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Periarticular Disorders
 

Periarticular Disorders

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Periarticular Disorders Periarticular Disorders Presentation Transcript

  • Peri-articular Disorders
    Patrick Carter MPAS, PA-C
    Clinical Medicine 1
    April 18,2011
  • 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
  • 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
  • Crystal Deposition Arthritis
    Gout
    Urate crystals
    Pseudogout
    Calcium pyrophosphate crystals
  • 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
  • Gout
  • 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
  • Risks for Acute Attacks
    Alcohol ingestion
    Changes in diet (NPO due to abdominal surgery)
    Rapid fluctuations in serum urate levels
  • Epidemiology
    90% of gout patients are men
    Usually age > 30
    Postmenopausal women
    5-10% of patients will also have uric acid kidney stones
  • 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
  • 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
  • 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
  • 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”)
  • 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
  • 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
  • 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
  • Sodium Urate Crystals
    Sodium urate crystals appear yellow under polarized light.
  • 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
  • Imaging Studies
    “Rat bite” is a punched out lesion with an overhanging rim of cortical bone
  • Differential Diagnosis
    Acute gout
    Cellulitis
    Acute infectious arthritis
    Pseudogout
    Chronic gout
    Chronic RA
    Chronic lead intoxication
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • Chronic Tophaceous Gout
  • 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
  • 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
  • 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
  • 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
  • Pseudogout Crystals
  • 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
  • Non crystal
    Peri-articular Disorders
  • 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
  • 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
  • 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
  • Shoulder
    Most common causes of shoulder pain
    Subacromial bursitis
    Rotator cuff Tendinitis
    Biceps tendinitis
  • 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
  • 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
  • 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
  • Rotator Cuff Tendinitis
    Treatment
    NSAIDS
    Steroid Injections
    Physical Therapy
    Surgical decompression if refractory to conservative treatment
  • 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
  • Bicipital Tendinitis
  • 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
  • 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
  • Subacromial Bursitis
  • Subacromial Bursitis
    Treatment
    NSAIDs
    Prevent aggravating movements
    Steroid Injection
    Ortho referral for refractory or recurrent
  • 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
  • Adhesive Capsulitis
    Treatment
    Refer to Ortho
    Arthrography confirms diagnosis
    Steroid Injections
    NSAIDs
    Physical Therapy
    Manipulation under anesthesia
    Difficult to treat once established
  • Elbow
    Most common causes of elbow pain are epicondylitis and olecranon bursitis
    Epicondylitis
    Medial – golfer’s elbow
    Lateral – tennis elbow
    Both are overuse syndromes
  • Olecranon Bursitis
    Posterior Elbow
    Acutely Inflamed
    Need to Aspirate fluid
    Gram Stain & Culture to R/O Infection
    Urate Crystals for Gout
    Treatment
    NSAIDS
    Prevent aggravating condition
    Inject Steroids
    • If Infection then Antibiotics
    • If Gout then Gout Rx
  • Lateral Epicondylitis
    Actually caused more by pulling weeds, screwdriver, briefcase
    Pain over lateral aspect of elbow
    Caused by small tears to extensor aponeurosis
  • Lateral Epicondylitis
    Treatment
    NSAIDs
    Rest
    Ultrasound Ionophoresis
    Steroid Injection
    Avoid activity x 1 month
    Forearm band
    Improvement takes several months
    Occasionally Surgical release required
  • 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
  • Medial Epicondylitis
    Treatment
    NSAIDs
    Rest
    Ultrasound Ionophoresis
    Steroid Injection
    No activity x 1 month
    Physical Therapy
    Occasional Surgical release if sx > 1 yr
  • De Quervain’s Disease
  • DeQuervain’sTenosynovitis
  • DeQuervain’sTenosynovitis
    Finkelstein’s test
  • 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.
  • 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.
  • Carpal Tunnel Syndrome
  • 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
  • Trigger Finger
  • Hip
    Hip has 3 main bursae
    Most clinically significant is the trochanteric bursa
    Trochanteric bursitis
    Hip pain
    Tender to direct palpation
    Full passive ROM
  • Trochanteric Bursitis
  • 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
  • Prepatellar Bursitis
  • Knee Effusion
  • Pes Anserine Bursitis
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • Compartment Syndrome
    Increased pressure within a confined space compromises the circulation and function
    Common Causes
    Fractures
    Ischemic-reperfusion injury
    Hemorrhage
    Crush Injury
    Burns
    Casts
  • Compartment Syndrome
    • Most Common site is level of tibia & fibula
    • Lower extremity
    • 4 Compartment
    • Anterior
    • Lateral
    • Superficial Posterior
    • Deep Posterior
  • Compartment Syndrome
    Upper Extremity
    Three Compartments
    Flexor
    Extensor
    Mobile Wad
    Hand & Upper Arm Less Likely
  • 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
  • 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
  • Compartment Syndrome
  • 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
  • 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
  • Questions?