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MUSCULAR DISEASE Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications Fibrotic myopathy Mus...

MUSCULAR DISEASE Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications Fibrotic myopathy Muscle sprain Defect in hamstrings muscle causing fibrosis - Altered gait Palpate fibrosis and US scar Surgery No inborn myopathy or muscle cramping - May have increased CK in association Visible defect in hamstring Stretching with exercise Slam the limb back down- because Massage - Defect in muscle palpable the hamstrings are shortened - Slamming down gait in HL Muscle strain Fibrotic myopathy Injury to muscle - Acute swelling and heat - Transient lameness Polysaccharide storage RER, SR Glycogen storage disorder – can use the glycogen that is in the - Gait abnormalities – short stride, Genetic tests for PSSM1 Acute management: Symptomatic therapy myopathy muscle - Atrophy muscles Sub maximal exercise testing – CK - Analgesia – careful kidney function Type one homozygous - Fasciculation should less than double or stay under - Fluid therapy to help kidney and muscle Type 2 anything that’s negative - Rapid muscle fatigue 1000 perfusion Emphasised by unfitness - Anxious, tachypnoeic, sweating - Rest and hand walking - Painful and hard muscles (esp triceps) on Chronic: manage!! palpation - High fat low sugar diet – takes 4 months - Reluctant to move - Regular daily exercise Drafts- atrophy and progressive weakness Paddock (esp PSSM) WBs muscle soreness and gait abnormalities QH – gait abnormalities if hetero, acute exertional rhabdomyolysis if homo Recurrent exertional PSSM, SR Genetic cause – fault with calcium regulation TBs and SBs - CK and AST 4-6 hrs Acute management: Symptomatic therapy rhabdomyolysis Predisposing factors anxiety and stress!! Being held back, young, lameness, being held - Hyperkal - Analgesia – careful kidney function back - Haemoconc - Fluid therapy to help kidney and muscle - Gait abnormalities – short stride - Myoglobinuria (and serial perfusion - Atrophy muscles samples) - Rest and hand walking - Fasciculation CK normal unless exercised Chronic: manage!! - Rapid muscle fatigue - High fat low sugar diet – takes 4 months - Anxious, tachypnoeic, sweating - Regular daily exercise - Painful and hard muscles (esp triceps) on - Paddock (esp PSSM) palpation - Reluctant to move Spontaneous RER, PSSM Usually management factors – worked in hot and humid - Hot and humid weather History and CS rhabdomyolysis conditions in excess of its ability - Electrolyte deficiency CBC, biochem, urinalysis - Endurance horses - Gait abnormalities – short stride, - Atrophy muscles - Fasciculations - Rapid muscle fatigue - Anxious, tachypnoeic, sweating - Painful and hard muscles on palpation - Reluctant to move Hyperkaliaemic periodic RER, PSSM, SR Genetic from “impressive” sire causing muscle weakness QH Genetic testing Low potassium diet can help paralysis QH - Recumbency and laryngeal paralysis Clostridial myositis Clostridial spores in environ inoculated into muscle → Different form the others- endotoxemia leading to US Create an aerobic enviro – cut muscles inflammation and necrosis cause spores to germinate a really sick horse. Recent injection of flunixin Aspiration with cytology, gram stain, Aggressive ABs and fluids - Depression culture - Fever CBC and biochem - Pain, swelling and emphysema - Toxaemia Atypical myopathy Sycamore trees toxin hypoglycin A Early winter, wet weather, very young or old Poor prognosis 40% horses Supportive care IV glucose and insulin - Sudden death - Recumbency - Weak - Not really painful - White muscle disease Selenium/ Vit E deficiency causing muscle necrosis Neonates often - Weak foals die – heart and resp muscles affected  THE FOOT Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications Bruises/ subsolar Most common cause of lameness. Bruise creates good bacto Can be very lame – 5-10/10 Clinical signs and localisation with Excavation and drainage abscessation environ → bacto proliferate and abscess travels and pushes - Increased DP hoof testers - Poultice through weakest part of hoof – white line or coronary band - Focal hoof tester pain Rads - NSAIDs – need to get them walking on the foot - Partial response to ASNB - Avoid ABs unless cellulitis present Thrush Bacterial infection of white line/ sole that invades and causes - Black necrotic exudate Management related – not enough exercise or trimming, lameness - Foul odour poor stable hygiene, wet ground - Lameness Treat by trimming back to health tissue and iodine Canker – chronic Proliferative and invasive bacteria invades Filamentous and cottage cheese look Manage bacterial infection – swab C and S hypertrophic moist Debride extensively – often until blood pododermatitis Club foot Excessive tension in DDFt causing pulling of the foot backwards Hoof shape clubbed Conservative: Analgesia and exercise restriction to reduce (standing on tiptoe) Short/ choppy stride DDFt pain, toe protection but NOT extension, gradually Valgus stance ? trim heels Toe point if in acute stage Surgical: tenotomy or cut inferior check ligament of DDFt, rasp heels, toe plate to protect toe Hoof cracks Horizontal – burst abscesses or trauma to coronary band Stabilise it!! Horizontal keep clean and grow out (6 Vertical – trauma at coronary band or sole months). Vertical shoes and casts Keratoma Benign growth of aberrant keratin tissue from chronic irritation or - Lameness Surgical only – remove slice of hoof wall with it in it up to infection between pedal bone and hoof wall/ sole→ pressure - History or trauma or abscess coronary band, then bar shoe with quarter clips reabsorption of underlying pedal bone and mechanical separation at white line Pedal bone fracture Trauma type 1, 2, 3, 5, 6 Recent trauma Rads Stabilise with casting/ shoeing Type 7 marginal in foals Lameness Fixation with screws type 3 Type 4 avulsions, overextensions or OCD – will often show no Recovery in 6-12 months, if under 3yo then good symptoms so don’t have to worry too much if shows up prognosis for athlete incidentally If type 4 lame- small fragments remove, large fragments be conservative or remove Navicular fracture ALWAYS check if bilateral – beware Can repair if acute but poor prognosis – especially for the congenital bipartite navicular bones smaller fragments Cast/ support maybe DJD osteoarthritis fetlock Capsulitis and synovitis → radiographic changes → chips, wear Often bilateral in jumping breeds Block DIP/ coffin joint If chip arthroscopy to remove lines and cartilage Degen Arthroscopy Supportive care Cartilage protectants, HA, IRAP, IA NSAIDs, PRP Controlled exercise to keep nutrients in the synovial fluid 6 weeks to 6 months recovery Solar penetrations Usually metal -depth and site of penetration change everything → Acute lameness Suspecting synovial involvement – Bone injury – ABs mostly simple subsolar abscesses, or a life threatening synovial rads and pic with nail still in. Synoviocentesis if suspect penetration to the nav bursa or infection Synoviocentesis and test fluid coffin joint – give intrasynovial gent while you’re there Distend joint/ bursa and look for tract Arthroscopic lavage and debridement Distend with contrast and see if leaks Pengent good BS combo – IVRP good to concentrate ABs on rads down there Raise heel of shoe Podotrochlear syndrome The new navicular syndrome (which isn’t a thing) Low grade chronic lameness MRI only really – STIR images good Roll toe and raise heel to unload navicular apparatus Erosion of navicular fibrocartilage and DDFt tears, navicular for seeing fluid signal around Intrabursal corticosteroids bursitis or adhesions, impar ligament desmitis, sesmoidian lig inflammation Analgesics desmitis 6 months rest DDFt tears Very common and in combo with other lesions MRI and navicular bursoscopy If fibrocartilage erosion very poor prognosis US?? Torn fibres exude so many inflamm mediators so MUST remove – debride the prolapsed tendon fibres from bursa Raise heel and roll toe to unload DDFt Bone bruising MRI fluid in bone on STIR images Difficult – prevent repeated trauma, rest and farriery, aspirin, biphosphates, months of rest Quittor Infection of collateral cartilages from a penetrating wound Chronic discharging tract proximal to the Poor AB penetration because avascular – topic potassium coronary band (lat or med). iodide may be the way to go Cart horses!! Bc stand on each other Surgical resection of required (complications with coffin joint) Laminitis Colic Inflammation and breakdown of laminae causing hoof wall to Big spectrum: CS and rads repeated to assess Reduce destructive forces so heeled shoe and chop toe if Rhabdomyolysis separate from pedal bone – forelimb more than HL - Pain on hoof testers changes acute, chop toe right back if chronic Bilateral hoof Causes: - Increased DPs Remove inciting cause!! abscesses - Force/ concussion - Swaying back to unload forelimbs and Analgesia and ace (makes them lie down) - Carbohydrate overload reluctant to move, lying down Optimise new hoof growth - Endotoxemia (colic and RFM) - Increased HR Ice slurry, Frog support, SAND! - Underlying metabolic disease - Prolapse of P3 through sole DDFt tenotomy maybe (salvage) Support limb laminitis Excessive weightbearing on good leg causes ischemia to laminae MUST START THEM MOVING  Analgesia of lame leg really important Synovial sepsis (any joint Articular fracture Wound, haematogenous (staph in systemic illnesses) (SEP types) - Lameness – usually broken legged lame Direct palpation Synoviocentesis and put pengent in here right away ofc) - Synovial fluid discharging Imaging – rads and US good ABs alone rarely successful – just delays euth. Use in - Joint distension Synoviocentesis with C and S, combo with IVRP and parentally with following - Wound near joint contrast study treatments – and use concentration dependent ABs Maybe open drainage but poor athletic prognosis Standing lavage High volume lavage via endoscope gold standard Assess recovery with SAA sampling, should decrease, high TP signals poor prognosis THE LIMBS (DM) Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications Ringbone Osteoarth manifestation laying down new bone in response to History- overuse, fracture, deep laceration, OCD, CS, rads and nerve blocks IA medication – corticosteroids, HA, IRAP, Arthramid stress → phalanges remodel and cause OA and chronic pain poor conformation (sloped coronet or offset Corrective shoeing to raise heel, balance foot, roll toe → aiming HIGH - at P1P2 joint (pastern) pastern) here to control the OA LOW – at P2P3 joint (coffin) Surgically- Pastern arthrodesis (HL>FL, fair prognosis), or neurectomy low ringbone (not v good) P2 fracture Plantar/ palmar eminence- usually from subluxation of pastern in Western horse CS Lag screw fixation and cast slid stops Nerve blocks- Maybe arthrodesis Rads Comminuted – trauma. Biarticular and bag of ice Trauma history Rads bag of ice Euth Acute 5/5 lame Maybe trans fixation cast Pastern subluxation Soft tissues disrupted causing severe instability (SDFt and distal Dropped pastern stance Rads Pastern arthrodesis – bone plate and screws sesamoid ligaments) Extreme pain Manage conservatively to end up pasture sound Swelling of joint Pastern OCD Subchondral cysts develop on weightbearing points Lameness Rads IA meds, bute and rest- aim to decrease inflamm and control size Cartilage flap can also be a thing Can be insidious Arthrodesis if severe Transcondylar screw across the cyst Sesamoid fracture Apical Top of sesamoid Usually associated with fetlock hyperextension – Rads and then MUST US suspensory Good prog with surg repair Mid body Halfway thru ses bone put under too much pressure lig – if this is damaged then not worth Surg- cast and 2 lag screws but guarded prog Basal Bottom of ses Acutely lame and swollen surgery Surg but guarded prog Abaxial At SL insertion NO SURG- not articular. Good prog Sagittal Through centre Surg but guarded prog Comminuted (traumatic) Shattered Surg- remove large fragments and repair. Prog guarded Sesamoiditis Adaptive remodelling of sesamoids that cant keep up to training Pain on exercise Rads- will see increased Rest and anti inflamms to allow the bones to return to forces – becomes painful because too slow Swelling heat ? vascularisation strength Fetlock OCD OCD of sagittal ridge of distal cannon - Effusion and increased synovial fluid in Rads (including flexed lateral Screw across cysts and IA corticosteroids Subchondral cystic lesion usually medial condyle a synovial cavity projection) No treatment if sagittal ridge lesion- can wait until From failure of endochondral ossification - Variable lameness- mild to moderate matured, if showing clinical signs arthroscopic removal of - Pain with flexion flap indicated Osteochondral chip Usually at medial dorso-proximal eminence of P1 Mild lameness IA anaesthesia and rads Arthroscopic removal but MUST get to them early – if left fractures of P1 Joint effusion can cause joint damage P1 sagittal fractures Short incomplete – less than 10mm down from sagittal surface 3/5 lame Rads – angle down 10-15 degrees on Stall rest 6 weeks then if still lame go surg with a lag Some effusion DP view screw Joint hot and swollen Potentially CT Can cause chronic lameness and risk of propagation Long incomplete - Propagated down more than 10mm but haven’t NWB lameness Lag screw through- basically wake up sound gone all the way down medially or laterally Joint hot and swollen Complete – to medial or lateral surface Sudden onset severe lameness – 5/5 Internal fixation with lag screws Fractures can spiral - Joint hot, swollen and painful to move Less of a good prognosis because they involve both joints - Crepitus if severe Comminuted Severe lameness – bag of ice Big euth energy If strut of bone spanning the two joints maybe repairable but seriously euthable Proximal/plantar P1 Type 1- articular- Small avulsion fracture May be incidental or cause low grade lameness at Pos to fetlock flexion and blocks out Good candidate for arthroscopy – good prognosis fragments high speed with IA NB Ignore if sound Rads Type 2 – non- articular – manifestation of OC Mostly SBs in the hindlimb Rads Rarely cause lameness – remove and lag screw if so Rarely lame POD – palmar/plantar Repeated hyperextension of legs causes microfractures, cartilage 3-4yo TBs in training IA fetlock anaesthesia Difficult to treat- rest and prevention but a guarded osteochondral disease damage, bone necrosis and lysis of the cannon (MT3/MC3) – - Moderate to severe persistent lameness CT (gold standard) prognosis if severe bone under so much pressure and doesn’t have enough time to - Joint effusion (can be mild) Bone scan -but lots of activity in 3- 4 If seeing flattening of palmar condyles will never race remodel properly - Significant pain on flexion year old bone anyway again - Cysts developing Rads VERY insensitive - Palmar condyles flatten  - Complete wear of sesamoid and cannon cartilage - Secondary sesamoid changes Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications Hygroma Synovial hernia False bursa dorsal to carpus from trauma Often have repeated trauma Palpation and aspiration – localise to Needle drainage then pressure bandage front of joint Inject CS Contrast rad Surgery US to confirm ECR and LDE are ok Prevent- padded stall Carpal chip fracture COMMON SITES: Poor conformation (back at the knee), shoeing Rads Arthroscopy if chip fractures – remove and debride - Distal lateral radius (RC joint) (toe too long), slippery racing surfaces predispose fragments - Distal radiocarpal bone (MC joint) Nsaids acutely and pentosan, cartrophen etc to try to - Proximal third carpal bone (MC joint) preserve the joint (+ IRAP, HA, PSGAG) Fatigue → instability → hyperextension Rest 4-6 months Hyperextension of carpus causes bones to lock and interdigitate – Prognosis related to amount of cartilage involved, create an uneven surface → increased pressure on dorsal carpal radiocarpal (bc more proximal) tends to be better than and distal radius midcarpal Carpal slab fracture Of C3- complete fracture from cortex to cortex – articular surface - 4/5 lame acutely after racing Rads- skyline view Internal fixation to articular surface - Carpal swelling Cast and arthrodesis if comminuted Can be frontal – with 3rd carpal bone - Won’t let you flex carpus Nsaids acutely and pentosan, cartrophen etc to try to Or sagittal – with third and accessory preserve the joint (+ IRAP, HA, PSGAG) Rest 4-6 months 50% will return to racing and good prog for paddock soundness Accessory carpal bone Traumatic – from cortex to cortex Support and stabilise carpus and rest 4-6months fractures Will heal with a fibrous union eventually Usually pasture sound Third carpal bone Third carpal adaptive remodelling not fast enough (same idea as Common in racehorses 2-3yo IA anaesthesia Predisposed to subsequent chip or slab fracture disease POD) → density increases, compliance decreases → subchondral - Reduced performance, shifting FL Bone scan 6weeks to 6 months rest pain lameness Rads- skyline view to see sclerosis Arthroscopy for severe lysis Plus- lots of weight on the medial aspect of FLs - Often bilateral and subchondral lysis of 3rd carpal IA and systemic chondroprotective agents bone The sclerosis will never go back to normal but can remove the subchondral pain Bone Spavin Stress on hock joints – force, concussion causing DJD, OA – Wedges and weighted shoes, cow hock, sickle History and CS Conservative: goal to get pain free activity basically joint degeneration of the hock hock, straight hock predisposes - Positive spavin test on Corrective shoeing – to improve conformation Jumpers, western lameness exam IA CS - Mild HL lameness (often bilateral) - IA nerve blocks Systemic NSAIDs, PSGAG, HA - Reduced performance - Rads to see 4 signs of OA- Surg: not that great - Breaking on turns osteophytes, sclerosis, lysis Arthrodesis of distal hock joints or laser ablation of and joint narrowing cartilage – takes pain away but can still be lame Bog spavin Effusion of tibiotarsal joint from OCD (hallmark sign), synovitis, Varying lameness Rads If just an effusion – CS, HA, IA NSAIDs, cold hosing and trauma or idiopathic Effusion around the hock bandaging to keep the inflamm away Arthroscopy if suspect quiescence OCD Hock OCD Sites: DIRT- distal intermediate region of tibia Causing bog spavin Rads and CS Arthroscopy good prognosis if before arthritis has started Varying lameness Capped hock Gastrocnemius bursitis Acquired bursa over the point of the hock – mainly cosmetic Not usually lame Stop inciting cause! Calcaneal bursitis Drain bursa with needle DDFt sheath effusion Topical and systemic AIs, pressure bandage Curb Soft tissue swelling on plantar aspect of tarsus – retinaculum, Plantar aspect of carpus looks convex US and CS IA topical and systemically – need to break the inflamm plantar lig or SDF Acute lameness with pain on palpation On US: cycle - Desmitis of long plantar REST ligament Inject area with CS if chronic - Tendonitis SDFT Freeze firing – to knock out chronic pain receptors - Inflammation and thickening Prognosis good but can recur of soft tissue generally Tendonitis Acute trauma or accumulated microdamage to fibres or fibrils – Risk factors – conformation, rain or uneven track US- for core lesions 12 months off (stall rest mostly) depending on size of especially forelimb, mid cannon surface, age – anything that can cause lesion – and will never return to full strength (but warmbloods tend to be upper hindlimb) overstraining of the tendon Acute: EARLY DIAGNOSIS AND AGGRESSIVE - Bowed/ swollen tendon look TREATMENT to stop the inflamm response from causing further damage - Cold therapy, Nsaids, tight bandaging - RJ bandage, splint, heel elevation if DDFt involved After 2 weeks – when inflamm has subsided: Intralesional treatment – IGF-1, bone marrow implant, stem cell therapy, PRP Surgery- Tendon stab/ splitting, ligament transection if annular ligament, check ligament desmotomy  Controlled exercise (swimming good) and serial exercise program based on serial US Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications Palmar annular ligament Injury to lig causing thickening and constriction Will see a little bulge over the thickened area (just CS and US IS CS and HA constriction above sesamoids) Nerve blocks Transection of lig - Mild lameness Looked buggered by 65% return to athletic – depends on - Pain on palpation and fetlock flexion chronicity and tendon damage - Notching of ligament palpable Suspensory desmitis Over stretching of the lig – can occur in origin (at top of cannon) STB HLs, TB FLs Nerve blocks Rest 4-6 months or body and can be both or one branch - Dropping of fetlock if significant or both US Controlled exercise branches Positive flexion test Bone marrow implantation - Variable lameness (if 30% fibre loss Rads maybe if worried about PRP with be very lame). avulsion of origin Surgical stab or spitting for branch lesions - Origin lesion 3/5 lame that improves Fasciotomy is chronic with rest then reoccurs Prognosis usually guarded - Pain on palpation and flexion - Swelling and heat Ulna fracture Dropped elbow Rads and CS 3 months stall rest if non- artic and non- displaced (not Limb drags Maybe crepitus that great so prefer surgery) Swelling and pain Support limb in bandage and splint to prevent contracture Loss of triceps function Screws and plates Shoe boil Trauma from heel of show or lying down on hard ground creating Acute pain varying lameness but largely cosmetic NSAIDs Olecranon bursitis a false bursa Needle drainage and CS in lesion Surg drainage En-bloc resection STOP THE CAUSE – pastern ring, bell boots, thicker bedding Sweeny Suprascapular nerve damage (from should trauma, brachial plexus Prominent scapular sign CS and EMG Try to stop too much luxation – stall rest 90d (60% damage or stretch from slipping) → atrophy of infraspinatus and Muscle atrophy recover) supraspinatus muscles Should luxates outwards Surgery if no improvement – release nerve from entrapping fibrous tissue, notch scapular Atrophy will never go away Upward fixation of Stringhalt Medial patella ligament locks over the medial femoral trochlear HL intermittently locked in extension H and CS Exercise program to strengthen quads – rigorous exercise patella Toe drags in thick sand for 6 weeks – 70% cure Not painful just an altered stride Irritate medial patella lig- injectable irritants, surg with stab incision into MPL. Desmotomy as last resort Rupture of peroneus Fibrous band from extensor fossa on distal femur to proximal Can flex stifle and extend hock at the same time US Rest, AIs tertius cannon (linking the hock and stifle) ruptures from overextension Controlled exercise program for 6 weeks of the hock (esp when in a cast) or direct trauma from hitting a jump May manifest as an avulsion fracture in foals Sacroiliac subluxation Trauma causing tearing of the SI lig → instability and pain Reduced performance and acute lameness CS and response to analgesia Rest 3 months Muscle spasm and pain on palpation Inject with cortisone or counter – irritants Hunters bump – asymmetric from behind Will heal enough for sport but bump will stay Infectious airway disease Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications Bronchopneumonia Aerobic: Strep equi subsp zooepidemicus most common, also Predisposing factors Racehorses, stress, viral CBC and biochem This can progress on to pleural effusion and Pasteurella, Bordetella, E.coli, pseudomonas resp disease, long distance transport - Look for neutrophilia pleuropneumonia Anaerobic – take hold as lung gets consolidated (poor prognosis Early signs: Fever (and thus anorexic), quiet, (abscess) and fibrinogen Thoracocentesis if fluid causing breathing problems and if these are here) – clostridium lethargic. inc, albumin dec and to clear bacteria and degenerate cells – makes them more Mycoplasma spp As progresses get clinical toxaemia – MM colour globulin inc comfortable and perfusion, increased DPs, resp signs - Azotaemia if kidneys If abscesses – direct centesis, rib resection to scoop out - Moist soft inducible cough fucked the fibrin - Increased RR Thoracic US – ring down artefacts, Placement of thoracic drain if extensive fluid - Nasal discharge fibrinogen, consolidation, fluid ABs Pleuropneumonia Aerobic: Strep equi subsp zooepidemicus most common, also Predisposing factors Racehorses, stress, viral Tracheal aspirate (infectious cause so - Pen 22000IU/kg BID (BS aerobes) Pasteurella, Bordetella, E.coli, pseudomonas resp disease, long distance transport don’t wash) and C and S – over 50% - Gent 6.6mg/kg SID (BS aerobes) Anaerobic – take hold as lung gets consolidated (poor prognosis Early signs: Fever (and thus anorexic), quiet, neuts sus, over 90% = defs bacto - Metronidazole 25mg/kg BID (anaerobes for if these are here) – clostridium lethargic. URT endoscopy consolidated areas) Mycoplasma spp As progresses get clinical toxaemia – MM colour Rads Anti inflamms and pain relief and perfusion, increased DPs, resp signs Thoracocentesis if fluid - Flunix best 1.1mg/kg (helps with endotox) - Pain over chest and stand with elbows Auscultation – right affected first - PBZ 2.2mg/kg pushed out with bacto - Butorphanol or morphine - Low head carriage Supportive therapy - Tachycardia - IV or enteral fluids - Dull and really painful - Digital cryotherapy Chronically- weightless and ventral oedema PROGNOSIS: Good with aggressive therapy with bronchopneumonia and bronchitis Pleuritis/ pleuropneumonia 40-80% survive and 40-60% return to racing COMPLICATIONS: Abscessation, pneumothorax, laminitis Cryptococcal pneumonia Fungal – cryptococcus gatii should be a ddx in WA Can progress to neuro disease – meningitis PCR Amphotericin B Can be granulomatous or miliary (diffuse) form Cough Neutrophilic monocytosis Fluconazole TTA – C and S For weeks to months! Keep an eye on kidney function Focal areas of consolidated lungs on and any neuro progression US Neonatal pneumonia Usually secondary to sepsis, can also be aspiration pneumonia Usually showing signs of systemic illness if CBC and biochem Ceftiophur best, cephalosporin if worried about kidneys (under 4 weeks) associated (from meconium in utero or milk) septic Blood gas analysis At metronidazole if concerned about consolidated lung - Quiet and lethargic, increase US – consolidation, pleural breaches, Supportive care recumbency, inapetent, reduced suckle ring down from coalescing - O2 reflex URT endoscopy – fluid in trachea, - Bronchodilators - Petechiae** in MM, congested and inflamed airways tacky Rads very helpful – fluid ventrally? - tachycardia Tracheal aspirate - pyrexia over 39 C and S resp: Auscultation wont need RB bag) - nasal discharge Important to rule out rib fractures!! - Cough (but rare!!) - Tachypnoea/ Dyspnoea - Abnormal thoracic auscultation Older foal pneumonia (1- Bacteria! – streptococcus equi sbp zooepidemicus, Rhodococcus - nasal discharge 12 months) equi, Pasteurella, Bordetella, Actinobacillus - Cough (but rare!!) Viral, Fungi, parasites migrating - Tachypnoea/ Dyspnoea Abnormal thoracic auscultation Rhodococcus equi (rattles) Gram + intracellular pathogen of resp macs in soil – enters lungs Usually 3 weeks to 6 months old (because takes CBC and biochem – evidence of Most foals with subclinical lesions recover without by aspiration or ingestion 3 weeks for abscesses to occur) abscessation, mature neutrophilia, treatment - with lesions between 1-10cm – and treating Causes a bronchopneumonia (acute) anaemia of chronic dz, increase these with microbials DOESN’T help them get better - Cough maybe fibrin and globulins, increased SAA faster. Treat only those with lesions above 10cm and a - Nasal discharge maybe US for abscesses temperature. Should screen all foals on far, once a week - Pyrexia almost always TTA- reactive macs and Degen neuts - Macrolide and rifampin combo good UNLESS - Tachypnoea/ dyspnoea depending how C and S resistance much lung involved PCR - Rifampin 5mg/kg PO BIG ON THE extra pulmonary disorders – can Rads to see how much lung affected - Doxycycline 10mg/kg PO  those two work have no resp signs!! together synergistically to penetrate the - GIT signs – colic, D+, wieghtloss abscesses associated with abdo abscesses or Careful of AB side effects- R discolours urine and coat, lymphadenitis Macrolides KILL ADULTs and stop foals thermoregulating Prevention- Plasma infusion! If endemic  - MSK – septic synovitis – lameness from - Limit stocking density immune complex deposition or - Segregate clinical cases bacteraemia - SCREENING!! - Uveitis – IC or bacteraemia Prognosis: poor if multiple EPDs - Neuro signs from spinal abscessation Usually 59-72%, up to 100% with screening Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications Strangles Strep equi sbp equi transmission direct, indirect, survives in Onset 3-14 days after exposure CULTURE!! Typically move severe in younger horses, 10% die from enviro 9 weeks Initially: PCR asphyxiation - Depression and reduced appetite ELISA Subman lymph nodes soften and rupture spontaneously, - Fever – FIRST SIGN retropharyngeal drain thru guttural pouches → - Mucopurulent nasal discharge complications empyema and chondrosis - Pharyngitis and laryngitis Once ruptured can flush and resolve - Cough Treatment: bug sensitive to penicillin but this has poor Later: abscess penetration - Suppurative lymphadenopathy (subman 1- Abscessed LNs but no airway obstruction- want and retropharyngeal) to mature abscesses to express- local therapy, - Purulent nasal discharge flushing, NO ABs, NSAIDs - Dysphagia 2- Early CS (fever and cough) but no LN abscesses - Asphyxiation – swollen guttural – isolate, penicillin, Nsaids to get them to keep pouches eating 3- Exposed animal but no CS – monitor for fever MAYBE pen!!? 4- UNCOMMON Retropharyngeal LN abscesses causing airway obstruction – Penicillin, rifampin justified to help pen penetrate, tracheotomy, US guided drainage Managing: quarantine new horses for 3-14 days, rest pasture 4 weeks CAREFUL OF ASYMPTOMATIC CARRIER- DETAILS IN NOTES Purpura haemorrhagica Immune mediated acute necrotising vasculitis occurring after 1- Vasculitis, petechiation, oedema, fever History of strangles or vaccination CS – dex – to treat vasculitis 2% of strangles cases 2-4 weeks after infection → immune Warm and painful oed Maybe ELISA for M protein Cold hosing and pressure wraps complexes bind to neuts and mast cells causing cytotoxin release Skin biop to confirm vasc ABs to cover antigen release Response to treatment Non- infectious airway disease Pharyngeal lymphoid Chronic inflamm of lymphoid tissues at pharynx/ nasopharynx Usually asymptomatic, but can be: Rarely indicated but maybe improve enviro- control dust, hyperplasia (PLH) Usually young horses, yearlings, horses starting prep - Bilateral nasal discharge let them put head down and graze Most racehorses grade 2 - Regional lymphanomegally - Cough - Rare poor performance Equine IAD – Exposure to irritants, allergic or non- specific reaction → Young racehorses and old performance horses Pulmonary function testing Try to ID early to reduce the amount of airway asthma inflammatory inflammation and airway remodelling→ pulmonary dysfunction - No increased resp effort at rest Tracheal mucus (from a lower remodelling that occurs airway disease - MAYBE: cough, serous nasal discharge, airway obstruction- remodelled) Enviro management! – get out of stable poor performance for >4 wks BALF cyto looking for airway - Improve ventilation - Poor recovery from exercise inflamm – curshmanns spirals - Dampen feed indicate increased mucus - Reduce dust Anti inflamms – reduce inflamm response - Heaves -RAO Exposure to irritants, allergic or non- specific reaction → Very geographical – Europe and north America, Pulmonary function testing corticosteroid (moderate to inflammation and airway remodelling→ pulmonary dysfunction rare in hot dry climates. Usually mature horses Tracheal mucus (from a lower - Inhaled lower risk of side effects- give in am- severe asthma) with genetic involvement airway obstruction- remodelled) dex - Increased resp effort at rest BALF cyto looking for airway - Systemic cheaper and ok – dex or pred Mild- Exercise intolerance inflamm - curshmanns spirals Bronchodilators – counteract bronchoconstriction -probs Moderate: cough, increased RR and effort, indicate increased mucus not needed – just corticosteroids will do the job marked exercise intolerance URT endoscopy, TTW (bc not If borderline – maybe try inhaled CS for a week )dex) Severe: Weight loss, heave line (hypertrophy of infectious), C and S abdo muscles), nostril flare, expiratory dyspnoea Atropine response test if in severe PROGNOSIS- mild to mod can be ok – exercise and distress (and should be good in 15 enviro modified can just have one treatment cycle mins) Seasonal – probs will need treatment forever Severe- Poor if chronic and doesn’t respond to atropine response test Exercise induced Bleeding from caudodorsal part of lungs with high intensity Usually no CS Endoscopy 30-90 mins post exercise Treat underlying IAD pulmonary haemorrhage exercise. Failure of pul capillaries? Pressure waves? Underlying - Epistaxis BAL to ddx acute vs chronic 4-8 weeks rest IAD? Upper airway obstruction? - Swallowing after exercise Race sparingly and in warmer weather - Poor performance ? - Collapse and death Upper resp tract Disease/ syndrome ddx Aetiologic agent/ path process/ explanation History and clinical signs Diagnosis Treatment/ management/ prognosis/ complications False nostril flutter Turbulence in nasal vestibule Nasal flutter No impairment usually resolves with speed Expiratory vibratory noise that resolves with speed Epidermal inclusion cyst Cyst in dorsal nasal diverticulum Not a big deal Can remove for aesthetics Atheroma Progressive ethmoid Encapsulated mass from ethmoid turbinates or within sinus from Intermittent unilateral epistaxis associated with History and CS Surgical excision via bone flap haematoma submucosal haemorrhage → can cause local damage by pressure exercise, brown tinged, low volume Endoscopy for masses Laser ablation necrosis Can induce a sinusitis CT IL injection of 4% formaldehyde 30-50% recurrence rate Primary sinusitis Usually following an URT infection in young horses – acute - Unilateral nasal discharge Percussion If chronic/ medial therapy fails – surgery required to re- onset and unilateral - Malodourous if dental origin Dental exam establish drainage – bone flap Strep equi zooepidemicus - Facial distortion sometimes Endoscopy, rads, trephination for C Most respond to medical treatment – systemic ABs, Secondary sinusitis Sinusitis due to underlying disease - dental (109 r 209), sinus and S, CT placement of a foley catheter via sinus trephination and cyst, trauma, ethmoid haematoma, neoplasia flush with saline BID Anti inflamms to reduce mucosal oed and help drainage Paranasal sinus cysts Usually genetic -fluid filled cysts in caudal maxillary sinus Usually under 1yo or over 9! Rads Bone flap removal of cyst and lining curative - Facial distortion Trephination and aspiration of - Swelling under eye yellow mucoid fluid - Unilateral mucoid nasal discharge - Secondary sinusitis Guttural pouch empyema Pus accumulation in guttural pouches secondary to resp tract Usually younger horses Endoscopy and C and S (check for Medical – ABs- systemic and gel in pouch, lavage with infection –