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224 Cards in this Set
- Front
- Back
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What is a diarthrodial joint?
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It is a "free-moving" joint with a cavity containing synovial fluid
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What are the five parts that make up a diarthrodial joint?
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fibrous joint capsule
articular cartilage subchondral bone synovial fluid in joint cavity synovial membrane |
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What makes up the synovium?
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intimal layer
subintima |
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What is contained in the synovial membrane?
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synovium
fibrous joint capsule |
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What is synovial fluid?
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ultrafiltrate of plasma plus secretions
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What is the makeup of normal synovial fluid?
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TNCC < 500/ microliter
synovial lining cells, monocytes, and lymphocytes = 90% 10% PMNs 0.5 mg/ml hyaluronic acid HA bs 2-3 mg/ml in humans |
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How does soft tissue lubrication occur (from synovial membrane lubrication)?
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occurs by boundary lubrication (hyaluronan and lubricin) --- based on a thin layer keeping the two boundaries separate
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Articular cartilage is _____________, ____________, and ____________.
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avascular
aneural alymphatic (chondrocytes obtain nutrients through diffusion) |
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What are the cellular zones of articular cartilage?
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superficial zone
middle or radial zone deep zone calcified zone subchondral bone |
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What is type II collagen and how is it different from type I?
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***specific to articular cartilage
85-90% of articular cartilage collagen increased lysine hydroxylation and more glycosylation vs. type I collagen tensile strength |
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What is the most predominant proteoglycan present in articular cartilage?
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large aggregating proteoglycan
aka ---- Aggrecan (most abundant) |
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How is the articular cartilage lubricated in low load situations?
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Boundary lubrication
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How is articular cartilage lubricated in high load situations?
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hydrodynamic and squeeze film
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What are the two parts of the biphasic material of subchondral bone?
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Inorganic and organic
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What does the inorganic matrix contribute to the biphasic material of subchondral bone?
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hardness and rigidity
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What does the organic matrix contribute to the biphasic material of subchondral bone?
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flexibility and resiliency
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Osteoarthritis represents a group of disorders characterized by 3 things. What are they?
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deterioration of the articular cartilage
changes in the subchondral bone changes of soft tissues of the joint |
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Can natural repair processes by adjacent tissues help repair articular cartilage?
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no they are incapable of producing tissue with morphologic, biochemical, and biomechanical properties of articular cartilage
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What is the etiopathogenesis of OA?
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-physical forces lead to bio material failure (traumatic injuries)
-chondrocyte response (deradation and repair) to insult ---(chronic synovitis) -extra-cartilaginous factors cause secondary cartilage changes ---(bony remodeling, synovial responses, microfractures, vascular changes, and other) |
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What occurs with synovial insult/injury?
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direct release of lysosomal enzymes
release of PGE2 release of free radicals release of cytokines source of pain (abundance of pain receptors in capsule; increase in interosseous pressure) |
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What are the biochemical changes that occur with articular cartilage degradation?
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decreased PG content
reduced PG aggregation increased water content change in collagen structure *****reduced compressive and tensile strength**** |
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What are the subchondral bone changes associated with OA?
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subchondral bone sclerosis
subchondral cystic lesions -----vascular infiltration -----focal osteonecrosis periarticular osteophyte formation |
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Osteoarthritis affects the ____________, ______________, and __________ simultaneously.
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sort tissues
cartilage bone |
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You need a _____ % to _____% change in bone density to observe a change radiographically.
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30-40%
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What are your therapeutic goals when treating osteoarthritis?
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decrease inflammation (soft tissues and cartilage)
alleviate pain lubricate joint restore normal environment/ halt disease improve cartilage repair |
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What are some challenges of treatment of DJD?
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specific joint involved
stage of lesions current and intended use of the horse age of the horse treatment cost response to therapy regulations |
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What are the 2 essential clinical features of OA that require attention?
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pain and loss of function
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What is the conservative approach (medical management) to treating OA?
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exercise modification
weight reduction anti-inflammatory drugs slow-acting, disease modifying, osteoarthritis agents supportive care |
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What is supportive care for OA include?
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--for acute trauma
cold 1st 24 hours, alternate heat, cold firm wrap provides warmth, minimizes swelling ROM/turn-out/exercise regular trim laser, mjagnet, acupuncture, shock wave |
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When do you use cold therapy and what is the benefit?
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decrease pain, inflammation, swelling
first 24-48 hours after each training session >10 min, <30 min (dry is best to preserve the foot) |
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what are the many levels of medical treatment for DJD?
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oral supplements
topical medications IM/IV medications IA joint medications NSAIDs |
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what are NSAIDs and how do they work?
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cyclooxygenase inhibitors
decrease pain and stiffness and improve function suppress inflammation due to trauma or degraded cartilage products attenuate release of synovial cell cytokines, oxygen-derived free radicals, and arachidonic acid metabolites |
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what are two major side effects of NSAIDs?
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GI ulceration
renal toxicity |
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What is COX-1?
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it is the good isoenqyme
--normal physiology for renal and GI (protective) |
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What is COX-2?
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it is the bad isoenzyme
it causes inflammation and pain |
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Which NSAIDs do we use?
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phenylbutazone (bute)
Flunixin meglumine (Banamine) Meclofenamic acid (Arquel) Naproxen (Aleve) Ketoprofen (Ketofen) Carprofen (Rimadyl) Aspirin |
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Why is phenylbutazone the most popular NSAID?
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ease of administration
good efficacy Cheap |
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What are the negatives to using Phenylbutazone?
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most toxic (however lower risk if given w/ the proper dosage)
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What are the characteristics of Flunixin meglumine (Banamine)?
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efficacy ---> seems less than bute for MS pain
---more expensive ---LESS toxic than Bute |
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What is the benefit of Ketoprofen (Ketofen)?
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both legs of the inflammatory cascade (possibly)
IV use for horses -efficacy appears to be less than bute but it has the LEAST toxic side effects |
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What is a topical NSAID used in horses?
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Diclofenac sodium
---selective COX-2 inhibitor --Liposome technology (multilamellar vesicles; > 20 lipid bylayers) ----research being done in both humans and horses (clinically beneficial, reduced side effects) |
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What are the goals of chondroprotection?
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support joint structure and function
normalize matrix synthesis decrease matrix degradation |
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What are some examples of chondroprotective agents?
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corticosteroids (choice of RX and dosing are critical)
hyaluronan Polysulfated glycosaminoglycans (Adequan) newer systemic chondroprotective meds (Cartrophen) oral, slow-acting agents (Cosequin, Glycoflex) Proteinase inhibitors |
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What are some intraarticular medications that we may give?
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corticosteroids
sodium hyaluronate PSGAGs NSAIDs newer systemic chondroprotective meds Oral GAG compounds IRAP serum VetSTem |
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What are the advantages to using corticosteroids?
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decreased MMP
decreased IL-1, TNF-alpha decreased fibrin deposition pain relief potent economical |
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What are the disadvantages for using corticosteroids?
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pain relief (may do too much on it???)
laminitis MPA (depo-medrol) --articular degeneration --chondrocyte damage --dec. matrix production (4 months) --steroid arthropathy |
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Corticosteroids may improve cartilage nutrition by controlling the severity of the synovitis by these mechanisms.
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enable return of normal synovial fluid properties
improve fluid exchange within the joint |
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Since corticosteroid suspensions used intra-articularly can cause laminitis, the maximum doses are....
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triamcinolone <18mg
methylprednisolone (depo-medrol) < 200mg betamethasone < 30 mg |
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What is the potency of the corticosteroid suspensions from most potent to least potent?
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flumethasone (most)
isoflupredone betamethasone triamcinolone methylprednisolone (least) |
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What is critical for the duration of action of corticosteroids?
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the rate of hydrolysis of the ester
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what are the short acting corticosteroids?
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hydrocortisone
flumethasone |
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what are some longer acting corticosteroids?
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triamcinolone
betamethasone methylprednisolone acetate |
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What is steroid flare?
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-when corticosteroid injections go wrong...
acute inflammatory response heat, pain, swelling, lameness 8-24 hours post-injection 2% incidence vehicle related ******DDx= infection****** |
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What are four rules/guidelines to follow with steroid application?
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choose wisely
low dose rest after use limit repeated doses |
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Sodium Hyaluronan is most effective in treatment of what?
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acute synovitis
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What are the mechanisms of action of sodium hyaluronan for treatment of acute synovitis?
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steric hindrance
scavenge free radicals reduction of bradykinin and prostaglandin increase in endogenous HA synthesis via cAMP levels |
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What is Legend?
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it has a streptococcal cell wall origin
give IV or IA acts on synovial fibroblasts to increase HA synthesis anti-inflammatory??? |
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What are the actions of Polysulfated Glycosaminoglycan (Adequan)?
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Inhibit MMP
Stimulate matrix synthesis (increase synth. of proteoglycans and collagen by chondrocytes) promotes HA synthesis |
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What are some adverse effects seen with PSGAG?
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-increased clotting times (dogs)
-thrombocytopenia (humans) -IA use: req. increased concentrations of abx against S. aureus |
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How does Autologous Conditioned Serum work? (IRAP)
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interleukin-1 receptor antagonist
---competes w/ IL-1 for binding ---preventss activation of receptor ---experimental evidence for dec. joint inflammation is strong |
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What do we use nutraceuticals for (we think they help)?
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cartilage support
cartilage protection |
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What are some current concerns with nutraceuticals?
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dietary supplements (functional foods)
little to no government regulation (purity and uniformity vary) validated analytical methods research: new human study not supportive labeling and claims |
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what are the mechanisms of action of glucosamine?
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stimulates proteoglycan and collagen synthesis by chondrocytes and fibroblasts
anti-inflammatory properties unrelated to effects on the eicosanoid pathway may increase hyaluronan synthesis by synovial lining cells |
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which joints are more difficult to image completely?
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stifle
cartilage lesions not visible with US |
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why would you do diagnostic arthroscopic surgery?
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certain joints are more difficult to image
even with multiple imaging modalities, arthroscopic visualization can be helpful cases that are no longer responsive to tx |
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What are some surgical techniques for OA?
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arthroscopic lavage and examination
removal of loose cartilage or OC fragments stimulation of fibrocartilage repair (curettage, microfracture, synovectomy) remove diseased bone cartilage resurfacing techniques |
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What are some risks/concerns of fetlock arthroscopy?
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risk of cartilage damage--> dorsal saggital ridge
synovial membrane attached to P1 ---debridement more conservative ---OC fragments often embedded |
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When would you perform stifle arthroscopy?
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cruciate ligaments
menisci meniscal ligaments large cartilage erosions cartilage lesions not visible otherwise |
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If cartilage is left alone, it does not _______.
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regenerate
---fails to restore function and structural |
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Surgery promotes cartilage ___________.
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healing
---implies replacement of tissue but does not restore normal function |
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cartilage regeneration is __________________________.
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specialized repair that reestablishes ORIGINAL tissue
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what is the primary goal of arthroscopic techniques for repair and how is this accomplished?
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enhancement of the repair
---quantity of the repair tissue ---quality of the repair tissue accomplished through: local manipulation OR cell or tissue transplantation |
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What are three types of arthroscopic repair?
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matrix flow
intrinsic repair extrinsic repair |
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What is matrix flow repair?
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marginal migration
<3mm of distance |
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What is intrinsic repair?
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limited repair within the cartilage
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What is extrinsic repair?
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mesenchymal ingrowth from below the subchondral plate
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When will you see intrinsic repair in the cartilage?
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---see with partial thickness injuries (non-healing, mild inflammatory response)
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What causes intrinsic repair to occur as a cartilage response to injury?
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limited mitotic ability of chondrocytes
ineffective collagen production (type III or I) limited proteoglycan production |
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What is the advantage of arthroscopic sx for partial thickness defects?
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remove loose cartilage
reduce further exfoliation (synovitis) |
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What is the matrix flow?
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the central flow of cartilage
-has a limited ability to "repair" |
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When is the cartilage response to injury extrinsic repair?
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with full-thickness defects
--deeper to calcified cartilage layer --improved healing response |
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what is the mechanism of repair for extrinsic repair of the cartilage?
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mesenchumal tissue inflow from subchondral bone
---hematoma-granulation tissue-fibrous tissue-progressive calcification to fibrocartilage |
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What are the requirements for extrinsic repair?
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removal of calcified cartilage
---allows fibrocartilage formation |
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What is curettage?
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superficial (2mm) intracortical debridement below calcified cartilage layer
exposes subchondral bone removal of eburnated bone to expose intracortical vessels allows for metaplasia of granulation tissue to fibrocartilage |
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What are the different tissue transplantation techniques for repair of cartilage?
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autogenous cartilage (articular, sternal or auricular)
pluripotential stem cell osteochondral chondrocyte periosteal perichondral |
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What are osteochondral grafts?
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may provide most secure attachment (bone integration)
provides immediate weight-bearing problems with donor site morbidity (must find less weight-bearing site) |
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What are the two stages of chondrocyte transplantation?
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autogenous collection:
1.digestion and culture for three weeks 2.implantation in fibrin vehicle *anabolic growth factors (IGF-1) incorporated |
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Articular cartilage injury benefits from __________.
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arthroscopic debridement
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Partial thickness injuries require _____________.
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minimal debridement
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Full thickness injuries have better healing with ____________.
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Modern techniques
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What do you see with End-Stage DJD?
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movement = pain
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What is a possible treatment for return to function as athlete for end-stage DJD?
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certain joints in the horse can be fused (arthrodesis) and the horse can function as an athlete
distal tarsal joints: DIT, TMT pastern: proximal interphalangeal joint |
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What joints can be fused for a possible treatment for end stage DJD that the horses can be salvaged for pasture pets/or for breeding?
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Fetlock (MCP/MTP) arthrodesis
Carpal arthrodesis |
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What are some ways that arthrodesis (fusion) can be performed?
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injection
laser drilling open approach remove cartilage LCP or LCDCP lag screws bone graft ***the more stable the fixation, the more comfortable post-op (shorter duration of cast application) |
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what is ankylosis?
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when the distal tarsal joints sometimes fuse on their own
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Pastern Arthrodesis
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hind > front
can be an athlete more stable -> less casting more stable -> less callus many surgical options |
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Carpal Arthrodesis
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salvage procedure
preferable to fuse either midcarpal or RC joint rather than pan-carpal arthrodesis usually consider for unstable joints, but occasionally severe DJD |
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When do we use fetlock arthrodesis?
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for breakdown injuries
also salvage for severe DJD newer system (LCP preferrable) |
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Where is CK found?
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skeletal muscle
cardiac muscle brain tissue (not readily exchanged between CSF and plasma) |
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Where is AST found?
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skeletal muscle
liver heart |
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Which three enzymes are routinely used to evaluate muscle health?
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creatine kinase (CK)
aspartate aminotransferase (AST) lactate dehydrogenase (LDH)- not muscle specific |
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What are the timings for CK and AST in relation to muscle damage?
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CK - usu. peaks at 4-6 hours after damage and rapidly returns to baseline
AST - rises more slowly peaking at 12-24 hours and may persist for 2-3 weeks |
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elevated AST with decreasing CK indicates no ___________________.
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ongoing myonecrosis
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What are the considerations for a bippsy?
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PE and lab work suggest muscle disease
---want to know is it sporadic ER, chronic ER, or PSSM *note - it can take 1-3 weeks for muscle fibers to return to normal after an episode of rhabdomyolysis |
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Where do you biopsy for suspected equine motor neuron disease (surgical biopsy)? ******
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Serocaudalis dorsalis medialis (tail head)
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When do you biopsy the semimembranosus/semitendinosus muscles?
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rhabdomyolysis
PSSM nutritional degeneration "shivers" (surgical biopsy)** |
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When do you biopsy the middle gluteal muscle?
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rhabdomyolysis
PSSM nutritional degeneration "shivers" (this is a needle biopsy)** |
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Where do you biopsy for neurogenic atrophy?
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the affected muscle
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How does a needle biopsy work?
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the biopsy needle is placed into the muscle of interest such that the open window is within the muscle belly (~ 8cm deep). The cutting device is then inserted into the biopsy needle until it cuts through the portion of the muscle that has entered into the needle. The entire unit is then removed and the stilette is used to remove the tissue sample from the biopsy needle.
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How does a surgical biopsy work?
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clip and prep in routine mannner
local lidocaine block sample size = .5-1.0 cm x 2 cm routine closure of the skin **incision is only 3.5-4 cm long |
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How should you fix your samples?
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either in 10% buffered formalin or frozen
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What will you see on a muscle biopsy with PSSM?
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subsarcolemmal vacuoles
periodic acid-schiff (PAS) + ve resistance to amylase digestion |
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What is grade 1 polysaccharide storage myopathy?
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aggregates of granular polysaccharide in the cytoplasm or under the sarcolemma
---> these aggregates are sensitive to amylase digestion |
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what is grade 2 polysaccharide storage myopathy?
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PAS positive, abnormal crystalline inclusions
---> the crystalline inclusions are resistant to amylase digestion |
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What is the genetic test for QH breeds for PSSM?
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GYS-1 (glycogen synthase)
- uni. Minnesota tests for 2 different genes of interest P- mutant gene causing classic PSSM MH- mutant gene that makes symptoms worse in QH and related breeds |
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what is grade 2 polysaccharide storage myopathy?
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PAS positive, abnormal crystalline inclusions
---> the crystalline inclusions are resistant to amylase digestion |
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What surgery can you perform for stringhalt?
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lateral digital extensor myotenectomy
--this is a field surgery --really only helps about half of the horses |
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What is the genetic test for QH breeds for PSSM?
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GYS-1 (glycogen synthase)
- uni. Minnesota tests for 2 different genes of interest P- mutant gene causing classic PSSM MH- mutant gene that makes symptoms worse in QH and related breeds |
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What is string halt?
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neurogenic etiology
australian form - dandelions (may have lesions within the left recurrent laryngeal nerve) --> many recover without treatment characteristic gait (exaggerated) can be unilateral or bilateral and should be differentiated from upward fixation of the patella |
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What surgery can you perform for stringhalt?
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lateral digital extensor myotenectomy
--this is a field surgery --really only helps about half of the horses |
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What is fibrotic myopathy?
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usu. unilateral hindlimb fait abnormality
fibrosis of semitendinosis muscle traumatic etiology characteristic gait (swinging foot in??) dx: observation of characteristic gait, palpate the fibrosed/ossified areas of the muscle usu. at the level of or immediately proximal to the stifle |
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What is string halt?
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neurogenic etiology
australian form - dandelions (may have lesions within the left recurrent laryngeal nerve) --> many recover without treatment characteristic gait (exaggerated) can be unilateral or bilateral and should be differentiated from upward fixation of the patella |
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What is fibrotic myopathy?
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usu. unilateral hindlimb fait abnormality
fibrosis of semitendinosis muscle traumatic etiology characteristic gait (swinging foot in??) dx: observation of characteristic gait, palpate the fibrosed/ossified areas of the muscle usu. at the level of or immediately proximal to the stifle |
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what is the surgical treatment for fibrotic myopathy and the prognosis?
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semitendinosis tenectomy
px: tenotomy alone has fewer complications to other procedures, but may not result in complete resolution of gait abnormality **if neuropathic form is present then recurrence is likely no matter what surgery is performed. |
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Is fibrotic myopathy painful?
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no it is a mechanical lameness not a painful lameness
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____________ and _____________ account for approx. 24% of septic synovial structures.
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puncture wounds and lacerations
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What is the pathogenesis for septic arthritis in adults?
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trauma
iatrogenic single joint |
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What is the pathogenesis for septic arthritis in neonates?
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hematogenous
polyarticular (50%) physitis first 30 days FPT blood culture 1.5-15% mortality |
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The degree of joint destruction due to septic arthritis depends on what?
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duration of infection
bacterial virulence and number pre-existing joint disease host age host health degree of inflammation |
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The defenses of the synovial membrane are overcome by __________________ and __________________ in SA.
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excessive numbers of bacteria
virulent/pathogenic organisms |
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What does inflammation in the joint cause?
|
joint effusion
fibrin deposition in the joint alterations in the cartilage matrix ultimately cartilage destruction |
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acture invasion of bacteria results in the activation of synoviocytes and neutrophils and results in the release of what inflammatory mediators?
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IL-1Beta
TNF-alpha oxygen free radicals |
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What do the inflammatory mediators activate?
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activate the chondrocytes to release more damaging enzymes such as MMP and decrease their production of proteoglycans in the cartilage matrix
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What is the end result of SA?
|
cartilage destruction and osteoarthritis
-if the damage is minimal the cartilage can recover -if not, the damage is permanent (this is why SA is so devastating) |
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Septic synovial structures are a _____________________!!!!!!
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EMERGENCY
THEY REQUIRE IMMEDIATE ATTENTION!!!!! |
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What are the clinical signs of SA?
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CS can vary depend. on how recent the insult, how aggressive the organism, and the degree of contamination with bacteria and organic debris
classic signs: swelling, joint effusion, lameness |
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what should you rule out when presented with severe lameness?
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fracture
sole abscess SA |
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How do you confirm a diagnosis of SA?
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demonstration of communication between the joint and the environment via leakage of synovial fluid or saline used to distend the joint
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If you are uncertain whether a synovial structure is involved....
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assume that it IS involved until proven otherwise and treat accordingly
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How is Radiography useful for dx SA?
|
rule out fractures
rule out osteomyelitis (very important in foals---often do serial studies) monitor progression of: -subchondral bone lysis -periosteal proliferation -narrowing of joint space -widening of joint space -ankylosis |
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When might scintigraphy be useful?
|
in special situations where a septic joint was initially diagnosed and treated effectively, but the horse remains more lame than expected with resolution of the SA
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What can synovial fluid appear like with SA?
|
yellow/bloody and turbid
TP>2.0 g/dl WBC > 5,000/microliter >50% neutrophils gram stain lactate >4.0 mmol/L perform culture and sensitivity |
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___________ is not more likely to generate a positive culture than fluid (SA).
|
Synovial biopsy
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How do you treat SA?
|
attack the problem on multiple levels
be aggressive as possible early and then be able to back off to less aggressive treatments if things are going well -supportive care -pain management -anti-inflammatories -antimicrobials -surgical management |
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What would supportive care for SA consist of?
|
IV fluids
stall rest passive motion pressure/support bandages appropriate bedding |
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What could you use for pain management for SA?
|
NSAIDs
Butorphanol CRI Epidural Catheter (great for hind limbs) --- may also consider ketamine or lidocaine CRI to control pain |
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What about antimicrobials for SA?
|
aggressive antimicrobial theraphy is critical and most often involves both systemic and regional routes of delivery
often use different antibiotic for regional delivery than systemic systemic treatment often >2weeks duration |
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What is the standard of practice for antibiotic delivery for distal limb injuries that could benefit from high tissue levels of antibiotics?
|
regional antibiotic perfusion (intraosseous or intravenous)
--30 min -aminoglycosides -ceftiofur -based on C/S (culture and sensitivity) |
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How do antibiotic-impregnated implants work?
|
provide a slow release of antibiotic into the surrounding joint or tissue that is very high initially and gradually declines over time
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What is considered the gold standard for septic synovial structures?
|
surgical treatment
-lavage, debridement, and drainage -wound repair - if lots of fibrin is present sx will be essential to remove all the fibrin |
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What are three different lavage methods?
|
needle
arthroscopy arthrotomy |
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How do you lavage a septic joint?
|
use balanced electrolyte solution (LRS) under pressure from a pressure bag or motorized pump to control pressure and maximize flow
-must use substantial fluid volume (5-10L/joint or more) |
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Why are tendon sheath infections often difficult?
|
because the horses are more painful longer as a result of mechanical issues and adhesion formation/soft tissue fibrosis and lack of range of motion
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What are the KEY points when treating septic synovial structures?
|
EARLY RECOGNITION
AGGRESSIVE TREATMENT |
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what are the layers of tendons and ligaments on a horses leg from superficial to deep at mid metatarsus?
|
superficial digital flexor tendon
deep digital flexor tendon inferior check ligament suspensory ligament |
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What do proteoglycans do?
|
regulate water content
provide lubrication control collagen fiber diameter |
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What are the three phases that occur in response to injury?
|
Inflammatory phase (vascular and cellular)
repair phase (fibroblast proliferation) remodeling phase |
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When performing an ultrasound examination of thetendons and ligaments you must use _____________.
|
both the transverse and longitudinal views
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US lesion classification: type 1
|
decreased echogenicity
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US lesion classification: type 2
|
core < 50% CSA
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US lesion classification: type 3
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Core > 50% CSA
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US lesion classification: type 4
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core entire CSA
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What will you see if the SDFT is lacerated?
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fetlock dropped
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What will you see if the SDFT and DDFT are lacerated?
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fetlock dropped
toe off the ground |
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What will you see if the SDFT, DDFT, suspensory ligament are all lacerated?
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fetlock on the ground
toe off the ground |
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how do you treat tendon/ligament lacerations?
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wound lavage and debridement
suture tendons/close wound (compound locking loop or three loop pulley system) |
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What is the prognosis for extensor tendon lacerations?
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75% sound
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what is the prognosis for flexor tendon lacerations?
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84% survival
45-82% survival |
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what is tenosynovitis?
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idiopathic
acute (trauma, tendon/mesotendon injury) OR Complex (chronic) -tenosynovial masses -digital sheath fibrosis -adhesions -annular ligament constriction Infectious |
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How do you diagnose tenosynovitis?
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CS: palpable thickening and/or masses
fluctuant fluid swelling chronic lameness US Exam: thickened synovial sheath tendon lesions synovial masses adhesions |
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What medical therapy might you do for tenosynovitis?
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physical therapy:
cold therapy controlled exercise range of motion Medical: NSAIDs Intrathecal HA |
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What are the three techniques for annular ligament transection?
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open technique
modified open technique endoscopically assisted technique |
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with tendonitis/desmitis you get more ____________ than ____________.
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catabolism than anabolism
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What medical therapies do you do for tendonitis/desmitis?
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control inflammation:
anti-inflammatories support bandage cold therapy controlled exercise serial ultrasound exams |
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What surgical therapies might you use for tendonitis/desmitis?
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superior check ligament desmotomy
percutaneous tendon splitting |
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What is the extracellular matrix?
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dual function proteins
-structural and functional controlled release of growth factors degradation results in release of biologically active proteins |
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What are bioactive factors?
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growth factors
cytokines |
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what do bioactive factors do?
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cell differentiation
recruit endogenous stem cells inhibit apoptosis inhibit fibrosis stimulate angiogenesis immunomodulation anti-inflammatory anti-pain |
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Where are two locations you can take a bone marrow aspirate?
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sternum
ilium |
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What is the stromal vascular fraction (stem cell section)?
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= nucleated cells...
fibroblastic cells pericytes immune cells vascular smooth muscle cells endothelial cells |
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What was the effect of adipose-derived nucleated cell fractions on tendon repair in horses with collagenase-induced tendinitis?
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no adverse effects
decreased inflammatory cell infiltrate improved tendon architecture (fiber linearity, uniformity, crimping) increased cartilage oligomeric matrix protein (COMP) --- critical role in collagen fiber formation??? |
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what are the advantages of platelet rich plasma?
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autologous
point-of-care multiple growth factors bioactive scaffold (fibrin) relatively inexpensive |
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what are the disadvantages of platelet rich plasma?
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patient variation
dosing is empirical |
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what does shock wave therapy do?
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neovascularization
achilles and patellar tendon healing decreased lesion size |
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initial endoscopy of a horse must be done _____________.
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unsedated
* if you lose sight of where you are - get it out - can reflect ventral to soft palate and be bitten |
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What is guttural pouch tympany?
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salpingopharyngeal osteum becomes a one-way valve trapping air in one or both guttural pouches
***air must be relieved |
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guttural pouch tympany sx in unilaterally affected foals
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fenestrate median septum to allow unaffected side to empty air
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guttural pouch tympany sx in bilaterally affected foals
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fenestrate median septum and relieve salpingopharyngeal obstruction on one side
OR relieve both pharyngeal openings |
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laser fenestration of median septum for guttural pouch tympany
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target tissue contains no vital structures
can be performed in standing horse minimally invasive procedure |
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Guttural pouch lavage used to treat guttural pouch empyema
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-use coiled catheters via nose
foley catheter via nose |
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guttural pouch mycosis
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mycotic plaque on internal carotid or maxillary artery
probably arterial wall disease (may affect cranial nerve function) topical Rx little value require embolization of regional arteries |
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Guttural pouch mycosis: clinical signs
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impressive arterial hemorrhage
often stops spontaneously first time unpredictable |
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Guttural pouch mycosis: treatment
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treatment is urgent
-unilateral carotid ligation useless bilateral??? how long ---endoscopy - sedate the horse (check metabolic status first) -careful entry into pouch ---DON'T DO IF INEXPERIENCED OR SCOPE IS TOO BIG |
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what is the appearance of the normal epiglottis?
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prominent vasculature
serrated margins pointed tip slightly curled |
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entrapped epiglottis
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think about turtleneck example
-probably happens b/c the mucous membrane becomes inflamed: when the tissue swells, air turbulence makes it swell more -soft palate is in normal position |
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Epiglottis entrapment tx
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cut them for surgery - so now it isn't as tight anymore and it doesn't entrap again - if it recurrs again then you haven't cut it enough because it shouldn't be tight enough to do it again
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_________ can occur due to atrophy of the epiglottis from the reperfusion injury (releasing the entrapped epiglottis).
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blunted epiglottis -- can get recurrent displacement with this
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epiglottal entrapment: prognosis
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thickness and inflammation vary widely
clinical picture is variable (noise, exercise intolerance) need to consider each individually healing process - can take a long time |
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hypoplastic epiglottis (in racehorses)
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typically due to atrophy
can take awhile to heal and so they will be out of work and they may have to start over training so if they are racing and winning money right now--they may be as good as they are ever going to be --discuss the value of taking the horse all the way down - maybe they only need to race a few more times to increase value and then they may never have to race again (esp. mare --> breeding) |
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it is almost always a mistake to operate on a _____________ airway.
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inflamed --- rest it, decrease inflammation, then work with it
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________________ is the most common complication after an epiglottic entrapment.
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dorsally displaced soft palate
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Dorsal displacement of the soft palate
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characterized by expiratory noise --- horse makes a gagging noise -- sometimes referred to as swallowing its tongue
--many of these are operated on hx rather than seeing them with a scope b/c they have spontaneous replacement |
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dorsal displacement of the soft palate: pathogenesis
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--most commonly cause by upper airway irritation
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dorsal displacement of the soft palate: treatments
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relieve inflammation
tongue tie strap muscle resection (don't really do anymore)/ST tenectomy --- the point of the sx is to release the larynx forward trim soft palate (not good idea) laser soft palate tie forward |
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what is an exception where you may trim the soft palate?
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if you have permanent soft palate displacement (not usual presentation)
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dorsal displacement of the soft palate: CS
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swallows tongue, expiratory noise
appears at work, subsides w/ o2 debt reduction may require racing speed to occur |
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What is the current approach for DDSP?
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standing ST tenectomy
soft palate laser heal 2 weeks and train tie forward if it doesn't work |
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what is laryngeal hemiplegia (roaring)?
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paresis/alysis of LEFT recurrent laryngeal nerve
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what is the expected appearance of a paralyzed left side d/t laryngeal hemiplegia?
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there is no swelling
it is very thin it just hangs there and doesn't move very much it obstructs airflow b/c that side collapses |
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what is the grading system for LLH?
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grade I: normal
grade II: asynchronous movement (full abduction possible with stimulation - particularly when swallows, can open it up completely but it is lazy) grade III: asynchronous movement, full abduction cannot be induced grade IV: no movement during any phase of respiration |
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what are the treatments for LLH?
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prosthetic laryngoplasty (with ventriculocordectomy)
ventriculocordectomy partial arytenoidectomy pedicle graft |
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What does the prosthetic laryngoplasty do for LLH?
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replace crichoarytenoideus dorsalis muscle
endoscopic control ventriculocordectomy after abx 3-5 days |
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what considerations should you have when performing prosthetic laryngoplasty?
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cricoid suture placed high at notch
arytenoid suture better medial to lateral for abduction don't penetrate lumen or break aseptic procedure |
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Laryngoplasty procedure: success?
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laryngoplasty alone decreased noise but not as well as VC. normal pressures
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Neuromuscular pedicle graft for LLH
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neuromuscular graft
nerve transplantation nerve anastomosis --- ventral branch of C1 to omo- and sternohyoid mm) to abductor branch of recurrent laryngeal n. 3-12 mo. for results -effect only seen during exercise |
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ventriculectomy alone for LLH: success?
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no improvement of ventriculectomy alone
PLP restored baseline values |
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prosthetic laryngoplasty and bilateral ventriculectomy for LLH: together success?
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48% race horses successful
-70% <3 successful -25% >= 3 successful 93% non race horses successful owner contact: 42% exercise intolerant 47% made noise |
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all LLH horses have _______________.
Race horses also have __________ |
ventriculocordectomy
tie back |
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right side presentation of recurrent laryngeal nerve hemiplegia
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not spontaneous recurrent laryngeal neuropathy
most common causes: retropharyngeal inflammation IV injection injury to RLN others: guttural pouch mycosis EPM treat medically to see where it will end |
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what is arytenoid chondritis?
|
superficial or deep infection of the arytenoid cartilage possibly resulting in:
mucosal ulcer granuloma abscessation deformity of cartilage dysfunction airway obstruction |
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what is the etiology of arytenoid chondritis?
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most likely begins with mucosal disruption leading to infection
possibly hematogenous from local infection/contamination |
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what are the clinical signs of arytenoid chondritis?
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coughing (less common)
upper airway noise (inspiratory) during exercise (usually presents earlier in course in horses in trraining -- can progress rapidly) may present as airway emergency Exercise intolerance |
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what are your endoscopic findings with arytenoid chondritis?
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mucosal ulcer
granuloma with or without tract to deeper tissue abscessation/purulent drainage deformity of cartilage immobility airway obstruction |
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what are the presentations of chondritis "complex"?
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mucosal defect alone
deeper involvement with potential salvage of arytenoid function *with or without tracts into the cartilage; with or without abscessation) invasive disease with permanent deformity and dysfunction |
