized to the patellar tendon Iliotibial band bursitis Pain over lateral aspect of the knee Tenderness confined to lateral aspect of the knee without effusion
77. Achilles Tendinitis Posterior ankle pain reproduced by active loading of the Achilles tendon Pain localized to the tendon There is a risk of Achilles tendon rupture with this
78. Plantar Fasciitis Pain along the plantar surface of the medial heel is most common complaint Severe pain with first steps of the day and gets better during the day Can worse with continued exacerbating activity
79. Plantar Fasciitis Risk Factors Obesity Excessive Pronation of the foot High arched foot Prolonged standing Excessive running Diagnosis based on History & Tender over inferior heel at insertion point of fascia
80. Plantar Fasciitis Imaging studies are not useful in acute cases (reserved for refractory) Treatment Removal of offending activity PT helpful in most cases Ice and Heat Strengthening exercises & Massage NSAIDs for analgesia and inflammation
81. Plantar Fasciitis Treatment Judicious use of intralesional steroid injections Plantar fascia rupture is a risk Plantar fasciotomy reserved for refractory cases after 6-12 months
82. Compartment Syndrome Increased pressure within a confined space compromises the circulation and function Common Causes Fractures Ischemic-reperfusion injury Hemorrhage Crush Injury Burns Casts
90. Compartment Syndrome Signs and Symptoms Severe Pain – Difficult to Control Pain with Passive & Active ROM & Squeezing Extremity Burning or Dysethesias or Paraesthesias Decreased Motor Function (late finding) Five “P’s” – Not as reliable Pain Paraesthesia Pallor Pulselessness Poikilothermia
91. Compartment Syndrome Measuring Compartment Pressures Normal Pressure < 10 mm Hg Intermediate 10-20 mm Hg Toxic Pressures > 30 mm Hg New Data supports “Delta Pressure” Diastolic minus Compartment Pressure < 30 mm Hg considered acute compartment syndrome
93. Compartment Syndrome Treatment Surgical fasciotomy with subsequent closure once edema decreased Medical Management Oxygen Maintain Blood Pressure Remove constrictive casts or dresings Elevate limb to level of heart – not higher
94. Compartment Syndrome Prognosis Permanent damage results with > 8 hours of ischemia Nerves begin to lose conduction within 2 hours Neurapraxia can occur within 4 hours Functional impairment unlikely when treated < 6 hours of onset
