DISH
- Diffuse Idiopathic Skeletal Hyperostosis |
- Calcification and ossification of ligaments, spine and peripheral entheses |
- Decreased ROM, Stiffness,dysphagia |
- ALL mainly affected , PLL can be affected and can cause spinal stenosis |
- Vertebral motion unaffected |
- Tx spine most affected (T7-T11) on the right - aortic pulsation |
DISH Demographics
- Rare in <50 years old patients |
- More males than females |
- Usually 3rd and 5th decade of life |
- White people affected more than any other race |
- Associated with Diabetes, obesity, gout, hyperlipidemia, HLA-B8 & hypertension |
- No association with HLA-B27 |
DISH Presentation
- Pain due to nerve impingement and/or bony growths |
- Decreased in ROM |
- Dysphagia, hoarseness, sleep apnea if in the cx |
- Spinal/extremity pain |
DISH Investigations
- CRP, ESR, RF, ANA normal |
- AP and lateral X-rays gold standard |
- CT and MRI for occult f# |
DISH on x-ray
Ossification of the Anterior Longitudinal Ligament (ALL)
- Radiolucent horizontal cleft
- Disc height preserved (OA)
- Bony bars
- No sacroiliitis/facet joint involvement (AS)
- Hyperostosis ends from mid-anterior portion of the VB (out and up) on 4 or more contiguous vertebrae
- Looks like flowing candle wax
- Can affect costotransverse, costo-vertebral and other joints
DISH in other areas
Most commonly in the pelvis, patella, calcaneus, and elbow - can affect any place where there is a ligamentous/tendinous insertion
"Whiskering" of the bone and ossification of ligament/tendon
DISH DDx
- AS |
- Spondylosis Deformans (no tx ALL ossification) |
- Seronegative spondyloarthropathies |
- Charcot Spine |
- Acromegaly |
- Psoriasis |
- Reactive arthritis |
- Pseudogout |
- Hypoparathyroidism |
Management
- Mobilisation and NSAIDs |
- Hip and Knee ossification may require surgery if severely affecting ADL |
- Exercise (ROM exercises, stretching of muscles, strengthening of muscles) |
- Bisphosphonates |
- Activity modification |
- Surgery if: F#, Cx myelopathy, lx stenosis, neurological deficits, infection, painful deformity |
Complications
Myelopathy |
Cx Radiculopathy |
Dysphagia |
VB f# |
Instability |
Heterotopic ossification |
Gout
- Most Common cause of chronic inflammatory arthritis |
- Build up of uric acid - after breaking down purines |
- Sodium urate builds up in joints |
Gout Causes/Risk Factors
- Hyperurcemia |
- Male (>40yo) |
- Obesity/ Hyperlipidaemia |
- Purine diet (fish, meats) |
- Alcohol/soft drinks |
- Medication (diuretics, low dose aspirin, ethambutol, pyrazinamide, cyclosporine) |
- Genetics (SLC2A9, ABCG2, SLC22A12, GCKR, PDZK1) |
- Kidney disease |
- Heart failure |
- Metabolic syndromes |
- Stress (surgery, trauma, starvation), diet, drugs can trigger a flare up |
Gout Presentation
- Usually 1st MTP joint, talar, subtalar, ankle and knee can be affected |
- Check tendons and bursas |
- Acute onset of joint pain |
- Wakes patient up/develops gradually over few hours (reaches max intensity within 24 hours) |
- Severe pain - sometimes tender to touch |
- Swollen, red, warm joint |
- Can also have systemic signs- fever, malaise, fatigue |
- Tophi on joints, ears, finger pads, tendons, bursae |
Gout DDx
- CPPD |
- Septic Arthritis |
- OA |
- RA |
- Psoriatic arthritis |
- Cellulitis |
Gout Investigations
- Synovial fluid (yellow and cloudy, crystals and white blood cells) |
- Synovial fluid in septic arthritis will be more opaque with yellow-green appearance, higher WBC count and positive gram stain |
- Polarising microscopy (needle-shaped, negative birefringent crystals) |
- Arthrocentesis (confirms diagnosis and rules out septic arthritis, lyme disease or pseudogout) |
- ESR, CRP, serum urate can be elevated |
- Urine uric acid |
- US (hyperechoic enhancement on the cartilage), DECT |
Gout vs CPPD crystals
Above is Gout and CPPD crystals under polarising light microscopy
Gout on imaging
Yellow Arrow = Over hanging margin sign
Red Arrow = Marginal Erosions
Green Arrow = Peri-articular Erosion
- Tophi around joints
- Paraarticular erosion + sclerosis and overhanging margin sign
- Feet, hands, elbow mainly affected
- Can destroy the joint if chronic
- "lumpy and bumpy"
Gout Management
- Reducing inflammation + suppresion of serum urate levels |
- Acute |
- Rx should be started within 24 hours of first flare up |
- Ice packs, NSAIDs, colchicine, systemic glucocorticoids for 7-10 days |
Non-acute: |
Urate-lowering therapy (ULT) |
Guidelines for ULT:
- Frequent Flares (>2/year)
- CKD stage 2 or more
- Tophus diagnosis on physical exam or imaging
- Past urolithiasis |
- Medications including Xanthine Oxidase Inhibitors (XOI) - stops synthesis of uric acid (Allopurinol, febuxostat)
Uricosuric: increases renal urate clearance (Probenecid, Lesinurad)
Interleukin-1 inhibitor: Blocks interleukin-1 (anakinra, canakinumab) |
- Modification of lifestyle: limiting alcohol, meats,seafood, sugar, weight loss, drinking more water |
Colchicine Contraindications: Older populations, patients with chronic kidney and liver problems, taking other medications that affect cytochrome P450 and P-glycoprotein should stop/modify medication.
Glucocorticoids can be offered instead to the above patients
Colchine side effects: Vomiting, nausea, diarrheoa, myotoxicity, myelosuppression
Gout Prognosis
- Depends on comorbidity |
- Mortality higher in people with cardiovascular problems |
- Most patients live normal life |
- Younger patients have gout more severelyr |
Gout Complications
- Tophi |
- Joint deformity |
- OA |
- Bone loss |
- Urate nephropathy and nephrolithiasis |
- Conjunctivitis |
- Uveitis |
- Scleritis |
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HADD
- Hydroxyapatite Deposition Disease |
- AKA calcific tendinitis |
- Common in shoulder, elbow, wrist, hip, knee, ankle, spine |
- Metaplastic transformation of tenocytes to chrondrocytes |
- Women 4th and 5th decade of life |
- Some can be bilateral |
- Critical area of suprapinatus tendon is most commonly affected then lower side of infraspinatous and preinsertional area of the subscapularis tendon |
HADD Stages
- Precalcific stage: Tendon transforms into fibrocartilaginous tissue |
- Calcific stage: Calcium deposits
Consists of formative and resorptive phase
Formative: Calcium crystals deposit into the tendon by chondrocytes
Resorptive: Vascular weaving + Macrophages phagocytose calcium, oedema and increased pressure in the tendon, calcium crystals may move into the bursa - Most painful phase |
- Postcalcific: Tendon remodelled by fibroblasts - lasts several months , complete healing occurs |
HADD Presentation
- Low grade pain |
- Acute/gradual restricted ROM |
- Can resolve spontaneously |
- +ve shoulder impingement signs |
- Can be severe and wake patient up at night |
Findings
- Toothpaste- Like |
- Low signal on both T1 & T2 |
- Outside articulating surfaces |
HADD radiograph appearance
- Type A: Sharply defined, homogenous, dense calcification |
- Type B: Sharply defined, dense in appearance, multiple fragments |
- Type C: Heterogenous calcification in appearance with dawny deposit |
- Type D: Dystrophic calcification in the tendon insertion |
- C and D = resorptive phase |
HADD Management
- Rest |
- Physical therapy (Shoulder ROM, scapular strengthening) |
- SMT |
- NSAIDs |
- Corticosteroid injections |
- Shockwave therapy |
- US therapy |
- Surgery if no better within 6 months (last resort) |
Charcot Joint
- Damage of the nerves, injured extremity due to lack of sensation |
- Decreased Pain sensation and proprioception |
- Joint is swollen + unstable |
- Thought to be
Neurotraumatic: Neuropathy + repeated microtrauma = joint destruction
Neurovascular: Increased peripheral blood flow= osteolysis + demineralisation |
- Dysfunction between Calcatonin gene related peptide (CGRP), nuclear factor-kB ligand (RANKL) and osteoprotegerin (OPG) |
Charcot Stages
Eichenholtz: |
- Stage 0: Red, hot, swollen foot with no deformity with normal radiographs |
Stage I: Erythema, foot oedema, elevated temperature, no pain
Boney debris, fragmenation of subchrondral bone, joint subluxation/f#/dislocation on X-ray |
Stage II: Decreased signs of inflammation
Absorption of boney debris + new bone formation, merging of large fragments with sclerosis of bone ends, stability slowly increases, however x-ray looks worse than stage I |
Stage III: Inflammation resolves, changes in foot architecture due to bone remodelling - risk of ulceration due to new pressure points |
Charcot Causes
- Diabetic Neuropathy |
- Spinal Cord injuries |
- Poliomyelitis |
- Leprosy |
- Syphilis |
- Syringomyelia |
- Chronic alcoholism |
- Charcot Marie Tooth Disease |
- Steroids |
Knee Involvement: Tabes Dorsalis
Talonavicular/ Tarsometatarsal: Diabetes
Charcot Presentation
- Erythematous Foot with oedema and calor |
- Unilateral, sudden onset after trauma/repetitive microtrauma |
- Inflammation |
- Gait and biomechanical altercations |
Charcot DDx
- Osteomyelitis (can trigger Charcot disease) |
- Cellulitis |
- Septic Arthritis |
- Gout/pseudogout |
- Foot/ankle sprain |
- F# |
- DVT |
Charcot in Imaging
- Dislocation + displacement of the joint rules out infection.
- Can present similar to DJD (ghost chrondrocytes, subchondral cysts, sclerotic bone, fragmented and irregular cartilage thinning) and Osteomyelitis
- Bone biopsy and histology to determine charcot joint vs osteomyelitis (OM has plasma cells, lymphocytes, neutrophills + reactive new bone formation + necrosis + capillary fibrosis and proliferation
- CT can also be prescribed - labeled white blood cell nuclear imaging
Findings
The 6 Ds |
Distended Joint |
Density Increase |
Debris |
Dislocation |
Disorganisation |
Destruction |
Charcot Management
- In early stages, immbolise foot and restrict weight bearing (crutches, wheelchairs) |
- Fractures may heal on their own in a stable position if not stressed |
- Bisphosphonates (to inhibit osteoclastic reabsorption) |
- Calcitonin supplements |
- Pamidronate, Zoledronic acid |
- Surgery (although controversial in acute stages) |
- Stopping smoking if relevant |
Charcot Prognosis
- 8 months recovery time |
- Majority develop ulcerations |
Charcot Complications
- Foot deformities (flatfoot, rocker bottom foot, hammer toes, ankle equinus contracture) |
- Boney prominences - ulcerations, infection, possible amputation |
- Condition can reoccur again |
- 5 year mortality = 13% |
CPPD
- Calcium Pyrophosphate Dihydrate Disease |
- Involves synovial and periarticular tissues |
- Can cause acute inflammatory reaction (pseudogout) |
- Chondrocalcinosis = deposition of crystals in cartilage |
- Can also be mistaken for RA |
- Affects large, weight -bearing joints |
CPPD Causes
- Imbalance between production of pyrophosphate and pyrophosphatases in the cartilage |
- Hyperparathyroidism |
- Gout |
- OA |
- RA |
- Haemochromatosis |
- Osteoporosis |
- Hypomagnesaemia |
- Chronic kidney disease |
- Calcium supplements |
- >65 years old, male |
CPPD Presentation
- Symptoms caused by the crystals causing an inflammatory response from the immune system |
- Joint Oedema |
- Erythma |
- Tenderness |
- Some can have a low grade fever |
- Waxing and waning of non-synchronous inflammatory arthritis in the non-weight bearing joints |
CPPD DDx
- Gout |
- RA |
- AS |
- Erosive OA |
- Haemochromatosis |
- Hyperparathyroidism |
- Wilson's disease |
CPPD Imaging
CPPD of the Knee
- Calcification in joint compartments
DJD presentation in an unusual location = CPPD
- In scapho - lunate ligament , causes a wide
scapho-lunate joint + collapse of wrist
- Arthrocentesis for synovial fluid analysis (rhomboid crystals) + radiography
- US for cartilage abnormalities
- MRI
CPPD Management
- Decrease inflammation and stabilising the underlying disease |
- Joint aspiration and intraarticular glucocorticoid if acute and 1-2 joints affected |
- >3 joints affected - NSAIDs if contraindicated, colchicine/systemic glucocorticoids |
- Rule out septic arthritis (synovial fluid cultures) |
- Ice packs and joint rest |
- If younger patient, screen for metabolic conditions (Hyperparathyroidism, haemochromatosis and family hx) |
CPPD Prognosis
- Self limiting usually involves within days-weeks |
- Complications:
- Degradation of menisci and synovial tissue
- Gout Tophi
- Spinal involvement (Mistaken for AS, DISH) |
Refer if
- Unclear aetiology with hyperuricemia |
- Unclear aetiology with normal serum urate levels |
- Patients with renal impairment |
- Failed trial of XOI |
- Multiple side effects from medications |
- Refractory gout (Level 1) |
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