ANZCVS 2013 Flashcards
- Linear external fixators can be used to stabilize comminuted mid-shaft long-bone fractures.
a) Name the type of bone healing that occurs in the above scenario (2 marks) and briefly describe the sequence of events that occurs with this type of bone healing from injury to one year post fracture repair. (8 marks)
Secondary bone healing: The healing process from injury to complete union can be divided into 5 partially overlapping phases: Inflammation, Intramembranous ossification, Chondrogenesis (soft callus), Osteochondral ossification (hard callus) and Remodeling.
- Inflammation: Begins immediately after injury with the formation of a platelet clot and degranulation of activated platelets, which release cytokines and growth factors to attract neutrophils (24 hours), macrophages (48 hours, via diapedesis of monocytes) and lymphocytes. Arachidonic acid from membrane phospholipids is converted into prostanoids and thromboxans via COX, leading to vasodilation and further platelet activation. Fibroblast and platelet-derived growth factors activate progenitor mesenchymal cells from periosteum and soft tissue origin. These cells differentiate into osteoprogenitor cells, as well as provide anabolic factors to stimulate the healing process and modulate inflammation. Macrophages release chemotactic factors that recruit and activate fibroblasts, which begin to lay a fibrin meshwork to form a cell, growth-factor and matrix-rich meshwork. The “scaffold” will be quickly permeated by blood vessels and remodeled into granulation tissue, known as the “external callus”
- Intramembranous ossification: Osteoprogenitor cells derived from the periosteum begin to lay new bone between the periosteum and the cortex, for partial “ramps” on both ends of the fracture. The new bone does not cross the external callus.
- Chondrogenesis: starts with the development of granulation tissue during the inflammatory phase, which is quickly remodeled into fibrovascular tissue and finally into fibrocartilage by the production of collagen type I and III over several weeks. Local conditions (low O2 pressure, growth factors) stimulate local stem cells to differentiate into chondrocytes. These will produce extra-cellular matrix rich in collagen Type II, known as “soft callus”
- Osteochondral ossification: The cartilage callus (soft callus) produced during the previous phase is still insufficient to reduce strain enough to allow survival of osteoblasts. Chondrocytes undergo hypertrophy and begin to mineralize the extracellular matrix, downregulating the production of collagen Type II and stimulating the production of collagen Type X (marker of osteochondral ossification). Upregulation of MMP’s will degrade collagen II as it is replaced by bone. Mineralized cartilage finally possesses enough stiffness to support osteoblast/osteocyte survival. These cells proliferate from the periphery of the callus (previous zone of intramembranous ossification) towards the center, laying woven bone. Radiographically this callus looks large and misshapen.
- Remodeling: The woven bone callus formed during the previous phase is not as strong as lamellar bone, and is thus gradually replaced. Osteoclasts and osteoblasts work as Bone Multicellular units (BMU) to replace woven bone with lamellar bone known and osteons. Osteons are composed of concentric layers of bone bound by cement lines and possessing a central Harversian canal containing blood vessels. Remodeling can continue for years and follows Wolff’s law.
- b) Discuss advantages and disadvantages of an external fixator that has been applied in a closed manner compared to open reduction and stabilization by a dynamic compression plate applied as a buttress/bridging plate. (8 marks)
External fixators applied in a closed manner (Closed reduction)
Advantages (biological fixation)
- Minimal disruption of the fibrin clot/granulation tissue and mesenchymal stem cells therein contained
- Minimal disruption of the endosteal, periosteal and soft tissue blood supply
- Minimal to no exposure of the fracture to biological contaminants such as cutaneous bacterial flora
- Minimal soft tissue trauma.
Disadvantages
- Inability to more closely restore the anatomical structure of the bone (understanding that true anatomical reduction is not possible in this case)
- Less stiffness, leading to higher strain at the fracture site which may delay healing and predispose the site to nonunion. (This is highly influenced by the type of fixator utilized)
Open reduction with Dynamic Compression plate applied in buttress/bridging mode
Advantages
- Allow more adequate reconstruction of bone fragments and realignment of the anatomical axis of the bone in comparison to ExFix applied in closed fashion
- The implant is positioned close to the mechanical axis of the bone, making it superior to ExFix in its ability to counteract biomechanical forces.
- Implant stiffness is typically greater than what can be achieved with ExFix, leading to lower strain and faster rate of fracture union.
Disadvantages
- Application disrupts the fracture site and early fibrovascular callus, potentially delaying healing.
- Disrupts periosteal and soft tissue blood supply
- Exposes the fracture and implants to pathogens (open surgical wound)
- The required approach predisposes the patient to iatrogenic damage to anatomical structures (vessels, nerves, muscles).
- c) Name four (4) categories of linear external fixator frame configurations and draw a diagram for each to illustrate the construct. (4 marks)
A, Type Ia, (unilateral uniplanar).
B, Type Ib (unilateral biplanar)
C, Type I-II hybrid (unilateral uniplanar combined with a bilateral uniplanar and a diagonal connecting bar).
D, Type II modified (bilateral uniplanar with combined full and half pins)
E, Type II (bilateral uniplanar with all full pins)
F, Type III modified (bilateral biplanar). Note the addition of the diagonal augmenting the type I-II hybrid frame (C) and the proximal and distal articulations placed between the cranial and medial connecting bars of the type III frame (F, right image).”
- d) List strategies to increase the strength and stiffness of an external fixator frame.
- Pre-drill before inserting positive-profile pins
- Increase pin numbers (up to 4 pins per bone segment)
- Increase pin size (up to 25% bone diameter)
- Place pins near the joints and near the fractures
- Decrease the distance between the bone and the pin/clamp interface
- Increase the diameter of the connecting bar or use double bars/augmentation plates
- Increase the number and planes of connecting bars
- Tie the intramedullary pin into the fixator frame
- a) Compare the pathophysiology of Hansen type I intervertebral disc disease with that of Hansen type II intervertebral disc disease.
Hansen Type I: The nucleus pulposus undergoes progressive loss of proteoglycans, becoming dehydrated and mineralized (chondroid degeneration). This leads to loss of ability to distribute pressure and causes secondary degeneration and rupture of the annulus fibrosus. This usually culminates in the expelling of nucleus contents towards the dorsally located spinal cord (thinnest part of the annulus) during an episode of mechanical stress. This is know as Intervertebral Disk Extrusion. The resulting injury leads to various degrees of contusion and compression.
Hansen Type II: The nucleus pulposus becomes progressively more dehydrated and is gradually replaced by fibroid tissue. This causes a gradual transfer of stress to the annulus, which eventually degenerates over a period of months to years. The degeneration typically leads to dorsal protrusion of disk material and compression of the spinal cord.
The clinical signs associated with these conditions can be similar since both cause various degrees of spinal cord compression. The main differences pertain to the acuteness and severity of the resulting clinical syndrome. Type I is typically associated with acute or peracute clinical signs caused by severe contusion or even laceration of the Dura Mater and spinal cord in severe cases. Type II usually leads to more insidious clinical signs secondary to inflammatory changes at the site of compression. Signalment is also different between Type I and II.
- c) You have examined the urinary bladder of a dog with an acute thoraco-lumbar intervertebral disc extrusion and a dog with a chronic severe lumbosacral compression. For each case listed above describe: (8 marks)
- the neurological classification of bladder dysfunction
Urinary bladder disfunction is classified as Upper Motor Neuron (UMN) or Lower Motor Neuron (LMN).
- c) You have examined the urinary bladder of a dog with an acute thoraco-lumbar intervertebral disc extrusion and a dog with a chronic severe lumbosacral compression. For each case listed above describe: (8 marks)
- the neuroanatomic localization of the lesion
UMN bladder is expected with lesions between the pons and L7 spinal segment, such as in the case of the dog with thoraco-lumbar IVDE
LMN Bladder is expected with lesions caudal to and including sacral spinal segment, such as in the case of the dog with DLSS, as well as with pelvic/lumbosacral plexus lesions
- c) You have examined the urinary bladder of a dog with an acute thoraco-lumbar intervertebral disc extrusion and a dog with a chronic severe lumbosacral compression. For each case listed above describe: (8 marks)
- the expected clinical examination findings pertaining to the bladder
UMN bladder is full, turgid and difficult to express
LMN bladder is full, flaccid and easy to express.
- c) You have examined the urinary bladder of a dog with an acute thoraco-lumbar intervertebral disc extrusion and a dog with a chronic severe lumbosacral compression. For each case listed above describe: (8 marks)
- how these abnormalities affect control of micturition.
Patients with UMN bladder have excessive urethral musculature tone, and are either completely unable to urinate of have difficulty accomplishing bladder emptying.
Patients with LMN bladder lack detrusor reflex and have reduced urethral muscular tone. They typically dribble urine constantly, and it is difficult to confirm bladder emptying via transabdominal palpation due to overt bladder flaccidity.
a) Draw and label a diagram of the normal microscopic layers of articular cartilage in a mature dog. (6 marks)
Superficial zone Transitional zone Deep zone Tidemark Zone of ossified cartilage
b) Define osteochondrosis and osteochondritis dissecans. (2 marks)
Osteochondrosis is a syndrome characterized by failure of endochondral ossification, leading to cartilage retention.
Osteochondritis dissecans is the clinical syndrome caused by dislodgment of a cartilage flap due to osteochondrosis.
c) Describe the pathophysiology of osteochondritis dissecans in a dog. (12 marks)
OCD begins with failure of osteochondral ossification at either the level of the physis or the articular epiphyseal complex responsible for epiphyseal bone growth. The cause of this failure is not well understood, and proposed etiologies include a combination of management, nutritional and genetic factors. The unossified cartilage becomes progressively thicker (osteochondrosis) and eventually outgrowths its nourishment sources (synovial fluid and subchondral bone). This end result is chondrocyte necrosis and loss of cartilage viability, leading to the formation of clefts between the deep zone and the zone of ossified cartilage. Normal activity eventually leads to the formation of vertical fissures in the cartilage, which communicate with the horizontal clefts to form flaps. This communication exposes the synovial fluid to cartilage fragments and inflammatory mediators, inducing joint inflammation which eventually leads to DJD.
d) List four (4) recognised risk factors for development of osteochondritis dissecans in the dog. (4 marks)
- Age (4 to 8 months of age)
- Gender (Males)
- Breed (Large and Giant breeds)
- Rapid Growth
- Nutrient Excess
e) List three (3) joints in which osteochondritis dissecans lesions occur in the dog. Identify the specific anatomic location most commonly affected within those joints. (6 marks)
- Shoulder – Caudal aspect of the humeral head
- Elbow – distal aspect of the medial humeral condyle
- Stifle – distal aspect of medial or lateral femoral condyles
- Tarsus – medial or lateral trochlear ridges
- a) Describe, with the aid of diagrams, the normal anatomy of the canine diaphragm. Include in your answer the muscular divisions and their attachments and the spatial relationship of the diaphragm to adjacent organs. (11 marks)
The diaphragm is a musculotendinous plate located between the thoracic and abdominal cavities. It is composed of a central tendinous region surrounded on all sides by muscles that stream in a radial pattern to attach to various arear of the thoracic ad abdominal walls. This muscular region is divided into Lumbar part, Costal part (on each side) and Sternal part. The diaphragm is convex on the thoracic side and concave on the abdominal side.
The central tendon occupies 21% of the canine diaphragm and consists of a triangular central area with dorsal extensions on each side. It contains the foramen of the caudal vena cava, located to the right of the midline as viewed from the abdominal surface.
The Lumbar part is formed by the right and left diaphragmatic crura which surround the aortic hiatus. The hiatus contains the aorta, azygous vein, hemiazygous vein and thoracic duct. The right crus is much larger than the left. They arise from a long bifurcate tendon located medial to the psoas minor muscle. The long part of this tendon arises from the cranial aspect of the body of L4 and the shorter part from the body of L3. The muscle fibers that arise from the lateral aspects of this tendon parallel the dorsal thoracic wall and extend ventral to the psoas muscles to form the lumbocostal arch. After crossing the lumbar musculature the fibers coalesce with those of the costal parts. Seen from the abdominal cavity, each crus is a triangular muscle plate that give rise to tendinous portions. The sympathetic trunk and splanchnic nerves cross dorsal to the lumbocostal arch. The musculature of the medial portion of the right crus is the thickest (5 to 6 mm) and originates from the terminal portion of the right column of the aortic hiatus. It extends ventrally to surround the esophageal hiatus and blends ventrally with the central tendon.
The costal part is composed of muscle fibers originating from the eighth (ventral portion) to the thirteenth ribs (dorsal part) which irradiate centrally to blend with the central tendon.
The sternal part may not exist in the dog. It is an unpaired medial part that originates on the base of the xiphoid cartilage and extends dorsally to blend with the central tendon.
The convex thoracic side of the diaphragm is lined with fascia endothoracica and pleura. It lies against the surface of the lungs. On the dorsal part of the mediastinum the aorta, azygous vein, hemiazygous vein and thoracic duct cross through the aortic hiatus. The esophagus passes through the esophageal hiatus together with the dorsal and ventral vagal nerve trunks. The caudal vena cava and right phrenic nerve reach the diaphragm in the plica vena cava and cross through the foramen of the caudal vena cava. The stomach and liver attach to the concave peritoneal surface via ligaments.
- b) Name the nerve that provides motor supply to the diaphragm. (1 mark)
Phrenic nerve (C5,6,7)