DCM Exam Flashcards
Compare and contrast the disease caused by the following viruses of cats: Feline Immunodeficiency Virus (FIV), Feline Leukemia Virus (FeLV), Feline Coronavirus (FeCoV)
* Nature of the viral agent that causes each disease
* Pathogenesis of each disease
* Clinical signs of each disease
* Diagnosis of each disease
A five month old cat presents with problems of sneezing, coughing, and weepy eyes. Describe your approach.
i) Questions you would consider importnat to ask the owner
ii) DDX
iii) Diagnostic tests to make a definitive diagnosis
iv) Treatment options
v) Advice to the owner
i) Questions you would consider importnat to ask the owner
When did they get the cat? Any recent changes? Recent medication e.g. corticosteroids? Did it come from a rescue shelter or colony? Multi-cat household? Vaccinated?
ii) DDX
Feline Herpesvirus 1, Feline calicivirus, Chlamydia felis, Bordetella bronchiseptica, Mycoplasma spp., Streptococcus, other viruses
iii) Diagnostic tests to make a definitive diagnosis
Based on history and physical examination.
iv) Treatment options
Dx is usually self-limiting and no specific treatment for viral disease. Supportive treatment (hydration and nutrition). Clean dry mucus and exudate from the eyes and nares frequently. Steamy bathroom or smallroom with vaporier for 15-20 minutes 2-3 x per day. If chronic or changes to severe mucopurulent oculonasal discharge– doxy or amoxicillin. FHV1 suspected? Famcyclovir– reduces viral shedding and may decrease clinical signs. Oral lysine to antagonize viral replication. Check for corneal ulcers– can treat with topical tetracyclines or topical antivirals.
v) Advice to the owner
Trivalent vaccine- FHV-1, FCV, panleukopenia. Come back if does not resolve in 7-10 days or if cats condition deteriorates. Warn that this could periodically occur and it is contagious to other cats in the household. Avoid stress, overcrowding.
A one-year-old Greyhound dog presents to you for the problem of coughing. The dog is unvaccinated. The dog has a temperature of 39.8C and the owner describes the cough as being harsh with retching. Describe your approach to this case: include in your answer possible infectious causes, diagnostic tests you would consider worth running (and why) and treatment options.
1) Approach to this case
** Young so likely infectious instead of heart problem, but cannot rule out until physical exam– so work towards making sure it is truly a respiratory problem– then is it URT or LRT… likely LRT….
Is the cough productive or non-productive? How long has it been going? Recent exposure to other dogs?
Physical exam- particular attention to RR, RE, auscultation noting which lung fields affected if any… MM, pulse oximetry, if you think it is indicated blood gas analysis…. which could lead to oxygen therapy (e.g. PaO2 < 80 mmHg or SpO2 <94%)
2) Possible infectious DDX
* Pneumonia- bacteria, viral, fungal, protozoal, parasitic, aspiration e.g. Bordetella bronchiseptica
* Canine Chronic Bronchitis complicated by secondary bacteria or Mycoplasma infection, CCB complicated by Bronchiectasis
3) Diagnostic tests to run and why
Haematology, cytology and culture- TTW
Thoracic Radiographs- 3 views–> both laterals (to view all lung lobes) & DV (not safe to take VD if dyspnoeic)
4) Treatment options
* Mild- oral antibiotics (amoxicillin)
* Severe/ septic- IV broad spectrum- ampicillin + fluoroquinolone OR aminoglycoside
* Bordetella? Amoxicillin or doxy
* Walk and coupage, change sides every 2-4 hours
* Airway hydration– IV fluids +/- humidify (nebuliser)
** Treat at least a week past resolution
Describe the treatment of infectious tracheobronchitis (kennel cough) in dogs
(Canine adenovirus 2, Canine parainfluenza virus, Canine Herpes, Bordetella bronchiseptica, Streptococcus equi supsp. zooepidemicus)
* Bordetella infection reduces mucociliary clearance by damaging the ciliated epithelium–> secondary bacteria pneumonia.
* most common with dogs of different ages and susceptibility congregate- kennel, vet clinic, dog show
** Most infections are self limiting within 2 weeks and antibiotics are usually not indicated
** rare to develop pneumonia but life threatening
** Vaccines do not prevent infection and none are completely effective in preventing clinical signs, but they will reduce severity of disease
TREATMENT:
* rest for 7 days, avoid exercise/ excitement
* Antitussive if cough is frequent but not used if productive
* Antibiotics are not indicated in most cases unless signs of resp involvement or < 6-8 weeks old as they can quick develop pneumonia (C&S ideally)– doxy for Bordetella and Mycoplasma
** Further investigation if not resolved in 2 weeks
Discuss the common arrhythmias that can occur in canine dilated cardiomyopathy (DCM), and describe how we would attempt to treat these arrhythmias.
* poor contractility of the heart as the primary problem, reducing CO, activating SNS and RAAS, eccentric hypertrophy, loss of myocytes and fibrosis over time. Cardiac enlargement stretches the AV valvular annulus so mitral and tricuspid regurgitation occur secondarily.
* At some stage the myocardial failure becomes so severe the ability of the CV system to compensate is overwhelmed and teh ventricular chambers can grow no larger. Left ventricular end diastolic pressure increases which results in pulmonary oedema (congestive heart failure).
* All of the heart is affected but left sided signs usually predominate (higher pressure system)
* ARRHYTHMIAS are also a feature of the disease– CO reduced and pressure inside the heart are increased even in diastole (at rest). This reduces coronary blood flow and causes ischaemia. Ischaemia and cardiac remodelling with the loss of myocytes and regions of fibrosis in the heart both promote arrhythmias. Atrial tachyarrhythmias can reduce CO and cause acute decompensation. Ventricular tachyarrhythmias can be fatal.
** Conversion to sinus rhythm unlikely so control ventricular rate instead
Atrial fibrillation:
* Digoxin (increase contractility by increasing intracellular calcium), diltiazem (negative inotrope, calcium channel blocker– reduce work on the heart– decreasing HR, contractility, and SV– reduce demand for oxygen and nutrients and increase the window of time for perfusion of cardiac muscle through coronary arteries), beta-adrenergic blocking drugs (same as diltiazem)
Ventricular tachyarrhythmias:
* acute: lignocaine (blocking sodium channels–> decreases the rate of diastolic depolarisation (decreases rate of contractions of the heart)… by raising the depolarisation threshold, the heart is less likely to initiate or conduct early action potentials that may cause an arrhythmia)
* chronic: mediletine (Mexiletine (INN) is a non-selective voltage-gated sodium channel blocker which belongs to the Class IB anti-arrhythmic group of medicines.) + beta blocker (or cats atenolol)
Cardiomyopathies are well recognized in both dogs and cats, but differ considerably between the two species.
a) what are the important pathophysiological differences between canine DCM and feline HCM?
b) In both canine DCM and feline HCM we may, on auscultation, hear gallop rhythms. Explain what this term means.
c) Both canine DCM and feline HCM may present with low grade systolic murmurs. What is the likely origin for this murmur in each case?
d) What are your priorities in the mangement of acutely presenting canine DCM?
a)
DCM-
* poor contractility of the heart as the primary problem, reducing CO, activating SNS and RAAS, eccentric hypertrophy, loss of myocytes and fibrosis over time. Cardiac enlargement stretches the AV valvular annulus so mitral and tricuspid regurgitation occur secondarily.
* At some stage the myocardial failure becomes so severe the ability of the CV system to compensate is overwhelmed and teh ventricular chambers can grow no larger. Left ventricular end diastolic pressure increases which results in pulmonary oedema (congestive heart failure).
* HCM- hypertrophy of the left ventricular free wall and interventricular septum is usually symmetrica–LA enlarged–myocyte hypertrophy and disarray– severe interstitial fibrosis +/- dystrophic mineralisation. Intramural coronary arteriosclerosis is reported in 75% of cats. Chamber stiffness increases– wall does not relax properly in early diastole, allowing less time for the ventricle to fill (and smaller eventually). Reduces SV and CO causing neurhormonal activation… high HR reduce filling further and worsens ischaemia. Cardiac structural distortion can cause anterior mitral valve leaflet to prolapse–> mitral regurgitation–> dynamic outflow obstruction–> further promotion of muscle hypterophy and progressive disease–> higher pressures needed to fill the left compliant ventricle–> fluid is retained, increasing preload–> and higher left atrial pressures so LA enlarges–> ischaemia worsens which worsens relaxation and increases filling pressures further.
b) gallop rhythm from atrial enlargement- presence of S1 and S2 with interceding sound or sounds in diastole. e.g. blood dumpingi nto a stiff left ventricle (DCM) or massive amount of blood dumping in a normal left ventricle in early diastole (e.g. mitral regurg). In cats with HCM, left ventricle is stiff, so both third and fourth heart sounds can be heard– but HR so high usually cannot determine.
c) Mitral valve disease, regurgitant murmur– in DCM due to enlargement of the heart– valve does not appose properly…. stretching of the annulus.
Cats–HCM– anterior mitral valve leaflet prolapses into the left ventricular outflow tract in systole causing mitral regurgitation due to cardiac structural distortion
d) Stabilise first– e.g. check CO signs, dehydration? pre-renal azotaemia? OR are congestive signs predominating? do not vasodilate or suppress respiratory drive with drugs. Oxygen supplementation. IV frusemide– high doses often required as likely to have pulmonary oedema. Consider treatment of arrythmia…. Cockspaniel?? Taurine and L-carnitine!
A dog presents to you with an odd snorting respiratory noise and gagging. There has also been one small episode of epistaxis. Discuss your investigation of this presentation.
* involvement of caudal nasopharynx
DDX
* Primary pharyngeal disease
* Caudal NP foreign bodies
* Post nasal drip
* Discharge from lower resp tract
* Neoplasia
* Fungal infection
History/ Questions:
Blood in faeces?
Unlikely but to be cautious perform CBC with PT and aPTT coag times
** Would then go onto round 2 quickly with retrograde rhinoscopy via soft palate for nasopharynx… prepared to take a biopsy if there is a mass
Pulmonary oedema is one of the expected signs of left sided congestive heart failure. Discuss how you would recognize its presence and severity, and how you would manage it, acutely and chronically.
Findings: severe dyspnoea, tachypnea, weakness, syncope, cyanosis, exercise intolerance, weight loss, coughing from the pulmonary oedema
* complete physical exam– auscultation would initially help determine how severe including degree of cyanosis, degree of dyspnoea, respiratory rate, respiratory effort, blood gas analysis
* IV bolus of frusemide… if RR does nto decrease– continuous rate infusion– titrate down as RR decreases
Chronic management:
* frusemide, pimobendan, ACE inhibitor, digoxin
Atrial fibrillation does occasionally develop in endocardiosis cases, but not commonly. Why might this be so?
Myxomatous degeneration commonly affects the mitral and tricuspid valves in dogs. Chordae tendineae are also affected by the degenerative process, making them prone to rupture. The exact cause is unknown, but in Cavalier King Charles Spaniels and Dachshunds it is an inherited trait. Myxomatous degenerative valve disease is the most common cardiac disease in dogs and accounts for ~75% of cardiovascular disease in this species
Left atrial enlargement promotes the development of atrial arrhythmias such as atrial premature complexes and atrial fibrillation. Due to higher blood volume as body is compensating for regurgitation with RAAS and therefore retained renal sodium and water.. therefore increased work on the heart therefore hypertrophy
What factors are believed to contribute to coughing in endocardiosis patients?
+/- cough depends on the type of heart failure that develops. If it is left sided = pulmonary oedema accompanied with a cough
What duration of survival would you predict for a dog with endocardiosis that has a murmur and mild evidence of decompensation (e.g. reduced exercise tolerance and some coughing)?
2-4 years… once signs of CHF 2-4 months
Explain the term “diastolic failure.” How does it apply in canine DCM?
Diastolic dysfunction is failure of the heart to relax and fill properly. The heart is stiff and poorly compliant. It refers to HCM. DCM is systolic failure- poor contractility.
End stage- end diastolic pressures increase resulting in pulmonary oedeam (congestive heart failure).
What is recommended regime for diuresis in acute pulmonary oedema due to canine DCM?
Frusemide
Clinical signs associated with traumatic coxofemoral luxation. What radiographic features would you assess in your treatment plan?
* Position of greater trochanter- loss of triangle
* thumb displacement test- thumb is placed between trochanter and ischium and the femoral shaft is externally rotated
RG:
- orthogonal views of the pelvis
- look for concurrent fracture
6 month old German Shepherd unilateral forelimb lameness. DDX. Three conditions—main clinical and radiological features
- glenoid dysplasia/ congenital shoulder luxation
* patients hold affected elbow flexed and adducted
* excision arthroplasty of glenoid or arthrodesis
- Osteochondrosis
*lameness or exercise intolerance, joint effusion
* flattening/ concavity of subchondral bone, often with sclerotic margins
* joint mice if mineralised
* subchondral defect and sclerosis in opposing bone surface = kissing lesion
* secondary osteoarthritis
- elbow dysplasia
*incongruence of the elbow joints from : UAP, FMCP, OCD of the medial humeral condyle, elbow incongruity
- ununited anconeal process- failure of fusion through growth plate closure of anconeal process growth plate
*Lameness, pain on elbow manipulation, effusion
* RG: maximally flexed lateral radiograph shows area of lucency between AP and proximal ulna
* Surgical removement of fragment
- congenital elbow luxation
*general joint laxity– different types e.g. type I- caudolateral luxation of the radial head
Diaphyseal fractures of the femur from trauma
List the common techniques used in the repair of these fractures. Pick two and compare their favorable and unfavorable features
*External Skeletal Fixation
* Plate-rod construct
* Interlocking nail (adv- neutral axis ability to resist bending forces acting in all planes, interlocking bolts or screws resists axial collapse and rotation, work best mid-shaft femur, tibia, and humerus, early return to function, absence of external bandages and wound care…disad- all the equip is expensive and specific- need a large inventory, need to ensure screws are appropriate size for dog to prevent premature failure or excessive bone disruption, most practices do not have fluoroscopy though there are methods to place without)
* Locking bone plate (disadvantages screw can jam making removal nearly impossible, screws carry more load and are at higher risk of failing, even more so true with non-locking screws, expensive equipment set up). (Advantages- the limiting factor is no longer the screw being tightened so close to the stripping point– ideal for poor quality bone e.g. osteopenic or thin bone, screw loosening is less likely, as the plate is not compressed onto the bone, periosteal and cortical blood supply are not disturbed)
With a traumatic fracture of the femur, it is a high energy fracture therefore likely there are more than three bone fragments. Dynamic compression plates can be used and buttress plating is performed when there is a large gap between the two main fracture segments, where anatomical reconstruction and load sharing of the bone at the fracture site is not possible. The plate must span the fracture site. Position of the pin in the neutral axis reduces bending and the plate resists axial collapse, rotation, and shear. Other advantages are the pin extends the life of the bone plate up to 10 times to hopefully allow the fracture to heal before the plate fails. Disadvantages
Three clinical conditions in dogs where the nature of boney reaction is often helpful in determining the diagnosis of skeletal problems. Clinical features and radiographical appearance
- Osteomyelitis– depends on the agent and below.
- Osteosarcoma- away from the elbow, towards the knee… rapid progression, worse prognosis. PNB formation– thin brush like, sunburst, amorphous– more aggressive lesions. Edge of lysis if it is poorly defined= more aggressive. Wide transition zone from lytic region to normal bone = more aggressive. Rate of change within 10-14 days, marked = more aggressive. Bone destruction– permeative = more aggressive
- Metabolic bone disease- non-aggressive reaction
* Lesion location, pattern of bone lysis, presence of cortical lysis, pattern of periosteal new bone formation, transition zone, rate of progression
18 month Rottweiler, intermittent, low grade lameness LH 3-4 weeks. Sudden onset of non-weight bearing LH lameness.
DDX
* OCD with secondary OA and a joint mouse causing pain and rapid onset non-weight bearing
* Medial patella luxation
* Osteomyelitis
* Neoplasia
* Panosteitis
Clinical findings that would support diagnosis of cranial cruciate ligament dz
* young dog so history of traumatic event often hyperextension/internal rotation, no OA on radiographs, +/- bony avulsion, positive sit test, pain on stifle manipulation: hyperflexion and hyperextension, effusion, positive cranial drawer test (hold the fabella and patella, other hand fibula head and tibial tuberosity– tibia translated cranially relative to the femur– test in flexion and extension… CAN also do cranial tibial thrust to detect stifle instability)
One suitable repair method—adv and disadv of your choice compared to other methods
TPLO- radial osteotomy made in the proximal tibia and tibial plateau rotated down to 6 degrees, then osteotomy stabilized with specialized plates and screws… flatter tibia, the hamstring muscles (particularly the biceps femoris) can act to stabilize the stifle
* Adv- quicker recovery and improved function, low rates of subsequent meniscal tears, improved longterm function
Disadv-
Six weeks post surgery dog is still lame with discharging sinus at the bottom of his suture line consistent with an infection of implanted materials. List the steps you would take in diagnosing and managing this condition
* Arthrocentesis for culture and sensitivity
* Radiographic imaging to assess lesion
* Management
- Depending on severity of initial lesion radiographically I would initially attempt to conservatively manage by treating with AMs based on C&S (treat empirically first if the RG show it is aggressive). I would use local antibiotics as concerned systemic AMs would not reach the joint at appropriate concentration to take care of the infection.
- I would assess one week later with instructions to bring the dog back if any changes with in that time (febrile, lethargic, etc.)
- If the antibiotics are doing no good and the infection is aggressive– could attempt to surgically lavage the joint… though it would be likely you would need to remove (in this case you would have to replace implanted materials).
Indications for surgical management of pelvic fractures in the dog and cat?
* Fractures affecting the weight bearing axis (sacroiliac joint, ilium, acetabulum)
* Articular (acetabular) fractures
* Significant pelvic canal narrowing (50%) present– if surgery not performed– constipation/ obstipation can be a significant post op complication especially in cats– often have to euthanise as life threatening
* Fractures associated with hernias e.g. pubic fracture associated with prepubic tendon rupture
* Fracture must occur in at least 3 places for significant displacement
* Concomitant soft tissue injury especially the urinary tract e.g. bladder or urethral rupture leading to uroabdomen
* peripheral nerve injury/ impingement e.g. lumbosacral trunk from craniomedial displacement of ilial fractures
The radius and ulna of growing large breed dogs are commonly affected by orthopaedic problems. List four conditions affecting the radius and/or ulna.
For each describe the characteristic RG features and give a prognosis for the owners.
- Congenital elbow luxation- Type I caudolateral luxation of the radial head. Typically large breed dogs. Lameness is mild and diagnosis delayed. Conservative management as often lameness is mild and poor success rate with surgery.
- Angular limb deformities- congenital or traumatic (premature closure of growth plate). Prognosis– Can lead to subluxation predisposing to FMCP and UAP and OA. Dogs do compensate well but secondary issues cause pain and lameness. If patients are corrected before the end of the growth period some of the correction can be lost with ongoing growth but waiting can allow more rapid progression of OA.
- Medial compartment disease
* Fragmentation of the medial coronoid process, OC/OCD of the medial humeral condyle, incongruity*** either ulna osteotomy or coronoidectomy (if mild incongruity)- no studies on prognosis
- Elbow dysplasia– series of conditons that lead to OA– UAP, FMCP, OCD, and elbow incongruity.
*UAP can be caused by short ulna possibly–
* Ulna osteotomy to allow proximal ulna to float proximally– prognosis is good
- Osteosarcoma- poor prognosis as young age, neoplasia tends to be more aggressive
Bouncer
5 yo indoor/ outdoor cat
Cat fight 3 weeks ago
lethargic, not eating
PE: mentation is dull and minimally responsive, BCS 4/9, coat is dull and scruffy, unkempt, dull cardiac sounds, febrile, muffled lung sounds, paradoxical lung pattern
- Sedation, oxygen and no diagnostics at this stage (may not sedate at this stage though)
Cat case– fight– pyrexic, paradoxical breathing
Likely consolidated
Do not put on its side for radiograph
Effusion into the pleural space, we know it is fluid v. air– TFAST is dark. Thoracic radiograph, if it was air you’d expect for it to be lighter… asthma would be train tracks and donuts
Most likely DDX of cat fight, paradoxical, pyrexic
Pyothorax- pyrexic, dull, cat fight, haemothorax– would have bled out and died by now (3 weeks ago)…
- Thoracocentesis & fluid analysis
No wrong answer though or multiple things at once BUT
** Chest drains are more invasive, so they require sedation or GA and so not possible yet as patient is unstable!!!
* Chest tube- bilateral– two tubes is better because adhesions can segregate pockets of pus
Diagnostic of Pyothorax
* Thoracocentesis- removed as much fluid as possible
*fluid sent for C&S- results about 3 days so empirical first (amoxyclav, enrofloxacin(be careful))
Treatment of Bouncer
Bouncer key points
3-5 with ongoing infection or no improvement– CT to look for FBs or anything else, may even go to exploratory surgery
Benson- paradoxical abdominal component of breathing, looks panicked, expiratory sounds.
What do you do next?
- conscious thoracic RGs
- Oxygen and sedation
- Arterial blood gas measurement
- Give furosemide
- oxygen and sedation
** unstable, arterial blood gas is painful so bad idea to do at the moment. Frusemide– he pees more but doesn’t improve. Radiographs– conscious dog too difficult
Benson
Low dose Ace
* Fentanyl- dose dependent resp depression- low dose– but wont do what we wnat
* Medetomidine- minimal resp depression in low doses- reversible!!! Benefit. Decreases CO, so may be a bad idea because what if he is in heart failure– we don’t know right now
* Propofol- GA and IPPV
* Ace-vasodilation- not much resp effect, sedation, may be good for heart if it is the heart, NOT reversible
* Midazolam- no resp effect, anxiolytic, not much sedation, can be excitatory** so may be a bad idea (benzodiazepines)
** BUTORPHANOL (opioid)- first choice for respiratory distress but need sedation- limits our ability to provide good analgesia with pure opioids… think ahead any inkling surgical issue in the next few hours go with a pure opioid… likely something obstructive or lar par but unlikely to go straight into surgery… tracheostomy where you could do local infusion LA… butorphanol is gone within 2 hours
Benson put in an oxygen cage, he looks relaxed.
One issue they get quite hot and CO2. If the dog is too big for the cage, could run out of oxygen.
Most likely DDX?
- URT FB
- Heart failure
- Lar par
- Pneumothorax
- LAR PAR
Heart failure?? but with paradoxical abdominal movement (which makes us think diaphragm problems, URT problems, pleural space problems)
* so heart failure doesn’t really fit
URT FB- inspiratory and expiratory trouble– so could be fixed
* change in bark– one support
Benson
Upper airway exam– do not want to GA at the moment
Patient cooling, dex for upper airway swelling, obtain arterial blood gas
* Thoracic RG if you think there is more going on with the chest but probably difficult to hear due to respiratory effort is so loud
Stabilize him over night, prepare for sedation for laryngeal exam… not ready to be unobserved so would transfer to hospital
* Ketamine- Bensons jaw is tightly shut (because no muscle relaxant given)
* Diaz + Fentanyl- benson bites surgeron
* Medetomidine- wakes up and bites surgeon
** Propofol best option here- slowly and to effect, depth of anaesthesia can change laryngeal movement
- even if they are bilaterally affected
Benson recovery
* risk for aspiration- opioids can induce regurg
NSAIDs– we gave dex last night… so may need to wait 48 hours
3 Aspiration Pneumonia
25 kg dog has had a radial fracture repaired 10 days ago with a plate and screws. Not using the leg. Swollen with small discharge from distal suture line.
List and describe steps you would take to assess this dog and treat the infection.
* Instability at the fracture site predispose to infection
* Must improve the ischemic, necrotic environment and disrupt the biofilm
* Must determine the viability and stability of the bone, virulence and antimicrobial sensitivity of the organism, the condition of the soft tissue envelope
* RG to assess periosteal reaction, amount of bony involvement, pattern of lysis, etc. aggressive or non-aggressive will impact need for rapid more aggressive intervention or allow a more conservative approach
* deep sample for C&S– Jamshidi or FNA
* TX:
- Address instability and remove loose implants
- fracture can heal under infection
- debridement– removal of bony sequestra, necrotic tissue, any foreign material including old implants
- biofilm disruption and destruction
- eliminate dead space, establish drainage… rigid fixation– mandatory
- placement of local AM drug delivery system (beads)
- if implants present infection almost always comes back once antibiotics are stopped, so antibiotics will be required until fracture heals.
** if owner cannot afford prolonged antibiotics, revision surgery, implant removal or cannot commit to prolonged after care– amputation option
*instability from failure to provide rigid fixation
* septic joint can be a factor in prevention union
* incomplete removal of articular cartilage
* lack of autogenous or allogenic bone graft– which increases healing time, which makes the joint more vulnerable to instability and makes premature implant loosening and failure more likely
* Inadequate reduction of adjacent bones can lead to poor bone-to-bone contact, which slows healing
* Results in complete osseous union and an unstable joint with painful ankylosis
Clinical and radiological features of the following conditions in a growing GS dog
- Nutritional secondary hyperparathyroidism
- rare– PTH hyperactivity and elevated PTH levels. Primary from neoplasia or secondary to nutrition or renal– dietary or mineral imbalances. PU/PD, reduced activity and stiff gait, spontaneous fracture of limb and jaw, facial swelling due to rubber jaw
- Blood tests- hypercalcaemia, hypophosphataemia, increased PTH, calcitriol levels may be elevated
- RGs: diffuse osteopenia of the limb and skull and thinning of the cortices, polyostotic (involving many bones) deformities associated with fracture remodeling
- Osteochrondritis dissecans of the humeral head
- one of the conditions that results in the incongruence of the elbow joint leading to OA– part of medial compartment disease
- OCD- flap, thickened cartilage- can show up on a RG as a kissing lesion.
- panosteitis
- RG: thumb-print shaped foci of increased meduallary opacity–> patchy IM opacity–> may extend the entire diaphyseal medullary cavity, lesions eventually resolve
- shifting lameness (different bones affected at different times), presentation 5-12 months, excellent prognosis– rest and NSAIDs
- Describe the methods in which an autogenous cancellous bone graft contributes to bone healing
- From the animal itself- proximal humerus, distal femur, prox tibia, iliac crest, rib
- Osteogenesis- formation of new bone by osteoblasts which survive the grafting process
- Osteoinduction- recruitment of undifferentiated mesenchymal cells present in the graft and the host differentiation into cells of osteogenic and chrondrogenic lingeage
- Osteoconduction- provision of a scaffold/matrix in which these cells can produce new bone
- Osteopromotion- enhance osteoinductivity of other material
- List the DDX for lameness associated with the stifle joint in an immature dog. Diagnostic tests for one of the DDX.
- Cranial cruciate rupture or partial
- Medial patella luxation
- Osteochondrosis (lateral femoral condyle)
- Clinical and radiological features of
- Nutritional secondary hyperparathyroidism
- Common in reptiles
- Poor diet– low Ca:P, vit D def ratio or poor husbandry (lack of UVB light, inadequate thermal provision)
- Anorexia, lethargy, swollen/distended mandible, maxilla or other long bones, pathological fractures, muscle fasciculations and tetany
- Diagnosis requires RG to document generalized demineralization of the skeleton and low plasma levels of 25-dihydroxycholecalciferol.
- Avascular necrosis of the femoral head
- Non-inflamm local ischemia–> necrosis and collapse–> deformation of femoral head and neck–> pelvic limb lameness
- Small dogs 4-11 months
- Chronic progressive lameness
- Radiolucent areas in the femoral head, increases width of joint space, thickening of femoral neck, deformation of the femoral head, OA in chronic cases
- Rupture of the cranial cruciate ligament
- Chronic history of lameness with some acute flare ups or acute traumatic event (depends on the age)
- positive “sit” test
- pain on stifle manipulation- hyperflexion, hyperextension
- Palpable effusion
- Muscle atrophy of the biceps femoris
- Medial buttress may be palpable– deposition of hard fibrous tissue on the medial aspect of the stifle joint
- Radiographic OA can be evident in chronic, effusion in the mediolateral view, compression of the infrapatellar fat pad cranially, periarticular osteophytes
- Pelvic fracture initial management prior to surgery
- Analgesia, assess for haemorrhage- MM pallor
- Ortho/neuro exam
- Palpate for crepitus instability
- Thumb displacement for coxofemoral luxation
- Assess neuro function– sciatic nerve– sensation on digits, withdrawal reflect
- Peroneal- knuckling?
- Tibial n.- Plantigrade stance
- Pudendal n. function- anal tone/reflex
- Cauda equina- tail tone/sensation
- Radiography-
- Orthogonal views
- Conservative management
- Analgesia
- Bladder expression or catheterisation may be required
- Elevated/padded bedding
- Cleaning urine and faeces ASAP to reduce scalding
- Monitoring closely for pressure sores, especially large dogs
- Clinical and radiological features of primary bone tumours in dogs
- Osteosarcoma
- loss of cortical bone, periosteal proliferation, palisading cortical bone (sunburst effect), periosteal lifting caused by subperiosteal haemorrhage, loss of the fine trabecular pattern in metaphyseal bone, and pathological fracture with metaphyseal collapse
- (Other primary bone cancers: chrondrosarcoma, fibrosarcoma, haemagniosarcoma)– FSA and CSA similar RG appearance
- Clinical signs
- Lameness and localised limb swelling
- Distal radius, proximal humerus
- Occasionally pathological fracture
- Osteosarcoma
- Compare and contrast radiological findings that you would expect to see in Canine Mandibular Osteopathy and Hypertrophic Osteodystrophy
- CMO
- Non-neoplastic, proliferative bone disease of the dog with a genetic element 4-7 months old, mouth cannot be fully opened, mandible is bilaterally thickened, intermittent fever
- Mandible and tympanic bullae are thickened and fused by extraossesous bone
- Bilateral and symmetric
- Teeth are normal
- Ankylosis of TMJ (poor prognosis)
- HO
- young, rapidly growing large and giant breed dogs
- Metaphyses of the long bones, mandible, ribs or scapula
- Irregular radiolucent lines are seen in the metaphyses
- Irregular widening of the growth plate may occur with new bone growth
- 6 month old Laborador with forelimb lameness of 3-4 weeks duration
- Osteomyelitis
- Osteochondrosis of the humeral head or shoulder
- Elbow dysplasia
- Glenoid dysplasia
- Angular limb deformity (unlikely)
- RG findings in 3 of the conditions
- Osteomyelitis
- Infection often starts in growth plate
- Soft tissue swelling
- Lysis of bone
- differs from OSA as less actual bone resorption
- chronically- areas of sequestration with dead bone lying in a pocket of cellular debris outlined by a sclerotic border, periosteal proliferative activity can occur and modeling of the entire cortex and endosteum and areas of bone lysis
- Osteochondrosis of the humeral head
- Joint effusion
- Soft tissue swelling
- Flattening/concavity of subchondral bone, often with sclerotic margins
- Joint mic if mineralised
- Subchondral defect and sclerosis in the opposing bone surface = kissing lesion
- Secondary osteoarthritis
- Elbow dysplasia
- Ununited anconeal process- lucency between AP and proximal ulna
- Fragmentation of the medial coronoid process- osteophytosis or subtrochlear sclerosis (lack of sensitivity)– arthroscopy better
- Osteochondrosis dissecans of the medial humeral condyle- flap, thickened cartilage, kissing lesions
- elbow incontruency- uneven alignment of the articular surfaces of the radius and ulna or abnormal shape of the trochlear notch of the ulna– humerounlar incongruence
- Osteomyelitis
- Comminuted mid-diaphyseal fracture of the radius and ulna in a 35 kg dog
- Plate and screws- least aftercare and successful outcome
- Important the plate is used in a buttress fashion to span longer than the fracture as all of the weight must go through the plate until the bone has time to heal
- Comminuted fractures can tolerate relatively greater motion since the strain is applied over a larger SA of fragments
- I would love to use a DCP with a butress plate in a plate rod construct, but would not be able to do this in the radius
- Comminuted femur or humerus
- Dynamic compression plate used as buttress plating. Plate spans the fracture site– no load on the bony column until the fracture fap begins to consolidate with new bone.
- Plate-rod construct with the pin in the neutral axis resisting axial collapse, rotation and shear.
- Oblique fracture of the vertebral body of the first lumbar vertebrae in a Jack Russell
- realignment of the spinal column and decompression of the spinal cord
- This is definitely a case for referral
- Cortical screw with lag technique across the fracture oriented perpendicular to the fracture line
- there are special plates called Lubra plates that are meant to stabilise fractures
- Oblique fracture of the femur
- Cortical screw with lag technique across the fracture oriented perpendicular to the fracture line
- Contour a dynamic compression plate to the lateral surface of the femur
- Hip dysplasia in a 6 month old lab
- Total hip replacement or femoral head and neck excision
- At this stage preventive surgery might still be possible
- Triple Pelvic Osteotomy (TPO)
- Improve femoral head coverage such that subluxation does not occur
- Age 5-11 months old
- Select patient properly- no OA, clinically affected, angle of subluxation is less than 10 degrees, angle of reduction is less than 30 degrees
- Pelvis osteotomized in three places: ischium, ilium and pubis to create a free floating fragment that contains the acetabulum– this is rotated 20-40 degrees to improve femoral head coverage. Stablised with custom stepped plate.
- Triple Pelvic Osteotomy (TPO)
- hip replacement is gold standard uncemented prostheses are coated with porous surfaces to encourage bone growth to result in longer term stability
- FHNE
- following excision fibrous pseudoarthrosis forms which results in a comfortable outcome with reduced range of hip motion
- At this stage preventive surgery might still be possible
- Total hip replacement or femoral head and neck excision
- Simple transverse fracture of the acetabulum in a 1 yr old kelpie
- perfect reduction required
- Greater trochanteric osteotomy typically required +/- transection of internal obturator and gemelli
- K wires placed to keep the fracture in reduction
- DCP plate for stabilitization
- FHNE if necessary
- Hyperextension injury to the carpus in a 5 yr old Newfoundland
- If it is a severe high grade injury- arthrodesis of the carpal joint
- Pan-carpal arthrodesis since these structures are slow to heal and frequently do not attain sufficient strength to support weight bearing if conservative approach is used
- Partial fuse intercarpal and carpometacarpal joint
- Pancarpal if the antebrachiocarpal joint is affected too
- Plate fixation, DCP
- functional– standing angle– measure on contralateral limb or use a table
- Removal of articular cartilage
- Autogenous cancellous bone grafting
- Lameness from the stifle joint in young dogs- three conditions and diagnostic features and treatment options
- Cranial cruciate rupture
- Avascular necrosis of the femoral head
- Osteochondrosis
- Eight month old great dane bilateral forelimb valgus deformity. Describe how you would investigate this case and indicate important issues that you are considering during your work up.
- considering is this congenital or much more likely given the breed– is this due to overfeeding and imbalance of Ca:P… or is it trauma? Ischaemia?
- Radiographs- mediolateral and craniocaudal– likely radius is shortened as valgus deformity
- Overnutrition/ excess nutrients– ask about the diet and suggest changes, if necessary to a commercial puppy diet fed to recommendations on the bag, regardless of the cause
- Are they given vitamins in addition to food?
- Carpal laxity syndrome– balanced diet, applying splints and/or robert jones bandages and limiting exercise to surfaces with good traction
- Describe the clinical and radiological features of fragmented medial coronoid process in a nine month old Rottweiler
- typical age onset between 6 and 18 months
- Disease in the medial coronoid process results in microcracks–> fissures–> fragmentation. Cartilage shows chondromalacia–> fibrillation–> fissures–> erosion
- Likely genetic with environmental factors– possibly trauma
- Clinical signs– forelimb lameness, may be bilateral, muscle atrophy over scapula, may stand with elbows adducted and antebrachium rotated laterally to reduce load on medial compartment, pain on elbow manipulation, effusion, reduced range of motion in chronic cases with OA
- Radiography has a lack of sensitivity– osteophytosis or subtrochlear sclerosis
- Arthroscopy a much better modality to diagnose– can see fragments, fibrillation, fissures,bleeding
- Clinical and radiographic signs of tarsal bone fractures in the racing greyhound. Outline treatment plan and prognosis for return to racing
- RH most common as last to leave the ground on the corner therefore bears all of the dog’s weight (or left MC5 or right MC2
- Lameness and swelling– presents when the greyhound cools down
- Joint fully extended to check for pain on the dorsal surface
- Radiography- different types… Central tarsal bone fracture– type I: dorsal slab fragment minimal displacement all the way to Type 5– comminuted fracture often involving other tarsal bones (medial buttress)
- Clinical signs seen in a dog with generalized Distemper
- Onset within 3-5 days of exposure
- Leukopenia
- Transient fever
- Anorexia
- Serous nasal discharge
- Lethargy
- Mucopurulent ocular discharge
- Gi and respiratory signs
- Encephalomyelitis may occur
- Hyperkeratosis of the footpads and epithelium of the nasal planum
- Clinical syndromes that may develop in a cat persistently infected with Feline Leukaemia Virus
- Anemia, malignancies (Lymphoma, Leukemia), immunosuppression, immune mediated disease, reproductive problems, enteritis, neurological dysfunction, stomatitis
- List the clinical signs, diagnosis and treatment of canine neosporosis
- Subclinical infection
- Progressive hindlimb ataxia associated with polyradiculoneuritis, myositis and muscle atrophy
- Adult dogs may have encephalomyelitis, focal cutaneous nodules, ulcers, pneumonia, peritonitis, hepatitis, myocarditis with use of immunosuppressive drugs
- List the treatment options for a dog with generalized tetanus
- Muscle relaxants
- Tranquilizers
- Sedatives
- Tetanus antitoxin
- Draining and cleaning wounds
- Antibiotics
- List the treatment options for a cat with nasal Cryptococcus neoformans infection
- Longterm antifungal therapy and follow up.
- Surgery or flushing to debulk nasopharyngeal cryptococcomas can bring immediate relief to breathing
- Fluconazole 1-2 months beyond resolution of clinical signs and ideallyuntil the LCAT is negative– can take months to years!!
Pulmonary oedema is one of the expected signs of left-sided congestive heart failure. Discuss how you would recognise its presence and severity, and how you would manage it, acutely and chronically.
** Stability of the patient is paramount when they first present before more intensive diagnostics such as imaging… so I would first assess their difficulty breathing by their clinical presentation– body language, do they look distressed?
* Immediately provide oxygen, ensuring to minimized handling if they are severely dyspnoeic
* When appropriate physical examination and auscultation can give us a lot of clues… as well as breed, we can make the most likely guess that we are presented with LSCHF
* Pulmonary edema: tachypnea, dyspnea, cough
The diagnosis of congestive left heart failure (cardiogenic pulmonary edema) in dogs is classically made radiographically. However, the inability to take a radiograph during a deep inspiration is a diagnostic obstacle. Consequently, the caudodorsal lung fields on a lateral radiograph, where cardiogenic pulmonary edema is usually identified, often have an interstitial density that is either mistaken for pulmonary edema or hides pulmonary edema. This is exacerbated in older dogs. Most dogs with severe pulmonary edema can be identified radiographically, but those with mild to moderate edema are often problematic. In these dogs, it is often beneficial to send the dog home (if it is stable) to have the owner count the dog’s sleeping respiratory rate (SRR). The owner must be taught how to count respiratory (breathing) rate and then count the rate preferably while the dog is sound asleep and in a cool environment. A normal dog has an SRR <30 breaths/min, so a rate greater than that is abnormally high (ie, the dog has tachypnea). All dogs with pulmonary edema have an increased SRR (are tachypneic). However, dogs with respiratory disease/failure can also have an increased SRR. Therefore, once an increased SRR is documented, the dog should be started on furosemide at a dosage of at least 2 mg/kg, PO, bid. If the SRR decreases, then the diagnosis of left heart failure is confirmed.
Acute: oxygen therapy, limitation of stress, frusemide and possibly nitrates
* oxygen cage can be the most hands off, least stressful
* care with continued use of frusemide due to azotemia, severe hypotension, electrolyte depletion and metabolic alkalosis
Chronic:
* frusemide and ACE inhibitors– compromises vasoconstriction of the efferent arteriole and can lead to elevation of serum urea and creatinine– wait 1-2 weeks to decide to give ACE inhibitors
- A one-year-old Greyhound dog presents to you for the problem of coughing. The dog is unvaccinated. The dog has a temperature of 39.8C and the owner describes the cough as being harsh with retching. Describe your approach to this case: include in your answer possible infectious causes, diagnostic tests you would consider worth running (and why) and treatment options.
39.9 is top of normal temperature range in a dog
Canine infectious tracheobronchitis
Collapsing trachea
Canine chronic bronchitis
Feline bronchial disease
Allergic bronchitis
Parasitic bronchitis (
Oslerus osleri)
* pulmonary neoplasia, pneumonia (aspiration or infectious agents)
What is anechoic? What is hyperechoic?
Normal parameters dog and cat
