Injection Techniques in Musculoskeletal Disorders Janak Parmar
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General Consideration in Injection TechniqueCHAPTER 1

 
Osteoarthritis is idiopathic slowly progressive disease of synovial joints occurring late in life and characterized pathologically by focal cartilage degeneration, subchondral bony thickening, marginal osteochondral outgrowths and joint deformity.
  • Primary osteoarthritis—unknown etiology.
  • Secondary osteoarthritis—trauma, stress, loads, infection, rheumatoid arthritis, gout, chondromalacia patellae.
  • It begins at second decade.
  • Women are more frequently affected.
  • Prevalent in obese.
  • Patients present with pain, stiffness, crepitus, osteophytes, decreased range of motion, locking.
  • X-ray—decreased joint space, sclerosis, subchondral cyst, osteophytes, bony collapse, loose bodies, deformity and malalignment.
  • Conservative treatment modalities—rest, exercise, support, traction, physiotherapy, corticosteroids.
  • Steroids have deleterious effects on articular cartilage impairing synthetic activity of chondrocyte and decrease prostaglandin content of matrix—it is reversible in 2 weeks.2
 
Rheumatoid Arthritis
It is chronic inflammatory joint disease affecting young or middle aged adult characterized by deforming polyarthritis affecting small and large peripheral with associated systemic disturbance and circulating antiglobulin antibodies rheumatoid factor affects synovial membrane, perineural sheath which causes joint destruction ankylosis, and deformity.
  • Male:female = 1:3 more common in females
  • Genetic influence—increase lymphocyte activation with defined HLA class 2 haplotype
  • Immune overactivity may be the cause
  • Infectious agents—Streptococcus, Bacillus, Mycoplasma
  • Endocrine—adrenocorticosteroids
  • Allergy—eosinophilia.
Diagnosis features:
  1. Morning stiffness
  2. Arthritis of 3 or more joints (pain on motion/joint tenderness)
  3. Arthritis of peripheral joints of hand swelling (soft tissue thickening) in at least 1 joint > 6 weeks
  4. Symmetrical arthritis
  5. Rheumatoid nodules
  6. Rheumatoid factor
  7. Radiological changes
  8. Poor mucin clot
  9. Histological changes in synovium.
X-Ray features of rheumatoid arthritis:
  • Soft tissue prominence around the joint, joint space narrowing, osteopenia delayed erosions, cystic spaces, subluxations and deformities, ankylosis.
  • Absorption of locally applied NSAIDs is usually not proper but have a strong psychological value.
  • Treatment is rest, splint, intra-articular steroids, NSAIDs, DMARDs, surgery.
 
Role of Corticosteroids
Intra-articular (IA) steroids produce marked improvement in symptoms, lasting for weeks to months. But repetitive large dose injections are associated with delayed repair and may lead to more cartilage damage. It is recommended that their use should not be more than 3–4 times a year. Inflammatory reaction to crystalline depot preparation may occur but it does not affect efficacy of the injected steroid.
Incidence of joint infection following steroid is low.
Steroids are useful for rapid disease control until DMARDs start acting. They have been shown to reduce progression, but should be administered not on routine basis because of their side effects. Intra-articular steroids should be used to treat disease limited to few joints, or to treat acute flare in a joint. Over enthusiastic and frequent use of Intra-articular steroids should be avoided, (not more than 3 joints it a time, not the same joint more than 3 times a year, and a minimum interval of 3 months between successive injections in the same joint).3
 
Crystal Induced Arthropathy
Diagnosis: Intra and/or periarticular calcification with or without erosions destruction or hypertrophic changes may be seen on X-ray. Definitive diagnosis depends on identification of crystals from synovial fluid or tissue. Hydroxyapatite crystals are very small, nonbirefringent and can only be seen by electron microscopy. Appetite aggregates may appear as 1–20 shining intra- or extracellular globules that stain bright red with alizarin red S (nonspecific calcium staining).
It is necessary to differentiate it from sepsis, late avascular necrosis and neuropathic joint.
Treatment: No specific treatment is available. Acute attacks usually resolves spontaneously over 1 to 3 weeks. NSAIDs, oral colchicine, aspiration of effusion and intra-injection of steroid shorten the duration and intensity symptoms. Destructive arthropathy usually requires joint replacement surgery.
 
Ankylosing Spondylitis
Chronic inflammatory disorder in late adulthood and young age characterized by progressive inflammation of spine, sacroiliac joints and large joints of extremity leading to fibrous or bony ankylosis and deformities associated with HLA B 27.
Primary site of affection is attachment of ligaments and capsules to bone with enthesopathy, fibrosis, calcification, ossification to para-articular structures-degenerated calcified and ossified, commonly anterior longitudinal ligament of spine but are friable and rupture and easily increase bone production adjacent to joint.
Rome criteria for ankylosing spondylitis—low back pain and stiffness > 3 months not decreased by rest, stiffness in thoracic and decreased motion of lumbar spine, decreased chest expansion, iritis and its sequelae, bilateral sacroilitis, with X-ray and one or more clinical criteria /4 of 5 clinical criteria are useful in diagnosis.
Tendons are made of specialized cells including tenocytes, water and fibrous collagen proteins. These collagen proteins weave together to form a strand of flexible tissue to make up tendon. They anchor to the bone and form a mineralized connection.
Tendons transfer force, and as a result are susceptible to injury when they are overused. With repetitive overuse, collagen fibers in the tendon may form micro- tears, leading to tendonitis; or more appropriately tendinosis or tendinopathy.
The injured tendons heal by scarring which adversely affects function and increases risk of reinjury adding to the problem tendons heal at a slow rate due to poor vascularization (Flow chart 3 to 5 of Annexure).
Chronic cases indicate that there is no inflammatory response, but rather a release of one's own natural growth factors for normal tendon repair with a fibroblastic and a vascular response called, angiofibroblastic degeneration. Due to this mode of healing, treatment options including dry needling, prolotherapy, and extracorporeal shockwave therapy are aimed at increasing inflammation rather than suppressing it.
Peritendinitis is inflammation of paratendon which causes, pain, tenderness and restricted movements of muscles.4
Tendinosis—degenerative changes in tendon. Macroscopically-degenerative changes in tendon with disorganized tissue, microscopically-degenerative changes to collagen with fibrosis. Inflammatory mediators are not usually present as more degenerative changes occur.
Muscle imbalance is a cause of tendinitis.
Tendinitis or Tendonitis is inflammation of tendon and the paratendon. Chronic overload cause microscopic tears in tendon which trigger's inflammatory response. Over use/overload cause sudden accentuation of tendinitis.
Bursae are sacs lined with a membrane usually located about joints or where skin, tendon or muscle moves over a bony prominence and may or may not communicate with a joint. They reduce friction. These are two types.
  1. Those normally present, e.g. patella and olecranon
  2. Adventitious bursae—Bunion, osteochondroma
Adventitious bursae are produced by trauma friction or pressure.
Mechanical theory—Repeated loading causes microscopic degeneration. fibroplasias occurs within tendon which in turn cause scar tissue.
Vascular theory—Areas of local vascular disruption.
Neural modulation—Neurally mediated mast cell degranulation and release of substance p. Treatment of bursitis is treatment of primary cause of bursitis.
Conservative treatment in form of rest, hot wet pack, elevation, where applicable immobilization should be done, is very effective most of the times.
Surgical procedures useful are:
  1. Aspiration and injection of appropriate drug
  2. Incision and drainage of acute suppurative bursitis which fails to response to non-surgical treatment—rarely indicated
  3. Excision of chronically infected and thickened Burse
  4. Removal of underlying bone prominence.
 
Traumatic Bursitis Respond Favorably to Aspiration
Adventitious bursa develops as a result of repeated trauma and is more susceptible to inflammatory changes.
 
Syringes and Needles Used
Syringes used for injection: 2 ml, 5 ml, 10 ml depending on the quantity of drug to be injected or aspiration to be done and site of injection.
Needles used are 18 gauge usually for aspiration and 22, 24 gauge used for injection (Figs 1.2, 1.4, 1.8 and 1.10).
 
INJECTABLE CORTICOSTEROIDS
 
Mechanism of Action
Decreasing inflammation in synovial tissue is primary effect in synovial tissue of depot corticosteroid. The effects particularly profound on edema as well as the 5number of lymphocytes macrophages and mast cells. It has also been found that there is production in inflammatory cell in joints after corticosteroid injection. Although this may be preceded by mild initial inflammatory response immediately following injection.
It also has systemic effects on non-involved inflamed joints.
Marked improvement in inflammatory markers such as ESR, CRP, can occur in patients with rheumatoid arthritis who receive corticosteroid.
Depot formulations are useful due to local effects for long-term. Less soluble agents are preferred.
Most commonly used corticosteroid is methyl prednisolone acetate (35%).
Ability of methyl prednisolone for use in both joints and soft tissues are likely to contribute to its widespread use compounds with lower solubility have more synovial levels for a longer time and produce low systemic levels then would compounds with greater solubility.
A lower systemic level of corticosteroid is generally viewed as favorable feature because of potential reduction in systemic toxicity.
Compounds with low solubility are well suited for intra-articular injections. They may not be appropriate for soft tissue injections because of associated side effects.
Injectable corticosteroid often combine with local anesthetics because injecting both agents not only can verify that site injected was the source of pain.
Uses: Used in osteoarthritis and rheumatoid arthritis other joint conditions such as juvenile. Rheumatoid arthritis, crystal deposition diseases, connective tissue disease psoriatic arthritis. Ankylosing spondylitis and arthritis associated with inflammatory gastrointestinal disorders.
Goal is to relieve pain and control synovitis associated benefit of reducing synovitis may be ability to exercise and muscle strength.
They have also been used after arthroscopic surgery and rehabilitation period.
Corticosteroids are also useful in nonarticular disorder like overuse syndrome (tendinitis, bursitis, ligament sprain, tenosynovitis) acute athletic injuries and nerve compression syndromes, rather than entering joint extra-articular sites are targeted.
Outcomes in patients who received accurately placed injections are good.
 
Safety
Glucocorticoid injection of joints and periarticular structures are safe and effective when administered by experienced physician, most commonly there is transient injection pain.
Rare long-term effect is subcutaneous injection causing lipodystrophy.
Absolute contraindication to corticosteroid is joint infection, presence of prosthetic joint or fracture in joint.
Caution should be used in patients with joint instability, coagulopathy or overlying cellulitis or infection.6
 
Side Effects
Most common side effects are postinjection flare, facial flushing and skin or fat atrophy.
Frequency of these events depends on frequency and dose of administration and how closely patients are followed up.
There was usually a lag time of 1 day between injection and postinjection flare present in 10% patients more commonly from chemical synovitis in response to injected crystals.
Treated with Analgesics and Ice Packs
Facial flushing is seen in 15% of patients, more in women subsides within maximum of 3–4 days. Skin and fat atrophy is reported to be approximately in 0.6% of patients. Effects lasted for approximately 6 months.
Joint sepsis of greatest concern, occurs very rarely due to strict asepsis maintained during procedure.
Other major concern is ruptured tendons after intratendinous injection which may accelerated degeneration of already damaged tissue.
Animals studies show deleterious effects of cartilage but not in humans.
 
Systemic Side Effects
Depends on agent used, dose, frequency and number of joints injected milder than other preparations.
Steroid can cause osteoporosis but intra-articular steroid has no effect on bone resorption and only a transient effect on bone formation.
Corticosteroid induced myopathy is also possible consequence but not reported after intra-articular injection. More common triamcinolone and dexamethasone suppression and hypothalamus pituitary adrenal axis is well documented but is mild and transient.
Prolonged hypothalamus pituitary axis suppression for 5–7 weeks after last injected has been reported, in one can accompanied by Cushing syndrome.
It can increase hepatic glucose synthesis and antagonize insulin effects resulting in worsening of glucose tolerance and increase in blood glucose transiently.
 
Structure Lesion Relationship
Tendon and tendon sheaths
Tendinitis, peritendinitis degeneration, rupture, tenosynovitis
Tenoperiosteal junction
Enthesopathies, apophysitis
Bursae
Acute and chronic bursitis
Fasciae
Fasciitis, Dupuytren's contracture
Ligament
Sprain and tear
 
TRIAMCINOLONE ACETONIDE INJECTION
Long acting depot preparation of triamcinolone it is 9-alpha derivative of prednisolone.7
It has highly selective glucocorticoid activity and anti-inflammatory actions acetonide ester of triamcinolone is long acting for several days or weeks. Patients have prolonged remission of symptoms.
Most important mechanism is limitation of recruitment of proinflammatory leukocytes at affected site.
Triamcinolone is short acting plasma elimination half-life is 200 minutes and biologic elimination half-life is 18–36 hours.
It crosses placenta and secreted in breast milk. Its mean residence time after intra-articular injection is 4 days. with IM injections suppression of adrenal glands tends to occur within 24–48 hours gradually reversing over next 1 month.
By intra-articular, intrabursal route or in intratendon sheath is indicated as an adjuvant for short-term administration of acute exacerbation of: synovitis in osteoarthritis, acute and subacute bursitis, acute gouty arthritis, epicondylitis, acute nonspecific tenosynovitis and post-traumatic osteoarthritis.
Contraindications: Systemic fungal or viral infection, tuberculosis idiopathic thrombocytopenic purpura.
Not recommended for children less than 6 years not given intravenously, should not be given to nursing mothers, overuse of joint should be avoided, unstable joints should not be injected, it is associated with skeletal muscle atrophy so prolonged dose regimen should be avoided. There is a possibility of adrenal insufficiency.
In general, it is contraindicated in those with peptic ulcer, diabetes mellitus, other cardiovascular disorders, glaucoma, osteoporosis and infection also not recommended in those with myasthenia gravis, diverticulitis, thrombophlebitis, psychotic tendencies chronic nephritis, and metastatic carcinoma.
Dosage for smaller joints—20 to 40 mg dose is sufficient when given in large joint or multiple joints or peritendinous 80 mg should be the dosage, but not exceeding that.
Side effects—muscle weakness and fatigue, pain at injection site, transient pain, post injection flare, post injection discomfort, subcutaneous atrophy, hypo- or hyperpigmentation and Charcot like arthropathy.
Note: Intramuscular route can be useful for some disorders.
 
HYALURONIDASE
Each ampoule contains 1,500 international units of hyaluronidase comes as white powder for solution for injection/infusion. Hyaluronidase is used to enhance permeation of subcutaneous or intramuscular injections, local anesthetics and subcutaneous infusions and to promote resorption of excess fluids and blood in the tissues.
 
Adult Dosage
Adults, children and elderly: With subcutaneous infusion (hypodermoclysis), intramuscular injections, with local anesthetics: 1500 IU.8
Extravasation, hematoma: Where dispersal rather than localization is indicated.
Immediately before use dissolve the freeze-dried powder in approximately 1ml of water for injections or directly in the solution with which Hyalase® is to be combined.
Care should be taken to control the speed and total volume of fluid administered and to avoid over-hydration, especially in renal impairment.
Contraindications: Hypersensitivity to hyaluronidase, not to be used to reduce the swelling of bites or stings or at sites where infection or malignancy is present. Not to be used for anesthetic procedures in cases of unexplained premature labor.
Special precautions: Do not apply directly to the cornea, or intravenously.
Solutions for subcutaneous administration should be isotonic (0.9% sodium chloride, with 4% glucose) with extracellular fluid. Use in hypodermoclysis has been reported.
 
Adverse Reactions
Rare reports of periorbital edema occurring with the use of hyaluronidase in conjunction with local anesthetics in ophthalmology. Severe allergic reactions including anaphylaxis have been reported rarely. Local irritation, infection, bleeding and bruising occur rarely. Edema has been reported in association with hypodermoclysis.
 
PLATELET RICH PLASMA (FIGS 1.3 AND 1.9)
It is defined as a volume of the plasma fraction of blood having a platelet concentration above baseline.
Autologous platelet rich plasma (PRP) was first used in 1987 by Ferrari et al
  • Platelets release many growth factor responsible for attracting macrophages, mesenchymal stem cells, and osteoblasts.
  • It promotes removal of necrotic tissue, and enhances tissue regeneration and healing. Growth factors stimulate recovery in non-healing injuries.
  • Varying results are attributed to the need for additional standardized PRP protocols, preparations, and techniques. Although some authors have reported improved bone formation and tissue healing with PRP, others have had less success.
  • Sample sizes are frequently small, there are few controlled trials. PRP has been found to be useful in chronic non-healing tendon injuries including lateral epicondylitis and plantar fasciitis and cartilage degeneration. It is an alternative to surgery by providing natural healing.
  • Other uses include diabetic wound management, treatment of non-unions, and use in acute tendon injuries.
  • Typically a blood specimen contains 93% RBC, 6% Platelets, and 1% WBC. The rationale for PRP is decreasing RBC to 5%, and increasing platelets to 94%.
  • Platelets are made in bone marrow with a lifespan of 7–10 days. Inside the platelets are many intracellular structures containing glycogen, lysosomes, 9and two types of granules. The alpha granules contain the clotting and growth factors that are eventually released in the healing process. Normally they are at resting state. Upon activation by thrombin, platelets changes shape and develop branches, called pseudopods that spread over injured tissue (aggregation). Eventually the granules contained within platelets release growth factors. Alpha granules are storage units within platelets, which contain pre-packaged growth factors in an inactive form.
  • Growth factors contained in these granules are platelet-derived growth factor (PDGF), stimulates cell replication, promotes angiogenesis, epithelialization, granulation tissue formation.
Transforming growth factor (TGF) promotes formation of extracellular matrix, regulates bone cell metabolism.
Vascular endothelial growth factor (VEGF) promotes angiogenesis.
Epidermal growth factor (EGF) promotes cell differentiation and stimulates, re-epithelialization, angiogenesis and collagenase activity.
Fibroblast growth factor (FGF) promotes proliferation of endothelial cells and fibroblasts stimulates angiogenesis.
Vitronectin is a cell adhesion molecule which helps with osseointegration and osteoconduction.
  • It is prepared by centrifuging blood for 15 minutes at 3,200 rpm, it is spread in a clock-like manner to achieve a more extensive zone of delivery.
  • Patients may experience minimal to moderate discomfort following the injection which may last for up to 1 week. This is likely due to the stimulation of the body's natural response to inflammatory mediators.
  • No studies have documented that PRP promotes hyperplasia, carcinogenesis or tumor growth. Growth factors act on cell membranes rather than on the cell nucleus and activate normal gene expression. Growth factors are not mutagenic and naturally act through gene regulation and normal wound healing feedback control mechanisms.
  • Relative contraindications include the presence of a tumor, metastatic disease, active infections, or platelet count/10.5/ul/Hgb/10 g/dl, pregnancy or active breastfeeding.
  • Although adverse effects are uncommon, they are infection, no relief of symptoms, and neurovascular injury. Scar tissue formation and calcification at the injection site are also rare risks.
  • Taylor et al demonstrated safety and efficacy while injecting autologous blood in white rabbits at the patellar tendon.
  • Berghoff et al retrospectively reviewed patients to access autologous blood product effects in patients undergoing total knee arthroplasty (TKA). The study included 66 control and 71 treated with autologous blood products at the wound site.
  • Everts et al reviewed 160 patients, who undergoing total knee replacements (TKR), in which 85 received PRP with sealants; which resulted in decreased blood transfusion requirements, lower postsurgical wound disturbances, shorter hospital stay, and fewer infections.
  • Non-healing cutaneous wounds represent a challenging problem and are commonly related to peripheral vascular disease, infection, trauma, neurologic and immunologic conditions, as well as neoplastic and metabolic disorders.10
  • Crovetti et al reviewed 24 patients with chronic cutaneous ulcers, who were treated with a series of PRP Gel treatments, 9 patients demonstrated complete wound healing 2 patients had wound infection, both with positive Staphylococcus aureus which were positively treated with oral antibiotics.
In a recent study by Ranly et al, PRP was shown to decrease osteoinductivity of demineralized bone matrix in immunocompromised mice. The timing of the assays looking at osteoinduction may have been too late to accurately access early bone formation.
McAleer et al involved 24 patients with 33 chronic non-healing lower extremity wounds. Patients failed conservative treatment judged by lack of reduction of surface area. Surgical wound debridement was initially performed to convert chronic ulcers to acute wounds, in an effort to promote wound metabolism and chemotaxis wound closure and epithelialization was obtained in 20 wounds. The mean time for closure was 11 to 15 weeks. There was No improvement in 5 wounds.
Diabetes impairs fracture healing with reduced early proliferation of cells, delayed osteogenesis, and diminished biomechanical properties of the fracture callus. Platelet rich plasma (PRP) shows favorable results in these.
Barett et al evaluated nine patients given PRP injections for plantar fasciitis in which 6 of 9 patients achieved complete symptomatic relief after 2 months. At 1 year 77.9% patients had complete resolution of symptoms. Again, this was a non-controlled study with a small sample size.
Kajikawa et al showed that there was increased quantity of circulation-derived cells in the early phase of tendon repair after injury versus controls study in the American Journal of Sports Medicine. Mishra et al evaluated 140 patients with chronic epicondylar elbow pain, treatment group noted 60% improvement at 8 weeks, 81% at 6 months, and 93% at final follow-up at 12–38 months. Additionally, there was a 94% return to sporting activities and a 99% return to daily activities.
In 2003 Edwards and Calandruccio, demonstrated that 22 of 28 patients (79%) with refractory chronic epicondylitis were completely pain free, following autologous blood injection therapy. This study is limited by its small sample size and lack of control group.
A study from Chen et al demonstrated that PRP might potentially play a role in prevention of disc degeneration maintaining arthrodesis in a posterolateral lumbar fusion can be challenging and may necessitate revision. Screw instrumentation, interbody fusion, bone morphogenic protein was employed in an attempt to promote arthrodesis also limiting risk factors such as smoking, NSAID and corticosteroid use are recommended. Platelet rich plasma (PRP) is not of much help in this was shown by few authors. Lowery et al retrospectively reviewed 19 spinal fusion patients with PRP after 13 months. There was no pseudoarthrosis seen on exploration or plain radiographs in 100% of cases.
Hee et al evaluated 23 patients treated by instrumented transforaminal lumbar interbody fusions with PRP versus control with a 2-year follow-up. They found accelerated bony healing in the PRP group.
Jenis et al explored anterior interbody lumbar fusions in 22 patients with autograph using iliac crest bone graft versus 15 patients with allograft combined 11with PRP at 12 and 24 months demonstrated an 85% fusion rate for autograft versus 89% with PRP and allograft.
Classification of soft tissue rheumatism
Localized
Generalized
Epicondylitis
Myofascial pain syndrome
Enthesitis
Chronic fatigue syndrome
Tendinitis
Psychogenic rheumatism
Tenosynovitis
Bursitis
Capsulitis
Ganglion
Periarthritis
Rotator cuff syndrome
Fasciitis
Dupuytren's contracture
Regional myofascial pain
Common sites of lesions
Shoulder
Rotator cuff disorders, capsulitis of joint
Elbow
Lateral and medial epicondylitis, olecranon bursitis
Wrist and hand
Carpal tunnel syndrome, Dupuytren's contracture, de Quervain's tenosynovitis
Trunk
Costochondritis, trapezitis, nonspecific neck and low back pain
Hip
Ischial and trochanteric bursitis, meralgia paresthetica
Knee
Bursitis and ligament sprain
Ankle and foot
Achilles tendinitis, peritendinitis, plantar fasciitis, bursitis around calcaneus
Noninflammatory arthritis
Inflammatory arthritis
Osteoarthritis
Rheumatoid arthritis
Trauma
Ankylosing spondylitis
Internal derangement
Crystal induced arthritis
Osteochondritis dessicans
Psoriatic arthritis
Charcot's arthropathy
Reactive arthritis
Villonodular synovitis
Polymyalgia
Acromegaly
Behcet's syndrome
Sickle cell disease
Leukemia
Lyme disease
Viscosupplementation with hyaluronan intra-articularly can provide symptomatic relief for several months when given weekly with less side effects (approximately 8%). It has shown to have reduced disease progression as evident by arthroscopy. It is effective in those with high intra-articular aggrecan fragment concentration, i.e chondrocyte residual activity remains.12
Hyaluronic acid is an important glycosaminoglycans component. It is an important ground substance of synovial fluid and vitreous of eye. Its concentration is high in embryonic tissue and is thought to play a role in permitting cell migration during morphogenesis and wound repair. It has ability to attract water in extracellular matrix thereby loosening it up. Along with chondroitin sulfate is important part of cartilage.
 
INTRA-ARTICULAR ASPIRATIONS
 
Indications
  • Rheumatoid arthritis
  • Osteoarthritis
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Lupus erythematosis
  • Traumatic arthritis.
 
Contraindications
Charcot's arthropathy, local sepsis, hemophilia, avascular necrosis of cartilage.
 
Complications
Septic arthritis, Charcot's arthropathy, traumatic arthritis, avascular necrosis.
 
SYNOVIAL FLUID (FIG. 1.5 AND FLOW CHARTS 1 AND 7 OF ANNEXURE)
  • It is ultrafiltrate of plasma to which proteoglycan is added by local synthesis by joint tissue contents are 96% water and 4% solutes
  • Gross appearance: clear pale yellow viscous does not clot-absent fibrinogen
  • Intra-articular pressure: 8 to 12 cm of water
  • Bacteriologically sterile
  • Specific gravity:1.008 to 1.015, with PH 7.3 to 7.6 (decreased in OA and trauma). Viscosity depend on concentration of hyaluronic acid (decreased in aging, OA and trauma)
  • Cytology: average 65 cu/mm, mostly lymphocytes and monocytes
  • Protein: about 2 gm/dl with 2/3 albumin mucin and globulin, the A/G ratio is 20:1
  • Mucin is responsible for viscosity with average 235 at 38°C ranges from 5.7 to 1160
  • For cytology methylene blue is added to the saline and nucleated cells are stained. Differential count is done on dried smears stained with Wright's stain mucus, amorphous deposits stains deeply basophilic
  • Sugar is measured by Nelson-Somogyi method13
  • Protein measured by electrophoresis method
  • Mucin and viscosity: known as Rope's test
  • Synovial fluid hyaluronate concentration: this test lacks specificity but bears correlation with presence or absence of inflammation, finding is nonspecific and alone is not diagnostic of single pathology.
Equal amount of fluid and 5% acetic acid added on glass slide—normal fluid produce long strings, inflammatory fluid produce short strings.
Reference range—mucin clot positive (firm clot).
 
Ultrasonographic Appearance of Tendons (Figs 1.6 and 1.11 and Flow chart 2 of Annexure)
Ultrasound usage: Use highest frequency available, use linear array transducer, avoid improper angling of probe to avoid false hypoechogenicity, combine longitudinal and transverse at same site, check contralateral tendon for reference, perform dynamic examination, use color from for Doppler imaging.
Machine of USG is compact and cost effective. Its use was most significant in
specialities outside radiology profession.
  • There is interobserver variability depend on number of years, number of cases per year and quality of training.
  • Limitation: Inability to penetrate beyond bony cortex, also true for intra-articular structures as cruciate.
  • Real time examination and visualization of needle helps in giving USG guided injections.
  • Tendons consist of linear fibrils of collagen with a supporting matrix fibrils are oriented in direction specific to forces applied to tendon, its vascularity is also important. Tendon show increase echogenicity and oval in cross section. It is used for conditions like tennis elbow and golfer elbow for identifying common extensor and flexor origin over humerus.
  • Long tendons running in osseofibrous canals are surrounded by fluid filled synovial sheath which facilitates free tendon movements. Long tendons which are not surrounded by synovia lie within a vascularized loose areolar and adipose tissue.
  • Fluid in synovial sheath is visible as thin hypoechoic rim surrounding the hyperechoic tendon.
  • Tendons may be surrounded by synovial sheath or dense connective tissue which appears echogenic and can be differentiated from tendon by thin hypoechoic boundary.
  • All normal tendons are highly echogenic they show fine parallel longitudinal echoes resembling fibrils. These echoes correspond to endotendinium septa running within the tendon. As frequency increase these fibrils becomes distinguish.
  • The attachment of tendons to their muscles appear as a crowding of muscular fibers with rapid reduction of volume of muscle.
  • Nerve is less echogenic than tendon. This phenomenon can be used in identifying carpal tunnel and median nerve in it. Normal ligaments appear 14hyperechoic with compact echotexture at USG. Individual nerve fascicle show honeycomb appearance, nerve fascicle appear hypoechoic and surrounding hyperechoic connective tissue element.
  • Examiner should hold the transducer near its footprint and spread the other fingers out to stabilize the transducer on skin.
  • Excessive transducer pressure and tendon tension can compress and artificially eliminate neovascularity.
Ultrasonography is reliable for tendon sheath or peritendinous injections while avoiding on intratendinous injections which are associated with tendon weakening and possible rupture.
Anisotropy is hypoechoic appearance of tendon due to angulation of transducer. Anisotropy is beneficial in confirming tendon position because artifact can be produced in normal linear tendon surrounded by nonlinear echogenic fat. Slight obliquity of the angle of incidence results in hypoechoic appearance which mimics tendon disease.
Active and passive movements can be used for dynamic evaluation of all tendons for tear severity and look for abnormal movement due to subluxation and adhesive tenosynovitis.
A linear multifrequency 9–15 MHz transducer is used for superficial structures; and 5 MHz transducer for deep structures. Structures should always be evaluated in their orthogonal planes for a focal soft tissue abnormality. Advantages: patient interaction, enabling a detailed history and direct correlation with findings from physical examination and perform a dynamic evaluation. Color and Doppler ultrasound helps to diagnose vascular abnormalities.
For a full dynamic assessment, muscles and tendons are evaluated while in a contracted and relaxed state. Knowledge of origin and insertion allows correct identification of tendons. Placing limb in different positions to stretch structure under evaluation is important. Tendons surrounded by fat, that appear hyperechoic. By gently angulating the probe, tendon ligaments will show anisotropy and become hypoechoic, thus allowing visual differentiation from surrounding fat. While holding transducer, the edge of the hand or fifth finger is in contact with patient for stabilization of the transducer and to allow fine controlled adjustments in transducer position.
  • Muscle fiber group makes fascicles which are separated by perimysium. On whole, muscle is covered by epimysium.
  • In transverse orientation of transducer to muscle, perimysium is seen as dot/ short line in hypoechoic background of muscle fibers. Inter and intramuscular septa produce reticular pattern and increased echogenicity.
  • In longitudinal scan perimysium shows obliquely parallel echogenic striae against hypoechoic background. Intramuscular extension of tendon—which is thick fribrillar and echogenic. Intermuscular fascia are bright and echogenic.
  • Contraction produce hypoechogenicity with increase angulation of echogenic septa.
  • Acute lesions are strains, tears, contusion, hematoma. Chronic lesions—fibrous scars, hernia, calcification.
    Ultrasonography signs of tendon tear are
    • Fiber discontinuity, hematoma, nonvisualization of tendon, bone avulsion if present.15
    • Tendinitis—altered echogenicity, blurred margins, calcification in chronic tendinitis, tendon thickening, vascularity (color Doppler).
    • Tendon without synovial sheath like Achilles tendon are surrounded by homogenous hyperechoic tissue within which it can move more freely.
  • Synovial bursae are hypoechoic elongated areas, which are rarely thicker than 2–3 mm.
  • In chronic bursitis there is illdefined margins, complex appearance with internal echogenic debris due to fibrin and microcalcifications. Color Doppler shows increased vascularity and thickened wall.
  • Ultrasound detect minor changes of tendon echotexture which predispose tendon to rupture, these can be recognized as focal enlargements of involved tendon.
  • Avulsion of tendon due to force applied to insertion of tendon usually involves tibial tuberosity, ischial tuberosity and iliac crest. When avulsion is incomplete, ultrasonography shows V shaped image at site of lesion with slight irregular adjacent bony surfaces.
  • Tendons may be enclosed in synovial sheath (wrist and ankle) or paratenon (patellar/Achilles tendon) many have adjacent bursae (rotator cuff/illiopsoas) overuse cause fluid in these structures before tendon abnormalities are seen. Ultrasonography diagnosis of tenosynovitis should be made if inflammatory changes are located to sheath and joint effusion is excluded.
  • In peritendinitis the peritenon becomes hypoechoic and thickened, tendon remains grossely unaffected. Peritendinous inflammation occurs in setting of adjacent tenosynovitis or bursitis. It is also use to assess the response to treatment overtime.
  • Tendinosis manifest as alteration of echogenicity.
  • In tenosynovitis inflammation of tendon sheath fluid in the sheath may be seen with minimal quantity. In chronic tenosynovitis there may be impairment of movement of tendon. Doppler shows increased vascularity of tissue.
  • In inflammatory conditions there is thickening of involved tendon whose structure will become heterogenous with alternating areas of hypo or hyperechoic representing degenerative and fibrotic changes.
  • Tendinosis can also manifest as angiofibroblastic response presence of hyperemia may help to localize the areas of tendon that may respond to intratendinous and peritendinous steroid/anesthetic agents.
  • There may be cortical erosion seen and microcalcification at insertion seen.
  • In transverse images of tendon if inflamed, hypoechoic fluid surrounding hyperechoic tendon sheath can be seen. Thickening of peritendon and adhesions, nodules heterogeneity and irregularity can be seen.
  • In degenerative conditions tendons show enlargements, irregularity in texture, small hypoechoic areas within tendon body and associated diffuse or focal microcalcification, scar, granulation tissue may be seen, predisposition of tendons for rupture can be found as altered echotexture. Tendon sheath may be hypoechoic in rheumatoid arthritis, initially there is marked thickening of tendon and then there is marked thinning.
Fibrous scar can lead to further tear extension in superimposed on injuries. Scar is hyperechoic/heterogenous, linear/stellate adherent to epimysium. Lesion does 16not change with muscle belly. Myositis ossification shows coarse calcification in hypoechoic mass similar to adjacent diaphysis.
If tendon is seen with jagged margins, degenerative changes in tendon is termed tendinosis.
  • Dystrophic calcification can be identified, focal calcified masses are seen.
  • Additional changes can be seen as focal or diffuse thinning of tendon.
Complete tears often diagnosed due to presence of gap of varying length. When torn, fragments are separated by large distance, tendon may not be visible at all. Example rotator cuff tear or tear of flexor tendon of finger.
In complete tears of tendon, the ends of retracted tendons can present as focal mass. USG shows swollen hypoechoic irregular ends of tendon with surrounding effusion. Color Doppler shows local hypoechoicity in acute tears.
Ruptures are associated with minimal focal hemorrhages.
Recent partial ruptures appear hyperechoic defects in tendon or its attachment. Increased vascularity can be seen in inflammatory conditions of tendon sheath in color Doppler, there is thickening of tendon sheath and reduced echogenicity in partial/complete tears.
Tears are most commonly associated with background tendinopathy, which weakens the tendon. Chronic tear/relatively minor injury precipitate complete tear.
  • Tendon margins can be separated by fluid, hematoma, herniated adjacent tissue. There is separation of torn margins with dynamic movement. USG is also helpful in diagnosing other similar conditions and associated injury to other structures.
  • Note: Fluid could be found in asymptomatic tendon thickening.
  • Associated microcyst and increased volume of tendon results in calcification, focal involvement may be seen.
  • In acute muscle injury muscles fibers show increase flow on Doppler. musculotendinous junction is most common site of overstretch grade 1 muscle strain—rapid recovery with no loss of power and function.
  • Ultrasonography: normal/focal increased echogenicity up to 50% show generalized hyperechogenicity, this should be differentiated by delayed onset muscle edema—geographic hyperechogenicity, symptom increase after first 24–48 hours and peak at day 3 and reduce at day 7.
  • Grade 2 intrasubstance tear—presents as pain and loss of function, USG shows discontinuity, perimyseal striae, intramuscular fluid surrounding hyperechoic halo. Dynamic scanning shows increased size and contrast of lesions. In this grade there might be partial detachment of muscle from aponeurosis. Grade 3—complete myotendinous/tendo-osseous avulsion. USG shows complete discontinuity of fibers and hematoma.
  • Gouty tophi are echogenic with posterior acoustic shadowing in patients with rheumatoid arthritis joint changes are marked. For examination of joints, USG should be done in static and dynamic phases and simultaneously comparing it with opposite side.
  • Fibrocartilage is hyperechoic (Fig. 1.7).
  • Hyaline cartilage is hypoechoic.17
  • Subcutaneous fat has variable and heterogenous (internal reflective echoes) appearance.
  • During Doppler examination tendon should be in position relaxed contrary to tensed position in which tendons are evaluated for tears and tendinopathy.
  • Tendinopathy can also be caused by external impingement. Normal tendons do not exhibit neovascularity, these findings are associated with severe symptoms.
  • Tenosynovitis can present as mass in significant synovial hypertrophy and thickening of retinacula, excessive local pressure with transducer can displace fluid and lead to false diagnosis.
  • Harmonic imaging results in improved axial resolution and diminished near field artifact. Spatial compounding results in speckle reduction of inherent haziness seen in ultrasound images.
  • Traumatic stump neuroma is disorganized proliferation of nerve fascicle after amputation/regeneration (Fig. 1.1).
  • Stump neuroma is painless/cause pain nonresponsive to conservative management, steroid can be helpful in reducing inflammation and loosening the connective tissue that surrounds and compromises the nerve.
  • Intramuscular phenol or botulinum toxin type A peri and intraneural decrease pain, phenol decreases focal swelling after intra/extrafasicular/intraneural injection and cause severe demyelination, axonal degeneration, edema and hemorrhage leading to architectural nerve disruption.
    • Glycerol is useful but highly viscous.
    • Alcohol is slowly acting more irritating and cause painful neuritis.
    • Neuromas had average maximal diameter 7.15 mm.
  • Twenty-one gauge needle is advanced towards nerve and slightly proximal to stump neuroma, if there is complete cessation of pain after injection identification of pain causing neuroma was successful.
  • Local anesthesia is given proximal to nerve. Same needle is advanced into nerve proximal to neuroma under vision and used to inject phenolic solution. When injection of nerve is successful, swelling is observed in USG.
Phenol can cause slight burning pain (so needle is flushed with saline to avoid spreading). Shape of neuroma does not change but pain decreases.
Intraneural axonotmesis chemically impair and destroy peripheral neural tissues and does not damage surrounding tissues.
Note: In various chapters emphasis is given on identifying the concerned structure on ultrasound. Reader must see the needle (which appears hyperechoic) extending from skin to concern structure and inject under USG guidance.18
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Fig. 1.1: USG appearance of neuroma
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Fig. 1.2: 5 ml syringe
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Fig. 1.3: Blood collection for injection platelet rich plasma
19
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Fig. 1.4: Epidural needle
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Fig. 1.5: Exudate
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Fig. 1.6: USG appearance of tendon
20
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Fig. 1.7: USG appearance of elbow arthritis
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Fig. 1.8: 2% lignocaine
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Fig. 1.9: Separated platelet rich plasma
21
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Fig. 1.10: Syringes and needle
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Figs 1.11A and B: USG guided injection position of probe and the needle
22
 
FURTHER READING
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