Exam 1 Flashcards
Lecture 1
Differentiate weakness due to muscle disease and weakness due to neurological disease
Muscle disease - weakness Considerations
-Generally not ataxic
-Postural reflexes are normal (e.g., patellar reflex)
Critical to perform a thorough PE and neurologic exam when presented with a weak patient
-Weakness
-Siff/stilted gait
-Trembling
-Ventral neck flexion (low head carrying)
-Lameness
-Exercise intolerance
-Swelling and pain in affected muscles
-Atrophy or fibrosis, with or without pain in affected muscle
Acquired
- Inflammatory (immune mediated and infectious)
a. Masticatory Muscle Myositis (MMM)
b. Extraocular myositis: focal, specific
c. Canine and Feline Idiopathic polymyositis
d. Dermatomyositis
e. Protozoal myositis (Toxoplasma gondi)
f. Fibrotic myopathy
- Traumatic
- Endocrine/Metabolic
Inherited
- Muscular dystrophy
- CNM of Labrador Retrievers
Masticatory Muscle Myositis
Etiology
History
Clinical Presentation
DDx
Diagnostic Plan
Treatment Plan
Prognosis
Etiology
-Immune mediated disorder
-IgG directed against unique myosin (2M) component of muscles of mastication (Master m., Temporal m., Pterygoid m., Digastric m.)
-Predisposition: large breeds, GS, Doberman, Retrieving breeds.
History
Clinical Presentation
-Early: pain opening the mouth, painful at palpation of masticatory mm., maybe swelling of temporals m. and master m.
-Late: marked atrophy and fibrosis of affected mm.
-Eyes sink into orbit, patient unable to open mouth full range.
DDx
Painful
1. Retrobulbar mass/abscess
2. Dental disease
3. TMJ or bulb disease
4. Neoplasia if unilateral
Non-painful
1. Trigeminal nerve disorder (bilateral disease, dropped jaw)
2. Diffuse polymiositis or polyneuropathy
3. systemic disease: Hypothyroidism, HAC, cancer cachexia.
Diagnostic Plan
-Suspected on clinical findings
-CBS: normal, possible mild anemia, neutrophilia, peripheral eosinophilia
-Chemistry: CK, AST and globulins maybe mildly increased
Circulating 2M antibodies (85-90% positive in acute cases) prior to steroid treatment
Immunohistochemistry on muscle biopsy
-EMG: fibrillations, positive waves, normal is quiet
Treatment Plan
-Glucocorticoids (PREDNISONE) 1-2mg/kg q 12 hours. Tapering dose after initial 3-4 weeks over 4-6 months
-Goal: LED, EOD, may be indefinite
-Commonly reoccurs if tampered too quickly
-Additional immunosupressant if not responsive (Azathioprine, Cyclosporine)
-Dietary management maybe necessary due to limited mouth opening function
Prognosis
-Guarded
Canine Idiopathyc Polymyositis
Etiology
-Presumed autoimmune, diffuse inflammation of skeletal mm. in dogs
-Can be PRIMARY autoimmune or SECONDARY to systemic immune-mediated disease, protozoal, or neoplasia
-Adults affected
-Predisposition: large breeds, GSD, boxers, Newfoundlands, Visuals over represented.
History
Clinical Presentation
-Mild to severe weakness
-Megaesophagus, regurgitation (signs that something else is going on)
-Dysphonia, Dysphagia (weak bark)
-Stiff-stilted gait, may be exacerbated by exercise
-Painful muscles in some dogs
-Prominent atrophy is masseter and temporalis mm.
DDx
-Neoplasia.. think paraneoplastic 2 lymphoma (substances produced by tumor, anal gland carcinoma)
-Systemic Lupus Erythematosus (SLE)
-Toxoplasmosis, Neospora
Diagnosis
-Neurologic exam usually normal unless concurrent polyneuritis
-ELEVATED CK (2-100 fold) and AST
-Elevated gamma globulins
-EMG demonstrates multiple muscle groups affected
-MUSCLE BIOPSY definitive diagnosis
Diagnostic Plan
-CBC, Chemistry, UA, joint taps, protozoal testing, ANA testing, thoracic/abdominal radiographs, ultrasound, fine needle aspirate
-Arthrocentesis
-Even normal size LNs can have abnormal cells and need to be aspirated
Treatment Plan
-Based on Dx findings
-Rule out or treat underlying disease
-Autoimmune diagnosis: PO PREDNISONE 1-2mg/kg q 12 hours, tapering dose at 14 days and 28 days if responding
-May require additional immunosuppressants
-Megaesophagus: elevated feeding, small and frequent meals. Monitor for aspiration
Prognosis
-Varies
-Good if no severe megaesophagus/aspiration
Feline Idiopathic Polymyositis
Profile
-RARE
-Causes diffuse weakness in cats
Very important to rule out common acquired causes of diffuse weakness: hypokalemia and Thiamine deficiency
Clinical Presentation
-Sudden onset of diffuse muscle weakness
-Ventral Neck flexion
-Inability to jump
- +/- muscle pain
Diagnosis
-Neurological exam generally normal
CK AST elevated
70% affected with mildly hypokalemia
-Additional testing for Toxoplasma, FeLV/FIV, thoracic radiographs (Thymoma)
-Muscle biopsy
-EMG: multifocal abnormalities
Treatment Options
**Treat for other more common underlying causes **
-Correct hypokalemia (IV fluids, oral supplementation)
-Treat for thiamine deficiency (IM injections)
-Consider toxin or drug-induced (ex: antibiotics)
-Empirical treatment for toxoplasmosis (Clindamycin) if indicated
Glucocorticoids
-4-6 mg/kg/day
-Tapering over 8-12 weeks
- PO PREDNIDOLONE is preferred in feline patient due to bioavailability. Cats have decreased efficiency of conversion. Less bioavailability
Prognosis
-Spontaneous recovery occurs 1/3 of cases, but recurrence is common
Hypokalemic Myopathy
Clinical Presentation
-Metabolic disorder that affects mainly cats
-Weakness, stiff-stilted gait, exercise intolerance and muscle pain
Diagnosis
-Straightforward with compatible signs
-Potassium <4.0 mEqL
Treatment
-Potassium supplementation and correction of underlying cause
-IV fluids and add Potassium Gluconate (Tumil-K) 1/4 Tsp per 4.5 Kg BW PO BID in food
Dermatomyositis
Profile
-Uncommon inherited autoimmune disease in dogs
-Characterized by dermatitis, vasculitis and polymyositis
-Predisposition: Collies, Shelties, Australian Cattle Dogs, Border Collies
-Skin lesions appear by 3-6 mts of age and may fluctuate
-Erythema, crusts, ulcers, scales, alopecia of inner pinnae on head, face, body
Diagnosis
-High index of suspicion on clinical presentation
-Skin and muscle biopsies
-EMG: spontaneous myofiber electrical activity
Treatment Options
-Oral tetracyclines and Niacinamide orPentoxifylline
-Myositis may require further addition of glucocorticoids when involving the muscle and leading to muscle weakness
-Low stress environment
-Minimize sun exposure
Prognosis
-Variable - overall good but may flair intermittently
Fibrotic Myopathy
-Non-painful disorder
-Characterized by the formation of fibrous band within the muscle
-Likely due to repetitive muscle injury
-Excessive jumping/sprinting can lead to inflammation, hemorrhage, edema, fibrosis in the affected muscles
-Predisposition: GSD, any breed
Clinical Presentation
-Mechanical lameness in the affected limb
-Neurologically normal
-Can palpate a tight, usually non-painful band within the affected muscle
Gracilis and semitendinosis muscles quadriceps, biceps femoris, and semimembranosus (pelvic limb); suprastinatus and infraspinatus mm. (thoracic limb)
Diagnosis
-Based on characteristic lameness and palpation of fibrotic band
-Ultrasound of affected muscle
Treatment Options
-Surgical approaches are described but recurrence is high
-Management through physical conditioning, rehabilitation, pain control as needed
Prognosis
-Guarded, usually not cure
-Quality of life and function can be good in affected patients
Acquired Myopathies - Endocrine/Metabolic (common)
-Glucocorticoid excess/deficiency
-Hyper or Hypo adrenocorticism, resp.
-Hypothyroidism (dogs)
-Hypokalemia (especially in cats)
-Hypocalcemia (especially postpartum)
-Thiamine deficiency (cats)
Postpartum Hypocalcemia
-Nutrition-associated
-Hypokalemic muscle weakness
-Ventral neck flexion
Treatment
-IV fluid and potassium administration
Hypocalcemia postpartum tetani AKS
Clinical signs
Intermittent tremors, painting, painful muscle twitching, disorientation, panting, Eclampsia-tremors
Tetanus
-Sustained contraction of extensor muscles
-No muscle relaxation
-Dogs»_space; cats
-Gram POSITIVE anaerobe Clostridium tetani
-Horses most susceptible, birds less susceptible
Clinical signs
-Appear 5-10 days after wound infection
Treatment
-Wound debridement
-Penicillin
-Antitoxin
-Control muscle spasm
Not a disease of the muscle
“Risus Sardonicus”
-Contracture of the facial muscles if localized “frowned look”
-Saw horse stance if generalized
Inherited Myopathies
-Muscular dystrophy
-Centronuclear myopathy (CNM) of Labrador retrievers
-Myotonia
-Inherited metabolic myopathies
CNM of Labrador Retriever
Inheritance
-Autosomal recessive
Gender
-Both
Clinical signs
-Stiff/stilted gait
-Bunny hopping
-Muscle atrophy
-Poor conformation
Tendon reflexes
-Often reduced
CK levels
-Normal to elevated
Therapy
-L-carnitine supplementation
-Avoid cold.stress/excitement
Prognosis
-Guarded
-Disease often stabilized by 1 year of age
-May have acceptable quality of life
Muscular Dystrophy of Labrador Retrievers
Inheritance
-X-linked
Gender
-Mostly Male
Clinical signs
-Stiff/stilted gait
-Dysphagia
-Tongue hypertrophy
-Ptyalism
Tendon reflexes
-Normal until end stage
CK levels
-Markedly elevated
Therapy
-None
Prognosis
-Poor due to progressive disease
Muscular Dystrophy in Cats
Profile
- X-linked in DSH, Maine Coon, Siamese
Clinical signs
-Appear at 5-6 mts of age
-Marked muscular hypertrophy
-Protruding tongue
-Stiff/stilted gait
-Bunny hopping
Diagnosis
-Muscle biopsy
**Markedly elevated CK >30,000 IU/ML
-Immunohistochemistry
Extraocular Myositis (FYI)
Profile
-Myositis confined to extraocular mm. in dogs
-Bulging eyes
-Predisposition: Golden Retrievers, Labradors, Large breed dogs, females
Lecture 2
Clinical Manifestations of and Diagnostic Test for Joint Disorders
General Considerations
-Animals with joint disease commonly present with a history of lameness or gait abnormality
-Lameness may involve ONE joint/limb or MULTIPLE
-Typically traumatic or developmental if ONE joint
-Typically degenerative or inflammatory if multiple joints involved
General Considerations
Inflammatory
-Suppurative cells: neutrophils
-Infectious: Borrelia burgdorferi, Staphylococcus, Ehrlichia spp., Pasteurella multicocida in cats.
-Non-infectious
Erosive: Rheumatoid-like arthritis, Erosive polyarthritis of Greyhounds
Non-erosive: IMPA, SLE, Reactive polyarthritis. Most common in dogs.
Non-Inflammatory
-Non-suppurative cells: mononuclear cells
-Developmental: UAP, FCP, OC/OCD
-Degenerative: hip dysplasia
-Neoplastic
-Traumatic processes
General Considerations
Inflammatory Joint Disease
Inflammatory Joint Disease
-Very painful joints
-Shifting leg lameness “walking on egg shells”
-Reluctance to exercise or move
-Multiple joints usually affected: as many as 25% of dogs with immune mediated polyarthritis DO NOT have obvious pain or swelling
Signs of systemic disease
-Fever, lethargy, inappetence, weakness, stiffness, exercise intolerance
General Considerations
Non-inflammatory Joint Disease
Degenerative
-Low-grade chronic discomfort
-Fluctuating/intermittent lameness
-Reluctance to exercise
-NO SYSTEMIC signs
-Multiple joints may be affected
-Signs are usually consistent from day to day
-Patient often “warms” out of lameness
PE
-Conduct physical examination to localize a region of pain or inflammation
-Animal’s posture and gait
-Manipulate and palpate the spine and muscles, bones, and joints of each limb
-Give equal consideration to systemic examination (e.g., auscultation and abdominal palpation).
PE - DDx for pain upon palpation
-Bones: trauma, panosteitis, hypertrophic osteodystrophy, osteomyelitis, bone neoplasia
-Muscles: myositis, strain/sprain injuries
-Neck: spinal cord or vertebral abnormalities such as IVDD, intracranial disease, meningitis, polyarthritis
-Spine: spinal cord or vertebral abnormalities, IVDD, diskospondylitis, intervertebral facet joint inflammation
PE - Decreased range of motion, crepitation and joint instability suggests:
-Articular damage and wear
-Osteophytes (Bone spurs, or osteophytes, are smooth, bony growths, usually near joints, develop over time in patients with arthritis or joint damage).
-Peri-articular changes
-Tendon/ligament damage
Enthesophytes, Osteophytes Reminder
Osteophytes can be defined as lateral outgrowths of bone at the margin of the articular surface of a synovial joint. An enthesophyte is a bony spur forming at a ligament or tendon insertion into bone, growing in the direction of the natural pull of the ligament or tendon involved.
Diagnostic - Imaging
Radiograph
-For initial diagnosis
-Two views minimum
-Only one joint clinically affected or crepitation, instability or restricted range of motion
-Abnormalities of joints, DJD, chronic septic arthritis, and erosive immune mediated arthritis
If presumed IMPA, NOT recommended if the response to treatment is rapid and complete. Abnormalities seen are mild joint capsule distention and soft tissue swelling
-Radiographs of infectious polyarthritis typically only demonstrate soft tissue swelling and effusion.
CT
MRI
Ultrasound
Radiographs
CT Imaging
Ultrasound
Blank
Diagnostics
Arthrocentesis/synovial joint fluid analysis
-Minimal risk
High diagnostic yield
-Sedation for dogs, general anesthesia for cats
-If Polyarthritis is suspected, fluid should be analyzed from at least 3-4 joints, including at least one carpus, one hock, one stifle.
-Sterile procedure
-Only very small amount of joint fluid (1-3 drops) is needed for determining viscosity, estimated cell count, differential WBC count, and culture
-Larger volumes are required for a cell count
Always aseptically prepare and wear gloves
Synovial Smears
-Should be prepared immediately: one drop of synovial fluid is placed onto each slide, a second is used to make a smear
-Additional drops of synovial fluid should be submitted for culture and sensitivity
Normal synovial fluid
-Thick, viscous fluid secreted by synovium
-Clear to slightly yellow in color
-High content of hyaluronic acid and additional molecules such as LUBRICIN
-Primary function is to lubricate articular surfaces and facilitate movement with the joint
No more than three WBC per high-dry power field (40x)
-Mixture of large and small mononuclear cells
** <10% neutrophils**
-Blood contamination = 1 neutrophil/500 RBC
Case
Synovial Fluid cytology chart
Other tests to rule out systemic disease
-Radiographs - chest, abdomen
-Bloodwork - tick-borne disease panels, immune panels (ANA, LE, RF)
-Cultures - Blood, urine, bone
Lecture 3
General Considerations Joint Disease
Non-inflammatory
Inflammatory
Non-inflammatory
-Developmental
-Degenerative joint disease (DJD) - most common
-Cytology: macrophages, mononcytes
Inflammatory
-Infectious: treated with antibiotics
-Immune mediated - non-erosive most common
1. Primary idiopathic
2. Reactive polyarthritis: secondary to something else going on
Common Infectious DDx
Dog
-Distemper
-Bacterial (Gram negative) Staphylococcus, Streptococcus (most common)
-Mycoplasma, bacterial L-forms (Tetracyclines Tx)
-Borrelia burgdorferi
-Leishmania
-Tick-borne: Ehrlichia spp, Rocky Mountain spotted fever, Anaplasma spp.
Cat
-Calicivirus (polyarthritis, oral ulcers)
-Feline syncytium-forming virus
-Feline infectious peritonitis
-Bacteria Pateurella multicocida, other (anaerobes)
-Mycoplasma, bacterial L-forms
General Considerations DJD
-Chronic progressive disorder of joints
-Articular cartilage damage and degenerative proliferative changes in the periarticular tissues
-Any breed (C/F), any size and age can be affected
Joint instability, trauma and developmental orthopedic diseases are the most commonly identified underlying causes
-Estimated 20% of canine population are affected. Periarticular elbows and hips
-Behavioral changes: can’t jump anymore
Clinical Signs
-NO SYSTEMIC signs
-Insidious onset of signs confined to the musculoskeletal system
-Low grade lameness, stiffness, sometimes only after exertion, muscle atrophy
Prevention and Treatment
Think Multi-modal
-Weight management: overweight/obese BCS associated with joint incongruity, negatively affects normal movement. Chronic pain and dysfunction.
-Exercise and physical fitness
-Pharmaceuticals
-Physical rehabilitation: water therapy
-Complementary therapies: dietary supplements, Omega3
Pharmaceuticals - NSAIDs
Arachiodonic Acid
Cox-2 vs. Cox 1 Inhibition
Firocoxib
Robenacoxib - Cats
Deracoxib
Carprofen
Meloxicam
Etodolac
Ketoprofen
Tepoxalin (off the market now)
Pharmaceutical - NSAIDs
-Grapiprant (Non-Cox) : PGE2 EP4 receptor antagonist
-All NSAIDs have the potential to cause GI side effects ranging from gastric ulceration to erosion
-Cox-1 sparing NSAIDs are associated with 50% less GI ulceration in humans and animal studies
Use NSAIDs Judiciously
-Dehydrated
-Hypotensive
-Geriatrics with comorbidities
Managing OA in Cats
Cats lack a certain type of enzyme, called hepatic glutathione-dependent enzyme, which helps metabolize or break down many NSAIDS in the body. This means that toxic levels are allowed to build up within your cat, causing damage to vital bodily organs.
-Roebenacoxib
-Meloxicam
-Use judiciously as part of multimodal therapy
Pharmaceuticals - Other analgesics
Opioids
-For Acute pain
-Not long term
-Butorphanol (mild to moderate pain)
-Methadone
-Hydromorphone
-Buprenorphine
-Morphine
-Tramadol
-Fentanyl
Cerenia prior to opioid to prevent emesis
Pharmaceuticals - Other analgesics
Novel Adjuctives
-Ketamine CRI - NMDA receptor inhibitor
-Amantadine - NMDA antagonist
-Amitriptyline - TCA with pain modulating
Gabapentin - associated with NMDA receptors
-Lidocaine (transdermal patches or liposomal encapsulated lidocaine cream)
Other Therapeutic Agent
Joint Injections
-Stem cell therapy
-Platelet rich plasma (PRP), autologous conditioned serum
-Hyaluronic acid
-Corticosteroids
Not great long term results
Synovetin - OA
-Uses radio-synovi-orthesis to break the cycle of pain and inflammation for chronic OA patients
-Novel radioisotope (tin-117m) is injected into the joint, engulfed by macrophages and synoviocytes, which causes apoptosis
92% success
-Can last 1 year!
Solensia (Frunevetmab injection) Cats/Dogs
-Newest OA drug
-MOA: anti-NGF monoclonal antibody once monthly injection
-Anti-nerve-growth factor
Septic Arthritis
Route of Infection
-Hematogenous
Direct inoculation: penetrating joint wounds are common, often resulting in single joint infection
-Spread from local, adjacent tissue
-More common in large breed male dogs
Staphylococcus spp., Streptococcus spp., and Colifrom organisms are most common in dog
Pasteurela multicocida most common in cats
Diagnosis
-Radiographs of affected joint
-Aerobic and anaerobic cultures of joint fluid
-Arthrocentesis with joint fluid analysis
-Additional tests as dictated by case - thoracic/abdominal imaging, UA with culture, blood cultures
Treatment
-Goal is to rapidly resolve infection, decrease inflammatory compounds in joint (enzymes, fibrin)
-Start antibiotics as soon as cultures are collected
-Initial choice: BROAD SPECTRUM, beta-lactamase resistent antibiotics (e.g., cephalosporin, clavamox).
Treatment
-Medical management with caution
-Chronic infections, foreign bodies, immature animals with open growth plates should have immidiate surgical management
Tick-borne Polyarthritis
Dx: IDEXX 4Dx Snap test, Tests for antibodies (C6 peptide) Does not react with vaccine induced antibodies
-Borrelia burgdorferi
-Spirochete related to Leptospira and Treponema bacteria
-Worldwide distribution
-90% of Lyme disease northeastern US
-Most dogs are asymptomatic
-No breed, sex, age predilection
Lameness and/or myalgia most common signs in dogs
-Acute onset with lethargy, inappetance, +/- fever, lymphadenopathy
Joint inflammation in one or more joints, painful on palpation
-Affected joints characterized by marked FIBRIN effusion, NEUTROPHILIC infiltration, thickened synovial membranes
-Lymphocytes and plasma cells replace neutrophils in chronically infected joints
Treatment
-History: recent exposure in endemic region
-Clinical signs
-Positive serology
-Prompt response to antibiotic therapy
-Dogs may respond within 24-48hrs of antibiotic therapy
Acute infections
-Tetracyclines (e.g., doxycycline, 10 mg/kg, q24 hrs)
-Lactams (e.g., amoxicillin, 20 mg/kg, q8 hr)
Chronic/refractory cases
-Azithromycin (5mg/kg, q12 hrs)
-3rd generation Cephalosporins (e.g., Cefriaxone, 20mg/kg, q12 hrs)
Steroid Therapy
-Should be used with caution
-Low dose anti-inflammatory doses only
-Immunosuppressive doses exacerbate infection
NSAIDs
-May be used for pain relief from arthritic complications, with the usual cautions of monitoring for GI and renal side effects
Tick-borne Polyarthritis
Rickettsial
-Rocky Mountain Spotted Fever
-Ehrlichia canis
-Ehrlichia ewingii
-Anaplasma phagocytophilum
Polyarthritis largely due to immune complex deposition in synovial membranes
Vasculitis, systemic disease association possible
-CBC abnormalitites, thrombocytopenia
Dx
-ELISA test
-PCR to confirm
-Response to therapy
-Fourfold rising IgG titer over 2-3 weeks
-Joint taps with cytology may be useful, especially during acute phase when serology is still negative
Treatment
-Tetracyclines (e.g., Doxycycline) for 3 or more weeks
-Concurrent glucocorticoid therapy (PREDNISONE, 0.5-2mg/kg PO q24hrs) if antimicrobial therapy alone does not eliminate the fever, lameness, and joint swelling.
Feline Polyarthropathy
Mycoplasma gatae and Mycoplasma felis
-Bacterial L-form secondary to bite wounds
-Septic arthritis secondary to foreign bodies or bite wounds
-Transient polyarthropathy associated with Calicivirus following vaccination of kittens
**Always rule out FeLV/FIV
Reactive Polyarthropathy
Reactive polyarthritis accounts for 25% of all non-erosive immune-mediated polyarthritis cases
-Chronic bacterial, fungal, or Rickettsial infections
-Neoplasia
-Drug induced (e.g., Trimethoprim-sulfa, Phenobarbital, Penicillin)
-Numerous systemic diseases (e.g., endocarditis, heartworm disease, pyelonephritis)
Idiopathic Immune-Mediated Non-Erosive Polyarthritis
Diagnosed ONLY by Ruling out other causes of polyarthritis and it’s the most common form of polyarthritis in the dog.. NOT CATS
Clinical Signs
-Cyclic fever
-Stiffness and lameness
-Multiple joints affected
IMPA
Diagnosis
-Synovial fluid analysis
-Failure to ID other infectious causes
Treatment
-Empirical treatment with Doxycycline while awaiting the results of synovial fluid cultures
Rapid and complete response to antibiotics makes it unlikely IMPA
**Cornerstone of therapy: PREDNISONE 2mg/kg q12 hrs for 3-4 days, 2mg/kg for 14 days if improving decrease dose by half every 4 weeks
-Additional immunosuppressants such as Azothioprine might need to be added
Lecture 4
Developmental Orthopedic Diseases
Most common developmental orthopedic diseases in dogs
- Hip dysplasia
- Elbow dysplasia
- Medial Patellar luxation
- Shoulder Osteochondritis Dissicans
- Panosteitis
Canine Hip Dysplasia (CHD)
Profile
-Multifactoral disease with genetic and environmental factors
-Factors can be coxofemoral joint laxity in affected dog, which leads to long term osteoarthritic changes within the joints
Pathophysiology
Proposed Causes
1. Primary joint laxity due to abnormal collagen type or fibers development in the joint capsule and ligament of the femoral head
2. Abnormal endochondral ossification of the acetabulum resulting in joint incongruency, joint effusion, and secondary subluxation and laxity
PennHip Distraction Index (Gold Standard)
OFA extended Hip view
Treatment
Medical
-Weight control - maintain lean body
-Exercise, low impact, strengthening and proprioception
-Surgery - TPO (triple pelvic osteotomy); Total Hip Replacement, FHO (femoral head osteotomy)
-Manage osteoarthritis
Prevention
-Selective breeding
-Promote slow, steady growth rate in puppies to achieve lean body condition
Elbow Dysplasia
-Ununited Anconeal Process (UAP)
-Medial Coronoid Disease or Fragmented Coronoid Process (MCP or FCP)
-Osteochondrosis of the Humerus (OCD) of medial humeral condyle
-Most patient are affected by only 1 or 2 of these conditions at the same time
Causes
-Multifactorial: genetic and environmental
-Dogs present with unilateral or bilateral lameness or stifness of the forelimbs with effusion, pain, and decreased range of motion of the elbow
Pathophysiology
- OC/OCD: disturbance in endochondral ossification, leading to a region of abnormally thickened cartilage, resulting in ischemic necrosis, flap formation (e.g., OCD).
- MCD (FCP) may be caused by abnormal load distribution across the elbow joint, caused by various joint incongruities, which lead to pathologic lesions affecting load-bearing joint surfaces.
- UAP hereditary abnormality in the growth plate leading to incomplete fusion of the anconeal process of the ulna
-Subsequent instability in the elbow may lead to fracture of the UAP and secondary arthritic changes
Treatment
Medical Management
-Weight control - maintain lean body mass
-Exercise - low impact, strengthening and proprioception
-Surgery - arthroscopy, arthrotomy
-Manage osteoarthritis
Prevention
-Selective breeding
-Promote slow, steady growth in puppies to achieve lean body condition
Medial Patellar Luxation
-Abnormal angular limb structure and forces result in medial displacement of the quadriceps mechanism
-This muscular displacement results in abnormal forces that predispose the patella to luxate medially
-Small breeds are predisposed, although it does affect some large breeds
Akita, Sharpei, Great Pyrenees
Pathophysiology
Coxa vara (e.g., decreased angle of inclination of the femoral head) and diminished anteversion angle (e.g., less cranially oriented) of the femoral head, results in medial displacement of the quadriceps mechanism
-Patellar luxation is graded from 1 to 4, depending on the frequency of luxation and difficulty of manual reduction
Complex skeletal abnormalities affecting the overall alignment of the limb, including:
-Abnormal conformation of the hip joint, such as hip dysplasia
-Malformation of the femur, with abnormal angulation and torsion malformation of the tibia
-Deviation of the tibial crest
-Tightness/atrophy of the quadriceps muscles, acting as a bowstring
-A patellar ligament that may be too long
Treatment
Medical management
-Weight control - maintain lean body
-Exercise - low impact, strengthening, and proprioception
-Surgical correction
-Manage osteoarthritis
Prevention
-Select breeding
-Selected exercises for Grade 1-2?
Osteochondrosis Dessicans (OCD)
Shoulder OCD
-Multifactorial, genetics, environmental factors (e.g., high protein diets, calories, calcium)
-Large breeds are most commonly affected, usually presenting with unilateral or bilateral forelimb lameness between 4-8 mts of age.
Panosteitis
-Self-limiting inflammation of the bone marrow in long bones
-Large breed dogs, particularly German shepherd dogs are commonly affected, although smaller breeds can also be affected.
Males seem to be affected more frequently than females
-Most patients are between 5-12mts of age
-Range 2mts to 5 yrs of age
Pathophysiology
-Etiology unknown
Involves the diaphyseal and metaphyseal regions of long bones
-Lesions include medullary fibrosis, and endosteal and subperiosteal bones deposition.
Panosteitis Treatment
Medical Management
-NSAIDs for pain management
-Allow patient to self-limit exercise but encourage low impact movement
-Generally, resolves in 3-5 days
-May recur in different leg at a later time Shifting leg lameness
