ANZCVS 2019

Question 1

a) State the most common reported signalment of cats that are diagnosed with idiopathic megacolon. Name two (2) additional causes, other than idiopathic, of feline megacolon.

Answer 1

• Signalment: Overweight, middle-age to early senior
• Additional causes:
1. Previous pelvic fractures with narrowing of the pelvic canal
2. Tumors partially blocking the colon
3. Neurologic impairment – typically LMN disease affecting the pelvic plexus
4. Colonic strictures
5. Anal atresia
6. Foreign bodies

Question 2

• List and justify appropriate immediate treatments for managing a cat presenting for the first time with feline megacolon.

Answer 2

1. IV fluid therapy: Patients with megacolon are frequently dehydrated by the time they present to a veterinary hospital. Dehydration contributes to further desiccation of colonic contents and poor motility.
2. Enemas: Necessary to remove the colonic obstruction, relieve discomfort and minimize the absorption of potentially toxic colonic waste. Also necessary to minimize further stretching of colonic smooth muscle and worsening of colonic motility.
3. Analgesia: Colonic distension and the often-necessary manual removal of feces can be painful (even though the procedure is performed under general anesthesia). Appropriate analgesia can be provided with a partial u-agonist (buprenorphine) with minimal deleterious effects on colonic motility.
4. Antibiotic therapy: Rarely necessary for stable cases of megacolon, but should be considered for severe cases associated with shock or SIRS.

Question 3

• Briefly discuss appropriate longer term medical management options for feline megacolon.

Answer 3

1. Correction of underlining cause (if possible): Pelvic obstructions caused by previous fractures, tumors or hernias must be corrected whenever possible. This does not apply to idiopathic megacolon.
2. Fiber-enriched diet: Considered by many the most important aspect of medical management of megacolon. Prescription diets supplemented with soluble and insoluble fibers (i.e. Royal Canin GI Fiber Response) improve fecal matter moisture and stimulate colonic motility.
3. Prokinetic drugs: parasympathomimetic drugs like cisapride can stimulate colonic motility and improve frequency of defecation. Metoclopramide is a centrally-acting antiemetic which decreases nausea and also has mild motility-promoting effects.
4. Fluid supplementation: Delivered in the form of water fountains to stimulate water consumption or subcutaneous infusions. Maintenance of adequate hydration is extremely important to prevent desiccation of colonic contents.
5. Lubricating enemas: Sodium docusate and lubricating enemas can be used sporadically or regularly to help maintain regular defecation.
6. Laxatives: lactulose

Question 4

c) Describe the blood supply to the terminal ileum, caecum, colon and rectum in the cat. You may use an appropriately labelled diagram.

Answer 4

• The ileum and cecum receive arterial blood supply from the ileocecal artery, a branch of the cranial mesenteric artery (Cr mesenteric A.). Venous drainage is provided by the Ileal + cecal Veins > ileocolic V. > Cr. mesenteric V. > Portal V.
• The ascending colon receives arterial blood supply from the right colic artery, a branch of the Cr mesenteric A. Venous drainage is provided by the right colic V. > Ileocolic V. > Cr mesenteric V. > Portal V.
• The transverse and proximal descending colon receives arterial blood from the Middle colic artery, a branch of the Cr. Mesenteric A. Venous drainage is provided by the Cr. Rectal V > left colic V. > Cd. Mesenteric V > Portal V
• The descending colon receives arterial blood from the Left colic artery, a branch of the Cd. Mesenteric A. Venous drainage is provided by the Cr. Rectal V > left colic V. > Cd. Mesenteric V > Portal V
• The proximal 1/3 of the rectum receives arterial blood from the Cranial rectal A, a branch of the Cd mesenteric A. Venous drainage is provided by Cr. Rectal V > left colic V. > Cd. Mesenteric V > Portal V
• The middle and distal rectum receive arterial blood from the Right and Left caudal rectal arteries, both branches of the Internal Pudendal A. Venous drainage to the Cranial rectum provided by Cr. Rectal V > left colic V. > Cd. Mesenteric V > Portal V. Venous drainage to the middle and caudal rectum is provided by Caudal rectal and Perineal veins > Internal Pudendal V > Internal Iliac V > Caudal Vena Cava

Question 5

d) Describe the physiological benefit of preserving the ileocolic junction when performing a subtotal colectomy. Include in your answer the consequences of removal of the ileocolic junction.

Answer 5

Preservation of the ileocecal junction is thought to prevent bacterial translocation from large to small intestines, which may contribute to malabsorption syndrome. Preservation is thought to minimize post-op diarrhea.

Question 6

e) State two (2) reasons why resection of the ileocolic junction may be necessary when performing a subtotal colectomy in cats with idiopathic megacolon.

Answer 6

• Inability to achieve a tension-free colocolic apposition

* Gross proximal colonic distension, cecal inversion or neoplasia

Question 7

f) Describe the healing of the colon and include an appropriate timeline for the healing process. State how this healing differs from that of the small intestine.

Answer 7

The healing of the colon can be academically divided in three partially overlapping phases:
1. Lag Phase (inflammation and debridement): First 3 to 4 days. Characterized by hemostasis, cell migration, debridement, and fibrin meshwork formation. Platelet-derived activation of COX converts arachidonic acid into inflammatory mediators such as prostaglandins, prostacyclines and thromboxanes. These substances promote vasodilation and chemotaxis of phagocytic cells like neutrophils and monocytes. Monocytes exit blood vessels via diapedesis (cellular extravasation phase of inflammation) and become macrophages. Macrophage and platelet-derived growth factors (PDGF activates TGF-B and FGF) stimulate differentiation and migration of fibroblasts leading to fibrin production. Fibrin provides minimal gains in tensile strength but serves as matrix for collagen deposition during the proliferative phase. Neutrophils and macrophages phagocytize devitalized tissue and microorganisms.
2. Proliferative phase: Approximately 3 to 14 days. Characterized by fibroblast proliferation and collagen production. Different from other organs such as skin, colonic collagen is produced by submucosal and smooth muscle fibroblasts. Collagen type remains predominantly Type III. Upregulation of MMP’s by macrophages promote ongoing collagenolysis, preventing meaningful gains in tensile strength. THIS IS WHEN DEHESCENSE IS MOST LIKELY TO OCCUR, PARTICULLARLY IN THE FIRST 3 TO 5 DAYS. Microorganisms like E. coli produce endotoxin lipopolysaccharide which induce further collagenase synthesis by macrophages. Colonic wound strength remains only 30% of normal in the first 3 days, and the repair is heavily dependent on surgical devices (sutures, staples). Vascular proliferation induced by VEGF promotes capillary growth and supports fibroblast survival. Oxygen delivery is essential for hydroxylation of lysine and proline, precursors of collagen (collagen production does not occur below 40mmHg PaO2). New collagen is deposited over previous fibrin, leading to gradual gains in tensile strength. Strength is near-normal by day 14.
3. Maturation phase: Collagen is gradually reorganized by layers according to tension lines. Non-functional collagen is removed by collagenase produced by macrophages. Neutrophil fibroblast and macrophage presence gradually diminishes. Collagen type III or replaced by Type I, which usually accounts for 68% of colonic collagen (with smaller amounts of type III and V). Collagen fibers become tick bundles, particularly in the submucosa (strength layer).
The colon regains tensile strength more slowly than the rest of the GI tract, and therefore remains more susceptible to dehiscence for the first 3 to 5 days. This may be due to local and/or systemic factors. Local factors include poor blood supply, susceptibility to tension at the surgical repair, high bacterial load (some of which, like E. coli, produce endotoxic liposaccharide which stimulate macrophage production of collagenase, further delaying gains in tensile strength) and distal obstruction. Systemic factors may include hypovolemia leading to tissue hypoxia (no collagen at <40mmHg PaO2), concomitant use of chemotherapeutic drugs that delay healing (i.e. cisplatin) and immunosuppressive diseases like Diabetes Mellitus.

Question 8

g) Name three (3) methods that can be used to overcome luminal disparity when performing an ileocolic anastomosis.

Answer 8

1. Routine end-to-end sutured anastomosis followed by partial suturing of the larger diameter segment.
2. Enlargement of the smaller segment via “spatulation” of the antimesenteric border, followed by routine end-to-end sutured anastomosis.
3. Functional end-to-end anastomosis followed by TA stapling or hand-suturing of the cut ends.

Question 9

h) Name two (2) alternative methods of closure for colocolonic or ileocolonic anastomosis other than a hand-suture pattern. State a potential advantage and a potential disadvantage for each method.

Answer 9

• GIA stapling: Creates a functional rather that “true” end-to-end anastomosis. Requires closure of the cut end with TA staples or hand suturing. Fast but relatively difficult to perform in small diameter intestines. Costly in comparison with hand-suturing techniques.
• EEA stappling: Creates a true end-to-end anastomosis. Easier to perform than a GIA anastomosis since the EEA device can be introduced transcecally, through enterotomy or transrectally. Fast but more costly that hand-suturing techniques. Transrectal introduction may be difficult or impossible in small cats.
• Biodegradable anastomosis ring

Question 10

a) Describe the findings expected on neurological examination of a patient with an L4 to S3 myelopathy. In your answer, state the spinal segments being tested when evaluating the spinal reflexes.

Answer 10

This patient is expected to present LMN deficits on the pelvic limbs. These may include:
• Muscle atrophy if affected by more than 5-7 days (denervation atrophy)
• Paraparesis or paraplegia depending on the cause and severity of spinal disease. Monoparesis/plegia possible with unilateral lesion.
• Decreased or absent withdrawal reflex
• Lumbar or lumbosacral hyperpathia
• Flaccid anus and decreased perineal reflex; fecal incontinence
• Depressed or absent postural tests
• Panniculus reflex absent caudal affected spinal segment
• LMN bladder (flaccid, easily expressed)
• Reduced myotatic reflexes
o Patellar reflex: hyporeflexive due to impairment of femoral nerve-associated spinal segments L4-6. Pseudo-hyperreflexia may be observed with lesions affecting only spinal segments L6-S1, associated with the sciatic nerve (loss of muscular antagonism)
o Gastrocnemius reflex: hyporeflexive due to impairment of spinal segments L6-S1, associated with sciatic nerve (common peroneal branch)
o Cranial tibial reflex: hyporeflexive due to impairment of spinal segments L6-S1, associate with sciatic nerve (tibial branch).

Question 11

b) Briefly explain the phenomenon ‘pseudohyperreflexia’ which may occur in an L4 to S3 myelopathy.

Answer 11

o Pseudo-hyperreflexia may be observed with lesions affecting only spinal segments L6-S1, associated with the sciatic nerve (loss of muscular antagonism)

Question 12

c) Briefly explain the difference between the anatomic pathways involved in the withdrawal response and nociception, including how these differences are recognised during neurological evaluation.

Answer 12

The withdrawal reflex assesses the integrity of the reflex arch, independent of central input or acknowledgment. This pathway involves a sensory afferent nerve, an interneuron located at the DRG and an efferent motor nerve associated with flexor muscles. Patients with intact withdrawal reflex (i.e. full flexion/retraction of the tested limb) DO NOT necessarily have intact nociception.
Nociception involves transmission of the action potential by ascending spinal pathways to the cerebral cortex, generating a physiologic or behavioral response. Patients with intact nociception will typically display signs of discomfort such as vocalization, tension of multiple muscles or attempting to bite. Less overt physiologic signs may also be observed, such as increase in heart rate, respiratory rate or mydriasis.

Question 13

d) Briefly describe the modified Frankel grading system for dogs with spinal cord injury.

Answer 13

Grade 0: para- or tetraplegia with NO deep nociception
Grade 1: para- or tetraplegia with NO superficial nociception
Grade 2: para- or tetraplegia with preserved superficial and deep nociception
Grade 3: non-ambulatory para or tetraparesis
Grade 4: ambulatory para- or tetraparesis with GP ataxia
Grade 5: spinal hyperesthesia

Question 14

e) Explain why the loss of deep pain perception in dogs with intervertebral disk disease (IVDD) is associated with a poor prognosis.

Answer 14

Noxious stimuli generate action potentials that are conveyed to the cerebral cortex via BILATERAL TRACTS in the lateral funiculi of the spinal cord. Considering this bilateral distribution of nociceptive pathways, loss of deep pain (nociception) indicates functional “transection” of the spinal cord. Such pattern is inevitably associated with similar damage to nearly all other spinal pathways, and therefore indicates a poor prognosis. According to current data, 88 to 96% of dogs operated for IVDE with preserved nociception will recover unassisted ambulation, versus only 50-60% of those without nociception.

Question 15

f) Briefly describe one (1) proposed etiopathogenesis of fibrocartilaginous embolism (FCE).

Answer 15

One theory proposes that IVDE-derived nucleus pulposus material is forcefully introduced into the paravertebral vasculature, causing local thromboembolism. Other theories propose that the fibrocartilaginous material may originate in the growth-plate cartilage of skeletally-immature animals or may arise from endothelial metaplasia.

Question 16

g) Briefly describe the most common signalment and clinical presentation for a dog with FCE.

Answer 16

Young to middle age, large or giant-breed canine. Typically, non-chondrodystrophic. Shetland sheepdogs and Schnauzers can also be affected (most common cause of myelopathy in Schnauzers). Patients with FCE myelopathy typically presented with a history of acute or peracute onset of pain and non-progressive neurologic impairment (mobility) during physical activity. Pain typically subsides within the first few hours but can still be elicited upon palpation of the affected area of spinal cord. Neurologic deficits may vary severity and location depending on affected spinal segments. Most commonly T3-L3 (33% cases) with MFS varying from grade 0 to 3. Neurologic deficits are asymmetric in 69% of cases.
FCE also frequently affects the brain. Neurologic deficits will vary according to the area of the brain affected. Common signs for dogs with cerebellar FCE include head tilt, ataxia with or without hypermetria, nystagmus, decreased menace response, postural reaction deficits and nonambulatory paresis. Dogs with thalamic or midbrain lesions may present with central vestibular dysfunction, ipsilateral head tilt and heads turn (expected with forebrain lesion).

Question 17

h) List two (2) poor prognostic indicators for dogs diagnosed with FCE.

Answer 17

• Loss of nociception
• Presence of underlying thromboembolic disease (CRD, cardiomyopathy, etc…)
• Presence of severe LMN deficits
• Client’s reluctance to pursue PT

Question 18

i) Name one (1) syndrome in dogs that closely mirrors FCE in its clinical presentation.

Answer 18

Hansen Type I (chondroid) Intervertebral Disk Extrusion

Question 19

a) Describe how the extent and severity of burns are classified.

Answer 19

Rule of Nines: 
o	Head: 9%
o	Neck: 1%
o	Forelimbs: 9% each
o	Hindlimbs: 18% each
o	Dorsal or ventral aspects of the abdomen/thorax: 18% each

Question 20

b) Name and describe the defined zones of a thermal burn.

Answer 20

1. Zone of Necrosis: central area where all tissues are devitalized, and blood vessels are thrombosed. No viable tissue remains.
2. Transition zone (zone of stasis): Characterized by reduced blood flow, intravascular sludging an potentially reversible tissue damage.
3. Zone of hyperemia: Characterized by local vasodilation, erythema and edema as a result of inflammation. Tissues are fragile but remain viable.

Question 21

c) Describe the local inflammatory response to severe thermal burns and the systemic implications of this response.

Answer 21

Local inflammatory response to burns is characterized by vasodilation, increased vascular permeability, edema and influx of inflammatory cells. Local perfusion is immediately upregulated by postganglionic autonomic stimulation and upregulation of nitric oxide synthesis within the burn area. NO also stimulated the production of substance P, another potent vasodilator. Vasodilation is further promoted by chemokines produced by resident cells. These mediators may include endotoxins, prostaglandin E2, histamine and activated complement.
Systemic effects are mediated by inflammatory chemokines and free-oxygen radicals, and may affect various organs and systems including lungs, heart, gastrointestinal, renal, hemopoietic, immune, neurologic and endocrine.
o Lungs: Effects mostly derive from inhalation of CO, Hydrogen cyanide and inorganic acids. Multiple implications including formation of carboxyhemoglobin/systemic hypoxemia, increased vascular permeability, laryngospasm/bronchospasm, venoconstriction/increased vascular resistance and pulmonary edema.
o Cardiovascular: within 10 minutes of a serious burn involving more than 25% of body surface vascular permeability to fluid and albumin increase drastically. The effect is mediated by complement activation, histamine and oxygen free radicals derived from the burn site. Vascular fluid extravasation quickly overwhelms the lymphatic system, leading to severe hypovolemia and generalized edema. Evaporation at the burn site also contributes to fluid losses (even a partial-thickness burn can increase evaporation by 33%). Erythrocyte deformability also decreases due to peroxidation of membrane lipids. Combined with hypovolemia this causes hyperviscosity syndrome, degrading the normal blood rheolic (flow) characteristics. The combined effects are hypoperfusion, thrombosis and metabolic acidosis.
o Myocardial effects: Oxidative damage to the sarcoplasmic reticulum leads to Ca leakage into the cytoplasm, leading to myocardial damage and decreased cardiac output. Inhalation of CO leads to carboxyhemoglobin formation which decreased ATP and leads to myocardial hypoxia and necrosis.
o Gastrointestinal tract: Oxidative damage increases the apoptotic rate of gut mucosal cells, leading to gut barrier compromise. This results in bacterial translocation, endotoxemia and septic shock.
o Renal system: Acute renal failure is frequently observed, likely as a result of hypovolemia, sepsis, glomerular accumulation of myoglobin, hemoglobin and cell debris. The use of nephrotoxic antibiotics may also contribute to renal failure.
o Hematopoietic system: Erythrocyte destruction at the burn site and intravascular hemolysis lead to significant RBC losses within only a few hours of a large burn. The condition is known as “burn anemia”.
o Immune system: Upregulation of TNF- leads to lymphocyte apoptosis. Macrophages express a hyperinflammatory phenotype that overproduces TNF, IL’s, NO and eicosanoids. This increases the patient’s susceptibility to sepsis.
o Neurologic system: Cell damage and local inflammation sensitize local nociceptors into a hyperalgesic state (peripheral sensitization). Intense pain leads to massive sympathetic discharge and promote the cardiovascular events associated with burn shock.
o Metabolic and Endocrine systems: Initially the body enters a “hypometabolic” state (ebb phase). This is quickly replaced by a hypermetabolic phase (“Flow phase”) characterized by increased catabolic activity induced by cortisol and catecholamines. Muscle catabolism and relative insulin resistance ensue, known and “burn diabetes”.

Question 22

a) Elbow dysplasia is a common inherited condition causing forelimb lameness in dogs. List the five (5) developmental abnormalities commonly associated with elbow dysplasia. In your answer, indicate which is the most common disease process.

Answer 22

o	OCD
o	FMCP (most common, over 96% of cases) 
o	UAP
o	Elbow Incongruence 
o	Articular cartilage damage

Question 23

b) Identify one (1) other developmental condition of the canine elbow BESIDES OCD, FCP, UAP, Elbow Incongruity and Cartilage Damage and state a breed commonly thought to be susceptible.

Answer 23

o Incomplete Ossification of the Humeral Condyle (American Cocker Spaniel, Labrador Retriever and German Shepherds)
o Ununited Medial Epicondyle (UME) – Labrador Retriever

Question 24

c) Draw a transverse, cross-sectional line drawing of the radius and ulna at the level of the distal articular surface of the elbow joint. Label in your drawing the following:
• medial and lateral orientation
1. medial coronoid process
2. lateral coronoid process
3. the articulation of the ulna with the radius
4. the radial incisure
5. the position of the biceps tendon.

Answer 24

Question 25

d) Describe the proposed etiopathogenesis and pathophysiology of medial coronoid process disease and the concurrent changes that can be seen on the medial humeral condyle

Answer 25

In 1983 Olsson proposed that MCD was the result of osteochondrosis. This theory was recently proven incorrect by micro-CT demonstration of absence of a separate center of ossification of the coronoid process. Ossification of the medial coronoid process appears to occur exclusively because of appositional ossification. The most recent data indicates that MCD occurs because of mechanical overloading of the medial coronoid process before 15 weeks of age. The disorder initially only affects the subchondral bone, disturbing endochondral ossification via delayed calcification of the Zone of Calcification. This leads to the development of microfractures in the trabecular bone of the affected coronoid process, causing loss of osteocytes and canalicular density. These abnormalities are most observed along the radial incisure, where most coronoid fissures happen.
Cartilage lesions affecting the medial humeral condyle (trochlea) may result from osteochondrosis/OCD or humeroulnar conflict, with or without medial coronoid disease. Most cases exhibit a combination of cartilage lesions affecting both the MCP and humeral trochlea (kissing lesions), but this is not always the case. Trochlear cartilage lesions have been reported in the absence of MCD, suggesting that not all cases can be attributed to mechanical interference between the humerus and ulna.

Question 26

a) List and briefly justify appropriate pre-operative diagnostic investigations of a dog with a mammary tumor.

Answer 26

o Thoracic radiography: Thoracic (pulmonary) metastasis occurs in 25 to 50% of dogs with malignant mammary neoplasia.
o Minimum database (CBC, Biochemisty, UA): Typically, non-specific for mammary neoplasia but recommended to identify paraneoplastic syndromes and coexisting disease that may affect prognosis (ie. Hypercalcemia, Renal disease, etc…).
o Regional lymph node aspirate: Detection of neoplastic cells within regional LN helps stage the disease.
o Aspiration or exfoliative cytology: Helps differentiate inflammatory from neoplasia, but typically unable to differentiate benign adenoma from malignant carcinoma.
o Incisional biopsy: Recommended when aspiration or exfoliative cytology are not diagnostic. Important to determine the adequate “surgical dose” for the case at hand. Evaluation of the excised tumor should still be performed to confirm diagnosis, establish margins, etc..

Question 27

b) Describe the lymphatic drainage of the canine mammary glands.

Answer 27

o Axillary lymph nodes: Cranial and caudal thoracic glands as well as cranial abdominal (glands 1, 2 and 3)
o Inguinal lymph nodes: Caudal abdominal and inguinal glands (glands 4 and 5)
Lymphatic connections exist between glands and across the midline.

Question 28

c) List the clinical features that would suggest that a mammary tumor is malignant.

Answer 28

o Size (large tumors more likely to be malignant)
o Presence of ulceration
o Attachment to underlying fascia
o Regional or sublumbar LN enlargement
o Local signs of inflammation (erythema, edema, discomfort)
o Lameness or limb edema
o Weakness, lethargy, weight loss

Question 29

d) List five (5) common, distant metastatic sites for mammary neoplasia.

Answer 29

o	Lymph nodes 
o	Lungs
o	Liver                            “LLLBB”
o	Brain 
o	Bone

Question 30

e) Briefly discuss hormonal influences on mammary tumor development.

Answer 30

Prolonged exposure to progestins has been shown to induce proliferation of mammary epithelial cells. This may increase the chances of “genetic errors” being expressed, subsequently leasing to neoplasia. The effect of early spaying on the development of mammary neoplasia has been described. In comparison to intact birches, dogs spayed before the first estrus were 0.05% as likely to develop mammary neoplasia. Dogs spayed after the first estrus were 8% and after the second estrus were 26% as likely to develop the disease. The effect of spaying after the fourth cycle or after 2.5 years of age was negligible.

Question 31

f) List the surgical procedures available for resection of mammary tumors (5)

Answer 31

o	Lumpectomy
o	Simple mastectomy
o	Regional Mastectomy 
o	Unilateral mastectomy
o	Bilateral mastectomy

Question 32

g) State the most appropriate surgical procedure for management of the left cranial abdominal mammary gland mass in this patient. Provide justification for your answer.

Answer 32

Regional mastectomy involving removal of the entire left cranial and caudal thoracic as well as the cranial abdominal gland is likely the most appropriate procedure. These three glands share lymphatic drainage into the left axillary lymph node and may contain similar neoplastic cells should the mass prove to be malignant. Glands 2 and 3 also share venous drainage through the cranial superficial epigastric vein. From a technical aspect gland 1 through 3 are fairly confluent, making single mastectomy more complicated than removal of all three glands.

Question 33

h) State the most appropriate surgical procedure for management of the right cranial thoracic mammary gland mass in this patient. Provide justification for your answer.

Answer 33

Single mastectomy is appropriate in this case. The right thoracic gland is the first of glands 1-3 to drain into the axillary lymph node, making it unlikely that neoplastic cells would extend into the caudal thoracic gland without gross evidence of involvement (i.e. palpable tumor). Venous drainage occurs directly through intercostal, internal thoracic and lateral thoracic branches.

Question 34

i) List the prognostic factors known to affect the outcome for malignant mammary tumors in dogs. Also list the factors that have been shown not to affect the prognosis.

Answer 34

Factors that negatively affect prognosis:
o Tumor size (>3cm)
o Cell proliferation markers (AgNORs, Ki-67, nuclear morphometry)
o Histologic type (poorly-diff carcinomas > carcinoma in-situ)
o Degree of invasion (tumor extending beyond the duct system)
o Degree of nuclear differentiation (poorly diff adenocarc.=90% recur 2yr)
o Clinical stage (TMN staging)
o OHE status (OHE at the time of tumor removal MAY improve survival)
o Presence of lymph node metastasis (80% recurrence in 6mo Vs 30% in 2 yr W/O metastasis)
o Distant metastasis (MST 5 mo Vs 28 mo W/O metast.)

Factors that DO NOT affect prognosis for dogs:
o Presence of multiple tumors
o Micrometastasis (<2mm) to regional LN (although lymphadenectomy may be of therapeutic value)
o Type of surgery (provided that the current tumor is completely excised)

Question 35

j) Name one (1) mammary tumor for which surgery is contraindicated.

Answer 35

Mammary inflammatory carcinoma

Question 36

2. A three-year-old, male neutered Kelpie presents with a non-weight-bearing lameness of the right thoracic limb. The patient is of normal mentation with normal general physical examination findings and is hemodynamically stable. Orthopedic examination reveals suspected right elbow luxation.
   a) Describe the pathophysiology of traumatic elbow luxation in dogs. Your answer should reference the functional anatomy of the elbow and its relation to the frequency of occurrence and the direction of the luxation

Answer 36

The humerus, radius and ulna form a complex but inherently stable joint. This is the result of active and passive stabilizers, but also due to the interdigitating effect between the anconeal process and the supracondylar foramen during elbow extension. The humeral condyle is also larger on the medial aspect (trochlea) and smaller on the lateral aspect (capitulum), creating a “slope” oriented distomedial to proximolateral as viewed from the frontal plane. Elbow luxation usually results from blunt force trauma against a partially or completely flexed elbow joint. The radial head and ulna luxate laterally in relation to the humeral condyle. This is accompanied by rupture or avulsion of the medial collateral ligament. The lateral collateral and muscle attachments can also be injured.

Question 37

b) Describe typical physical examination and radiographic findings of traumatic elbow luxation associated with the most common direction of elbow luxation state.

Answer 37

Physical exam findings typically include swelling, pain and loss of range of motion on the affected joint. The patient is unlikely to bear weight on the limb, which is carried in flexed position. The ante brachium is abducted and supinated. The radial head is prominently palpable and the and the lateral humeral condyle is indistinct.

Question 38

c) Discuss, in detail, all available options for the management of traumatic elbow luxation, including aftercare.

Answer 38

Medical management (closed reduction): performed under general anesthesia with the patient in lateral recumbency, with the affected limb facing up. A thick rope or rolled towel is placed under the axilla and held by an assistant for counterforce. The elbow and carpus are fully flexed. The forearm is supinated and medially directed pressure is applied to the lateral aspect of the radial head as the elbow is slowly extended. The forearm is also moderately abducted during this maneuver. This is done with the intent of “hooking” the anconeal process into the supracondylar foramen to function as a leverage point. Once anconeal engagement is noticed the elbow is further extended, abducted and pronated as firm pressure is continuously applied to the lateral radial head to “slide” it over the humeral capitulum. Once the joint is reduced, stability is confirmed by flexing the elbow and carpus 90 deg and pronating/supinating the forearm (Campbell test). If the medial collateral ligament is intact, the paw can be rotated laterally to 45 deg. If the ligament is ruptured, rotation to 90 deg is possible. During internal rotation (supination) an intact lateral collateral ligament will allow 70 deg of rotation, while 140 deg will be possible with ligament rupture. Flexion/extension cycles are repeated for 15 minutes to remove blood clots and joint capsule folds from the joint space. Radiographs are obtained to verify reduction. The lib must be placed in an immobilizing extension splint (i.e Spica) for 14 days, followed by strict exercise restrictions and physical therapy for another 6 weeks.

Open reduction: Recommended for all cases of reluxation following closed reduction. Also recommended for close-reduction cases in large breed dogs when collateral ligament damage is also present. The joint of approached via the lateral aspect, including subperiosteal elevation or myotomy of the anconeal muscle. Reduction is achieved as previously described for closed reduction. Protect the joint cartilage and use a blunt instrument between the radial head and the humeral condyle to “lever” the joint into reduction. If reduction is not possible due to triceps contraction, perform an osteotomy of the olecranon. Once the joint is reduced and thoroughly flushed stability can be assessed. The lateral collateral ligament is repaired with non-absorbable monofilament sutures (Polypropylene) using modified Bunnell or Locking Loop pattern. Avulsion fractures can be stabilized with single screw/washer repair. Alternately bone anchors or screw/washers and braided polyethylene sutures (FiberWire) can be applied to the lateral humeral epicondyle and medial aspect of the radial head. Ruptured medial collateral ligament is repaired in similar fashion, typically through a separate medial approach. If an ulnar osteotomy was performed, it is stabilized with double-IM pin/tension band. Closure is performed in standard fashion. Post-op radiographs are obtained to verify reduction. Post-op care is like what was described under closed reduction.

The use of trans articular external fixators to augment joint stability after open of closed reductions has also been described.

Elbow arthrodesis: Only recommended as a last-resort salvage procedure as functional outcome is not ideal. Begin by pre-determining the angle of arthrodesis by comparison to the contralateral elbow (goniometry). Performed a caudolateral approach to the elbow and osteotomize the olecranon. Incise the lateral collateral and elevate the origin of the forearm extensor muscles to improve joint space exposure. Remove the articular cartilage of the humeral condyle, radial head and ulna using a high-speed burr, following the contours of the joint. Temporarily stabilize the joint with a K-wire introduced through the lateral humeral condyle and into the ulna. Contour a locking plate to fit the caudal aspect of the humerus and ulna, allowing room for at least 3 screws on each bone. Removal of a section of the proximal ulna is often recommended to facilitate implant placement. Add screws in lag fashion through the plate and arthrodesis to improve compression, always checking limb alignment, rotation and angulation prior to final fixation. Add cancellous bone graft obtained from the lateral proximal humerus. Reattach the olecranon top either side of the plate using a lag screw. Lavage and closure are routine. Obtain radiographs to evaluate limb alignment, apposition, and implant positioning. Place the limb in a soft padded bandage for 1 week or a Spica splint for 6 weeks if concerns over stability exist. Serial radiographic reevaluation every 4 to 6 weeks and strict exercise restriction are strongly recommended until radiographic union is documented.

Question 39

d) Identify relevant prognostic factors and discuss the prognosis for return to normal function in patients with traumatic elbow luxation.

Answer 39

Positive prognostic factors may include:

o Recent injury
o Relatively easy closed reduction followed by palpably stable elbow
o Small breed
o Less active patient

The prognosis for return to normal function is generally good after closed reduction. The prognosis following open reduction will largely depend on the chronicity of the injury and the degree of articular cartilage damage. Some degree of osteoarthritis is likely inevitable, but typically not debilitating expect in chronic cases associated with extensive periarticular fibrosis and joint cartilage damage.

Question 40

e) Briefly describe a Monteggia fracture and how it is most often treated. Discussion of specific fracture classification is not required in this response.

Answer 40

A Monteggia fracture is an ulnar fracture combined with luxation of the radial head. The ulnar fracture may or may not involve the trochlear notch. Repair is typically accomplished via caudal plating of the ulna to compress the fracture and counteract the pull of the triceps brachii, reconstruction of the annular ligament, reduction of the radial head and radio-ulnar fixation with lag screw.

Question 41

• Briefly describe the anatomic and functional abnormalities proposed to be involved with urethral sphincter mechanism incompetence (USMI)

Answer 41

A true bladder sphincter does not exist in the bitch. Urinary continence is governed by the balance of autonomic input (i.e. hypogastric nerve-derived alpha-adrenergic contraction of the proximal urethral smooth musculature), hormonal effects and distribution of intraabdominal pressure upon the proximal urethra. Proposed contributing factors to incontinence include urethral hypoplasia, intrapelvic positioning of the bladder, OVH, obesity and congenital abnormalities.

Question 42

• List two (2) medications commonly used in treatment of USMI and state their mechanism of action.

Answer 42

Phenylpropanolamine (PPA) – Alpha-adrenergic agonist

Diethylstilbestrol (DES); Estriol (Incurin) – synthetic estrogens

Question 43

• List four (4) surgical procedures described in the treatment of urethral sphincter mechanism incompetence.

Answer 43

1. Colposuspension
2. Cystourethropexy
3. Periurethral injections of polytetrafluoroethylene (PTFE) or collagen
4. Artificial urethral sphincters
5. Urethral slings
6. Urethral lengthening procedures

Question 44

Discuss Colposuspension - typical use, technique and prognosis

Answer 44

Colposuspension (Most common surgery utilized for the treatment of USMI)
Place a large gauge urinary catheter. Perform a ventral prepubic abdominal approach of sufficient length to allow exposure of the urinary bladder and vaginal tract. Use atraumatic tissue forceps or stay sutures to apply cranial traction to the vagina. Apply two simply interrupted nonabsorbable monofilament sutures (2-0 Prolene) on either side of the urethra, between the vagina and the prepubic tendon. The sutures are placed as to utilize the vaginal canal to apply pressure against the urethra, as well as to position the urethra within the abdominal cavity. The urinary catheter is in place to prevent overtightening of the sutures which may cause urethral obstruction (one possible complication). Other complications may include inadvertent urethral suture penetration and failure to regain continence.
Prognosis for return of continence is considered fair. Available papers report that 54 to 82% of treated patients regain full continence.

Question 45

a) A three-year-old Labrador is presented immediately following a road traffic accident. Radiographs reveal that the patient has sustained a mid-diaphyseal, closed, minimally comminuted single large butterfly fragment, caudally displaced left femoral fracture. In relation to this fracture:

• List the forces acting across this fracture that must be neutralized during surgical repair.

Answer 45

Bending, axial loading and torsion

Question 46

• Define interfragmentary strain

Answer 46

Interfragmentary strain is a measure of fracture instability, defined by the displacement of fragments divided by the original gap size.

Question 47

a) A three-year-old Labrador is presented immediately following a road traffic accident. Radiographs reveal that the patient has sustained a mid-diaphyseal, closed, minimally comminuted single large butterfly fragment, caudally displaced left femoral fracture. In relation to this fracture:

• For each of the fracture repair planning approaches: ‘open anatomic reconstruction’ and ‘biological osteosynthesis’, state the intended effect on both fracture gap and interfragmentary strain.

Answer 47

During open anatomical reconstruction the goal is to rebuild anatomy as closely as possible, thereby minimizing or eliminating fracture gaps and quickly reducing interfragmentary strain. The intention of this approach is to achieve “absolute stability”, allowing the bone to heal by direct union (contact or gap)

Biological osteosynthesis aims to preserve as much of the “soft callus” and blood supply around the fracture as possible. Stabilization is applied with the intention of achieving “relative stability”, sufficient to bring interfragmentary strain below 20-40% which will allow secondary bone healing.

Question 48

a) A three-year-old Labrador is presented immediately following a road traffic accident. Radiographs reveal that the patient has sustained a mid-diaphyseal, closed, minimally comminuted single large butterfly fragment, caudally displaced left femoral fracture. In relation to this fracture:

Provide two (2) questions specifically relating to this fracture configuration that should be considered to determine whether to plan the repair as an ‘open anatomic reconstruction’ procedure, or a ‘biological osteosynthesis’ procedure.

Answer 48

1) Can this fracture be anatomically reconstructed?

2) Can load sharing be achieved?

Question 49

a) A three-year-old Labrador is presented immediately following a road traffic accident. Radiographs reveal that the patient has sustained a mid-diaphyseal, closed, minimally comminuted single large butterfly fragment, caudally displaced left femoral fracture. In relation to this fracture:

• List three (3) appropriate internal fixation techniques for repair of this fracture. For each technique, state whether this is a planned ‘biological osteosynthesis’ procedure or an ‘open anatomic reconstruction’ procedure.

Answer 49

1. Interlocking nail (Biological osteosynthesis)
2. Lateral plate and IM pin (open anatomical reduction unless done as MIO)
3. Lateral locking plate (open anatomical reduction unless done as MIO)

Question 50

• List the two (2) general causes of delayed fracture healing or non- unions and provide two (2) specific examples of each.

Answer 50

1. Instability: Inappropriately selected implant or application for the patient’s size.
   Examples:
   - IM pin/cerclage for short oblique mid-diaphyseal femoral fracture
   - Cerclage/lag screws for oblique mid-diaphyseal femoral fracture in a large dog (without IM pin)
2. Inadequate vascular supply: excessive disruption of soft tissue envelope by injury or surgical repair. Anatomical location
   Examples:
   - Fractures of the distal radius in toy breeds
   - Excessive soft tissue dissection with periosteal stripping of any diaphyseal fracture

Question 51

b) A 10-year-old Border collie is presented for persistent hindlimb lameness after undergoing a right femoral fracture repair 16 weeks ago. Radiographs show reduced radiopacity of bone proximal and distal to the previous short-oblique fracture. The fracture appears to have been repaired with a lateral dynamic compression plate and a single cerclage wire applied at the level of the fracture. At this point, you are concerned about the development of a dystrophic or early atrophic non-union.

• Discuss a specific surgical plan, including each technique to be performed during surgery that would maximize the chance of attaining bone union in this patient. Justify each technique by discussing its intended effect on promoting bone healing.

Answer 51

The revision surgery will involve debridement of the fracture ends, reopening of the medullary cavity, improving upon the stability of the repair, obtaining samples for bacterial culture, and stimulating bone healing via the addition of cancellous bone autograft. The graft can be obtained from the wing of the ilium, femoral condyles or proximal tibia.

The first step should be evaluation of the radiographs for evidence of plate/screw loosening, breakage, or peripheral lucency. It is impossible to discuss specifics without having radiographs available to review. Plate size, length and application must also be carefully evaluated. Removal of all implants is advisable if signs of infection, inadequate implant size or implant failure are observed. The addition of an intramedullary pin may sufficiently augment the site but may not be able to “restart” the healing process, still requiring fracture debridement. This option must be weighed against the possibility of lack of healing due to persistent infection, likely justifying the complete removal of all implants. The description of “reduced radiopacity of bone proximal and distal to the fracture” as well as the time elapsed since the initial repair suggest that the addition of an IM pin will not be sufficient to stimulate healing.

A lateral standard approach to the femur is performed between the vastus lateralis and biceps femoris. Additional exposure of the trochanteric fossa for normograde IM pin placement can be achieved via a separate stab incision slightly dorsal to the greater trochanter. This will provide enough exposure for the revision.

The suspicion of atrophic nonunion justify debridement of the fracture with the intention of reopening the medullary cavity. This is done to improve revascularization, growth factors, and access to bone marrow-derived mesenchymal stem cells. Any necrotic, contaminated, damaged or infected bone and soft tissue should be debrided. The lateral plate, screws and cerclage are assessed for loosening and removed if unstable. It is important to highlight the fact that infected surgical sites under treatment do typically heal despite the presence of metal implants, provided that such implants provide absolute stability. The assumption that all implants must be removed in this case stems from the provided radiographic description and time from initial repair.

The fracture site is swabbed for bacterial culture prior to the administration of antibiotics. Tissue, bone fragments and implants are also cultured to improve the chance of bacterial growth, identification, and proper antibiotic selection. Samples should be collected from 5 separate areas of the wound if infection is suspected. Cytological examination of samples obtained directly from the fracture may help determine if antibiotics are necessary while awaiting culture results (presence of bacteria proves infection), although this may be a low-yield test. This is due to the typically low numbers of planktonic bacterial colonies in comparison to bacteria encased in biofilm. Newer PCR-based techniques allow bacterial detection and antibiotic selection with higher sensitivity and often without the need for culture.

Low-pressure (7-8 psi), high volume (2 to 3 liters) irrigation with Lactated Ringer’s solution is performed to decrease contamination (if present) and remove non-vital debris. This can be achieved with the use of a pressure cuff around a 1 Liter bag, pressurized to 300 mmHg and delivered through an 18G needle.

An intramedullary pin measuring 30-40% medullary cavity and extending from trochanteric fossa to the proximal aspect of the trochlea is added in normograde fashion. The pin will provide fracture alignment prior to plating and augment the stability provided by the lateral plate.
A lateral femoral DCP plate should span roughly 80% of the diaphysis and accommodate at least three bicortical screws for a total of 6 cortices on each fracture segment. Screw diameter should not exceed 40% of the bone diameter to avoid weakening the bone. Alternately a locking plate can be used to further improve the stiffness of the repair. For a Border Collie this likely means a 3.5mm plate/screws, but adequate implant size should be confirmed based on pre-op radiographs (typically dictated by maximum screw diameter). The use of a lag screw across a short-oblique fracture will create interfragmentary compression. This is desirable to provide load sharing and minimize strain but may not be possible if the fracture ends are partially resorbed and no longer matching. An interlocking nail would be another very good option to stabilize this fracture.

Cancellous bone graft can be obtained from the wing of the ilium, lateral aspect of the femoral condyle, proximal tibia or proximal humerus. Graft is added into any resulting gaps and around the fracture. This will provide fibroblasts, osteoblasts and MSC’s (osteogenesis), growth factors (osteoinduction), inorganic matrix (osteoconduction) and stimulate local cell activity (osteopromotion). The surgical wound is closed in standard fashion by apposition of fascial planes with monofilament absorbable sutures (0 PDS), followed by subcutaneous (3-0 poliglecaprone 25) and skin (3-0 Nylon).