Dogs and Cats 16 Flashcards
1
Q
pathogenesis of periodontal disease what is the primary and secondary factor and how is calculus involved
A
- Primary factor = plaque bacteria -> HAS TO BE PRESENT
- Secondary factors = tooth crowding, persistent deciduous teeth, malocclusions, non-abrasive diet, periodontal trauma, genetic predisposition, systemic illnesses (FIV in cats
- Calculus
○ Bacterial plaque is often attached to calculus
○ Calculus is merely mineralised plaque and in itself is not harmful
○ However, it provides a roughened surface for plaque to adhere to
○ Gingival recession exposes cementum which is more plaque retentive
2
Q
What are the first 4 steps in the pathogeneiss of periodontal disease that finishes at gingivitis
A
- Bacteria attach to tooth surface by adhering to tooth pellicle (salivary glycoproteins)
- Start forming seconds after teeth prophylaxis (fully formed after 4 months) - Once attached, plaque can only be removed via mechanical means
- Bacteria which attach are initially gram positive, non-motile aerobes
- Gingiva becomes irritated by this plaque -> swells and lifts from the tooth (gingivitis)
3
Q
What are the 2 steps after gingivitis that leads to periodontal disease
A
- If plaque is left undisturbed it eventually penetrates subgingivally
○ Subgingivally, population changes to predominantly gram negative, motile anaerobes -> initiation of periodontal disease - Bacteria and their toxins penetrate the sulcular and junctional epithelium -> rapid acute inflammatory response
○ This leads to soft tissue damage and alveolar bone resorption
○ Formation of periodontal pockets & tooth mobility and eventual tooth loss
§ Allows for more subgingival movement -> cycle continues
○ Localised disease but can also lead to bacteraemia & possibly other organ involvement
4
Q
What are the clinical signs and diagnosis of periodontal disease
A
Clinical signs - Halitosis - Difficulty or pain when eating - Hypersalivation, blood tinged saliva - Plaque and calculus - Bleeding or ulcerated gingiva - Gingival recession - Furcation Exposure - two roots split in multiple rooted teeth - Tooth mobility Diagnosis - Periodontal probing ○ Evaluate presence and degree of attachment loss - Dental radiographs ○ Evaluate bone loss as well as complications such as endodontic disease
5
Q
Periodontal disease what are the 4 stages and attachment loss
A
STAGE 0 - NORMAL
STAGE 1. gingivitis, 0% attachment loss
STAGE 2. Early PD, 25% attachment loss
STAGE 3. moderate PD with 25-50% attachment loss
STAGE 4. severe PD with >50% attachment loss
6
Q
What are 7 indications for dental treatment
A
1) periodontal disease
2) broken teeth - especially carnassial (UPM4)
3) discoloured teeth (pulpitis)
4) mobile teeth
5) retained deciduous teeth
6) resorptive lesions
7) stomatitis - inflammation of mucous membranes of mouth - may benefit from full mouth extraction
7
Q
Endodontic disease what is the main one and causes
A
- Pulpitis – inflammation of the pulp
○ Can be reversible or irreversible - Pulpitis causes
○ Blunt trauma to tooth
○ Uncomplicated and complicated crown fractures
§ Uncomplicated -> no exposure of pulp cavity
§ Complicated -> exposure of pulp cavity
○ Enamel & dentine hypoplasia
○ Haematogenous route
○ Iatrogenic causes (inappropriate use of polishing or scaling devices, restorative materials)
8
Q
What is the pathogenesis of pulpitis
A
a. Pulp injured -> pulpitis -> pulpal oedema or haemorrhage
b. Pulp exposure through fracture -> exposed to bacteria and becomes infected.
§ This leads to inflammation and oedema.
c. Inflammation + oedema + haemorrhage -> pulpitis + pain
d. If no treatment -> pulpal strangulation (compartment syndrome) -> death of dental pulp
e. Liquefaction of necrotic pulp, and escape of liquid through the apex.
f. Bacteria penetrating the apical delta -> periapical granuloma
g. Severe periodontal disease
§ Bacteria may gain access through apical delta, infected cementum or lateral canals
9
Q
How to diagnose pulpitis
A
○ History
○ Visual examination - draining tracts
○ Transillumination - shine bright light through the teeth (non-vital teeth no transfer of light - appear dull or dark)
○ Radiology - pulp cavity that is wider than the other teeth (as grows becomes narrow)
10
Q
What are the main options for treatment of pulpitis
A
○ Two options for tooth with pulpal death
§ Endodontic Therapy
§ Extraction
○ No treatment -> chronic pain and infection
○ Endodontic therapy
§ Pulpectomy - entire pulp is removed and dental cylinders created within the pulp cavity - closed off to the rest of the body
§ Vital pulpotomy - fracture site is sealed off
§ Surgical apicectomy
11
Q
dental radiography indications and equipment
A
- Indications ○ Teeth which are discoloured, fractured, missing, abnormally shaped or placed, mobile § Pre- and post-extraction § Oral masses/swellings § Tooth Resorption - Equipment ○ Wall-mounted vs handheld unit ○ Reusable intraoral plates ○ Processor ○ Personal protective equipment
12
Q
Dental radiograph what are the 2 techniques
A
- Parallel Technique
○ Used generally only on mandibular premolar and molar teeth
○ Film placed parallel to long axis of tooth root and perpendicular to x-ray beam
○ Provides the most accurate image - Bisecting angle technique
○ Most common positioning technique used in veterinary patients
○ Place film as parallel as possible to long axis of tooth root(s) of tooth being radiographed
○ Then approximately bisect the angle between tooth and film
○ X-ray beam perpendicular to this plane
13
Q
Dental radiography what to do with superimposition of structures, correcting elongation and foreshortening
A
○ Superimposition of structures
§ Change angle of incident beam
○ Correcting elongation and foreshortening
§ Angle between your incident beam and long axis of tooth root is either too acute or too obtuse
Shadow of building analogy -> if roots seem too long
14
Q
What are the 12 steps within dental treatment program
A
1) presurgical exam and consultation
2) supragingival cleaning
3) subgingivial plaque and calculus scaling
4) residual plaque and calculus identification
5) polishing
6) sulcal lavage - optional
7) fluoride - optional
8) oral evaluation with periodontal probing and dental charting
9) dental radiographs
10) treatment planning
11) application of barrier selanat - optional
12) client education during post-surgical discharge
15
Q
presurgical exam and consult for dental treatment what is involved
A
○ Comprehensive physical exam and pre-anaesthetic screening as required - blood work
○ Discuss findings with owner and counsel on treatment options based on anticipated level of disease (remember, though only 50% of disease present can be detected on a conscious exam)
16
Q
supragingival cleaning for dental examination what is the goal and the 2 types of instruments used, what need to be careful of
A
○ Goal is to remove large accumulations of calculus, usually via a combination of mechanical and/or hand scaling
1. Mechanical scalers
§ The ultrasonic scaler is the most commonly used and comes in 2 main types, magnetostrictive and piezoelectric
§ Work by providing different patterns of vibration
§ Produce heat which can damage the tooth - DO NOT SPEND MORE THAN 10 SECONDS PER TOOTH
2. Hand scalers
§ Most commonly used is the universal scaler
§ Triangular instrument with two sharp cutting edges and a sharp tip
§ To be used ABOVE THE GUM ONLY - the shape and sharp back and tip can easily damage the gingiva
17
Q
Subgingival plaque and calculus scaling in dental treatment how important, what equipment used and how done
A
○ This is THE most important step
§ Subgingival calculus is more difficult to remove due to limited access, bleeding, and adherence to tooth surfaces
○ We used to do this by hand (using a curette), but now many mechanical (ultrasonic) scaler tips are safe for use subgingivally (BUT CHECK BEFORE YOU DO SO)
○ Open root planing - raise a flap to properly clean subgingivally, if pockets >6mm (dog)
18
Q
Residual plaque and calculus identification and polishing during dental treatment what is involved and what need to be careful of
A
Residual plaque and calculus identification
○ If possible, check with a dental explorer and/or use a plaque-disclosing solution
○ IC plaque ->stains plaque red after clean place on and make sure haven’t missed anything
5. Polishing
○ Goal is to smooth the tooth surface to help decrease plaque adherence after scaling
○ Performed with rubber prophy cup on slow-speed handpiece
○ No longer than 5 seconds at a time per tooth to avoid damage
19
Q
Sulcal lavage and fluroide in dental treatment how commonly done and why
A
Sulcal lavage (optional?)
○ Not routinely done in most general practices but could be beneficial - removes microscopic debris from gingival sulcus
○ Recommended to lavage with 22-25 gauge cannula, using sterile saline or 0.12% chlorhexidine solution
Fluoride (optional)
○ Controversial
○ Application may decrease patient sensitivity after subgingival scaling
20
Q
Oral evaluation with periodontal probing and dental charting what technique use, normal sulcus depth and what is important to consider with this sulcus depth
A
○ Establish a system and do this the same each time
○ Preferred technique is to start with first incisor at each quadrant
○ Use modified triadian system to report and try to probe at least 4, possible (6), depths around EVERY TOOTH
§ Normal dog sulcus depth 0-33mm - NEED TO KNOW
§ Normal cat sulcus 0-0.5mm - NEED TO KNOW
○ In patients with gingival recession, remember that the attachment loss is the probing depth plus the gingival recession
21
Q
Dental radiographs where should be taken, when and what is gold standard
A
○ Taken at a minimum of every area of pathology noted on your exam
§ Deep periodontal pockets, furcation
§ Fractured/chipped/mobile/discoloured teeth
§ Missing teeth (retained roots? Dentigerous cysts)
§ Masses/swellings
○ Many clinicians advocate for full mouth radiographs but we are often limited by client funds and time
22
Q
treatment planning after dental examination what need to take into account and options
A
○ Take into account:
§ Exam findings
§ Radiographic findings
§ Overall patient health, also is the GA going well
§ Willingness of owner to perform home care
§ Likelihood of owner to follow up
§ Owner finances
○ Don’t forget that referral is an option
§ Root canal, restoration
○ Planning for extractions at the end
23
Q
Application of barrier sealant (optional) during dental examination what done, why optional and what is the most commonly used product
A
○ Waxy substance applied to teeth at end of the procedure after all is clean and dry
○ Clinically proven to decrease plaque and calculus however some dentists do not feel this is effective
○ OraVet is the most commonly used production
24
Q
Client education after dental examination what do you need to discuss and when should you do it
A
○ This is the best done by the treating veterinarian during the post-surgical discharge
○ Review the radiographs, discuss homecare and schedule follow up
§ Professional care has been shown to be of little valve without homecare
§ Most veterinary dentist suggest that owners should be doing at least 2 types of care, once a day
Homecare is comprised of MECHANICAL AND CHEMICAL modalities
25
What are 6 examples of mechanical homecare for teeth and which shouldn't you advise - rule of thumb
1) Tooth brushing (gold standard)
® DOG/CAT TOOTHPASTE, not human
® Daily
® Start slow… lots of patience and rewards
® Small, soft brushes. I really like cotton buds/Q tips
2) Dental diets (Hill's T/D, Royal canine dental)
3) Chews (oravet chews, greenies, dentastrix)
4) Toys
5) Pig ears -> no evidence that these works, reports of bacterial contamination
6) Bones -> NOT ADVISED, tooth fracture, GI obstruction
§ IF WOULDN'T WANT TO WHACK YOURSELF OVER THE KNEE WITH THE TOY THEN TOO HARD FOR PET
26
What are 6 examples of chemical homecare for teeth
1) Chlorhexidine based products (Hexarinse, curasept)
2) Zinc ascorbate (Maxiguard)
3) Xylitol (aquadent)
4) Miscellaneous (healthy mouth)
Other examples
1) Dental wipes
2) Oravet weekly application
27
What are the 6 reasons you MUST DO teeth extractions
1. Complicated crown fracture
2. Oronasal fistula caused by periodontal disease
3. Advanced PD (grade 4 >50% root exposure, grade 3 furcation, excessive mobility)
4. Advanced feline tooth resorption (dogs are more complicated)
5. Tooth in a fracture line
6. Retained deciduous teeth
28
What are 6 situations where extractions are negotiable
1. Is the owner able/willing to perform homecare, will the animal tolerate it?
2. If willing, what level/type of care will be performed
3. Is this the only dental likely to be performed for a long time or will they recheck as instructed in 3,6,12 months
4. Is the tooth important/strategic (canines, carnassials)
5. If you extract, what are the potential consequences (mandibular carnassial contracting site of maxillar carnassial, tongue protuding, lip getting caught by canine)
6. Are there other treatment options (refer for root canal, orthodontics, guided tissue regeneration, restoration
29
what are the 6 main tools needed for extraction
1. Dental X-rays
2. Luxators + elevators
3. Tooth extraction forceps
4. Dental base with triplex, high speed handpiece and burrs
5. Periosteal evevator
6. Small surgical kit with fine instruments
○ Scalpel (11,15 probably most common) and holder
○ Scissors
○ Needle drivers
○ Rat tooth tissue forceps
○ Suture material (usually 4-0, 4-0, absorbable)
30
What are the 7 steps in a simple extraction of a tooth
a. Dental xrays should proceed ALL extractions
b. Gingival incision
c. Luxation
d. Removal of root
e. Management of alveolus
f. Post extraction radiograph
g. Suture (usually 4/0,5/0, absorbable)
31
What are the 2 ways to do a double root teeth extraction and when would you do each
1) Simple extraction -> can do without use of a flap only if tooth is very diseased and you expect the roots will be removed without complication
2) creating a flap - surgical extraction
32
What are the 6 steps in the surgical extraction of multiple root tooth
1) Creation of vertical releasing incisions in making a mucogingival flap
§ Make incisions on the line angle of the roots of the teeth, just caudal and rostral to the target
§ Making the incisions slightly divergent will provide a broader vascular base
§ The vertical incision must be placed OFF the target tooth so as to avoid a TRAMPOLINE EFFECT on closure
§ Making an incision along the sulcus
§ Use a periosteal elevator to lift the attached gingiva, then the mucosa
- Be patient, tissue is delicate and tears easil
2) Flap is lifted exposing buccal bone and root structure, now can section and elevate
3) After sectioning the tooth, luxate the roots individually, remove buccal bone as necessary
4) To ensure extraction is complete, palpate the root tip (it should be smooth) AND take a post extraction radiograph
5) Lay the flap down, there should be no tension
6) Routine closure with simple interrupted sutures
33
Deciduous teeth when identify, why extract and why may fracture occur during extraction
○ Really important to identify in kittens and puppies
○ Extracted due to: fracture, crowding and malocclusion
○ Care is required when extracting - if done incorrectly
§ Damage may be done to the adjacent adult tooth - root damage or if not yet erupted, enamel damage
○ Fracture may occur
§ The roots of these teeth are VERY long, with the crown:root ratio often nearly 1:3.
§ This conformation requires extensive elevation before extraction is possible
§ These teeth have large pulp chambers with thin dentinal walls and are not tolerant of the exertional forces typically used to extract adult teeth
34
What are 6 main complication of teeth extractions
- Root fracture -> displacement of root tips (into places that you might not want to retrieve them from)
- Jaw fracture
- Oronasal fistula
- Haemorrhage
- Soft tissue injury (need to be careful of the tongue)
- Injury to the operator or assistant
35
What are 6 main ways to avoid complication
- Be patient!
- Don't use excessive force
- Use proper technique
- Know your anatomy, radiographs will help
- Use extractions forceps ONLY when the root is loose
- Alevoplasty before closing the flap; no tension on closure
36
Feline chronic gingivostomatitis other names, what is it and causes
- Nomenclature: Stomatitis, Caudal Stomatitis, Caudal Mucositis, Feline immune dysregulated stomatitis
- Persistent inflammation of the oral mucosa
Aetiology
- Aetiology has not been identified
- Multiple aetiologies may exist
- Viral (Calicivirus, FIV), Bartonella henselae, altered immune status & exaggerated inflammatory response to bacterial plaque have all been postulated
37
Feline chronic gingivostomatitis diagnosis and goals of treatment/management
Diagnosis
1. Visual examination
○ Affected gingiva and oral mucosa have varying amounts of inflammation, proliferation and ulceration
○ Lesions are often bilaterally symmetrical, friable oral tissue that bleed easily
- Gingivostomatitis and periodontal disease can present with severe gingival inflammation
○ Main differentiating clinical sign is the presence of caudal inflammation (Distal to the teeth)
2. Biopsy can help rule out neoplasia
Goal of treatment/management
- Goal is complete resolution of oral inflammation
- Managing a state of reduced inflammation is in some cases the best that can be achieved
38
Feline chronic gingivostomatitis what are the 2 main treatment options and options within
○ Surgical management
§ Extraction of all molars/premolars
§ Full mouth extraction
§ Laser treatment to remove inflammatory tissue - generally not done
○ Medical management - differing views on effectiveness
§ Chronic immune-suppressive treatment (i.e. cyclosporine, corticosteroids, Imuran)
§ anti-inflammatory treatment (Corticosteroids, NSAIDs)
§ antibiotics
§ feline omega interferon
39
Feline chronic gingivostomatitis what is the most successful long-term therapy, response and what if bad
- Most successful long-term therapy is extraction of all pre-molars and molars
○ Extraction of canines and incisors is indicated when the inflammation extends to include the gingiva surrounding them
○ If choose to keep in then need good dental homecare
- Majority of cats will have an excellent response to the treatment
- Poor response may require medical management
○ These are cats which have already had chronic immunosuppressive drugs
○ These cats may respond to low doses of immunosuppressive drugs and antibiotics
○ Check for retained root tips – DENTAL RADIOGRAPHS
40
Tooth resorption what also called, where originates, type based on and cause
- AKA Feline odontoclastic resorptive lesions, neck lesions, cervical erosive lesions, dental resorptive lesions
- Typically originates in the cementum, may progress into root dentin and then either progress through root, into the crown or both.
- Tooth Resorption type based on radiographic appearance
- Many hypotheses but the cause has not been proven
41
Diagnosis of tooth resorption what are the 3 things needed and what defines the 3 types
- Visual Examination + use dental explorer + dental radiography
- Type 1
○ Periodontal Ligament and roots remain distinct on radiographs of teeth
Still have black line between root and alveolar bone
- Type 2
○ Ligament and roots of teeth become radiographically indistinct as they are replaced by bone
Periodontal ligament resorption
- Type 3
○ Both Type 1 & Type 2 lesions present
42
What is the treatment for type 1 and 2 tooth resorptive lesions - EXAM
- Type 1
○ Extraction of the tooth is the only reliable treatment
- Type 2
○ Intraoral resorptions – extraction or crown amputation
○ Crown amputation performed only in teeth with confirmed type 2 tooth resorption
43
Caries what is it, how common and pathogenesis
```
tooth decay
- Bacterial infection of the tooth that destroys enamel and dentin
- Common in man, uncommon in do
- Not been accurately documented in cats
Pathogenesis
- Pathogenesis not well-studied in dogs
- In humans, begins with acidic destruction of teeth when plaque bacteria ferment dietary carbohydrates
- Genetic susceptibility
```
44
Management of caries and what necessitates extraction
- Dental radiographs to check for endodontic disease - important to check if present
- Carious lesions that do not involve pulp – restorative dentistry is an option
- Endodontic (pulp cavity) involvement necessitates root canal treatment or extraction
45
Enamel hypocalcification what also called, why occurs and what is the most common types seen
- AKA Enamel Hypoplasia
- Interference with amelogenesis
○ Lack of enamel or abnormal enamel formation
- Most common type seen in dogs is Environmental enamel hypoplasia
○ Systemic syndrome damages cells of enamel organ and impedes their function
- OR trauma common
46
Enamel hypocalcification management
- Restorative dentistry – all poorly attached enamel removed using ultrasonic scaler
- Bonding agent or dental sealant applied to occlude dentinal tubules
○ Prevents tooth sensitivity and ingress of bacteria into pulp
- If endodontic involvement – endodontic or exodontic therapy is indicated
47
oral massess what are some options, is it a common site for malignant neoplasia and the 2 main types
- Oral masses include benign/malignant neoplasia, gingival hyperplasia, fungal lesions, cysts etc
- Oral cavity is 4th most common site for malignant neoplasia
- Tumours
a. Odontogenic (AKA Epulides)
b. non-odontogenic (based on tissues of origin)
48
Odontogenic Tumours what are they, what include and what is the main one
- Epulis – any gingival growth
○ Historically epulides referred to benign locally invasive tumours
○ Epulides comprise 20-30% of oral tumours
Canine Acanthomatous Ameloblastoma
49
Canine Acanthomatous Ameloblastoma what also called, what arise from, character, predilection site and management
- AKA Acanthomatous epulis
- Arises from epithelial rests of malessez, adjacent bone and/or periodontal ligament
- Locally aggressive (invade bone) but are benign (so do not metastasise)
- Have a predilection for mandibular incisors and premolar regions
- Management
○ Wide surgical margins that include a section of normal bone - as locally aggressive EVEN THOUGH BENIGN
50
Non-odontogenic tumours what are the most common canine and feline ones
- Most common canine oral tumours are malignant melanoma (30-40%), squamous cell carcinoma (20-30%), fibrosarcoma (10-20% and male dogs predisposed), osteosarcoma (<10%)
- Most common feline tumours are squamous cell carcinoma (70-80%) and fibrosarcoma (13-17%)
51
Canine Malignant Melanoma predispoition, character and size for better prognosis
- Occurs in older patients and a male predisposition has been suggested
- Breeds with increased oral pigment are over-represented
- Highly-metastatic
- <20mm in size tend to have better prognosis
52
Feline oral SCC how common, risk factors, most common site, character and median survival time
- Most common feline oral tumour
- Risk factors include smokers in house, flea collars and canned tuna/food
- Most common site is sublingual
- Tumour is invasive and local disease is often cause of death
- Median survival time is 45-60 days
53
Diagnosis of oral massess what is involved
- Full and thorough clinical examination
- Imaging – CT vs radiographs
- Careful inspection and palpation of the tumour and drainage lymph nodes
- Biopsy – incisional recommended as benign and malignant masses have similar appearance.
○ FNA and impression smears can be unrewarding - generally under GA anyway so just take biopsy
- Histopathology – proper management starts with accurate diagnosis
- Clinical staging – TNM system from WHO
○ Tumour: extent of primary tumour
○ Node: involvement of regional lymph node
○ Metastasis: absence or presence of distant metastases
54
Gingival hyperplasia what also called and the 2 main types of causes
- AKA Generalised Gingival Enlargement
- Non-specific causes
○ Chronic inflammation
- Specific causes
○ Drug related - cyclosporin
○ Hereditary
55
Management of gingival hyperplasia how to diagnose and treatment
- Biopsy -> Histopathology and dental radiographs (to ensure no bone involvement)
○ Dental radiographs should be normal except for increase in soft tissue density of enlarged gingiva
- Removal of plaque + calculus + excess gingiva followed by strict homecare
- Gingivectomy – return gingiva to normal contour
56
Malocclusion what is the most common cause and what is important for the owner
- Either genetic or non-genetic origin
- Hereditary is most common cause
○ Mating of parents with dissimilar jaw sizes
○ Other genetic causes include
§ tongue size
§ lip and cheek tension
§ presence of cleft palate
- Genetic counselling for owner - is this animal suitable for breeding? NO
57
Malocclusion class I what is called and what involved
○ Jaws are of the correct length with a scissors bite but one or more teeth are out of alignment
○ Mesioversed maxillary canines (lance effect)
○ Base narrow canines
58
Malocclusion class II what is it called and what involved
○ AKA overshot, manidibular brachygnathism
○ Lower molar positioned distal to the upper molar
○ Jaw length discrepancy, mandible is shorter than maxilla
○ Considered primarily a genetic condition
59
Malocclusion class III what is it called and what is involved
○ AKA undershot
○ Jaw length discrepancy – mandible is longer than maxilla
○ Generally considered genetic however such non-genetic causes such as severe infection or nutritional diseases should affect both jaws equally
Some class III malocclusions considered normal for certain breed standards
60
Malocclusion class IV what is called and what is involved
○ AKA Wry bite
○ Jaw length discrepancy – two mandibles are of different lengths
○ Shift of the mandibular midline
○ Primarily a genetic condition
○ Other reported causes include trauma with bone scarring or physeal closure
61
Management of malocclusion diagnostics and treatment options
- Visual examination is diagnostic
- Dental radiographs - looking for trauma that may have led to the malocclusion
- Options
○ If purely cosmetic – no treatment indicated
○ Exodontic therapy - not ideal - removal of teeth
○ Orthodontic correction
○ Endontic therapy - Coronal amputation and vital pulp therapy
62
trauma for tooth and are the 2 main things that occur and most common teeth affected
- Luxation & avulsion
○ Tooth luxation – tooth may still be partially attached to alveolar bone but deviated from its normal position
○ Avulsion – complete displacement of a tooth from its alveolus
- Most common teeth affected are maxillary canine and incisor teeth
63
Management of trauma damaged tooth what are the options, factors that influence decisions and what is saving the tooth
- Decide to save or abandon the tooth
○ Factors -> Strategic value of tooth, time between injury and treatment, owners’ dedication
- Pulp is going to become necrotic due to disruption of blood supply
○ Endodontic therapy will be needed in future
- If saving tooth - referral to veterinary dentist
a. Avulsed tooth placed in milk, sterile saline or balanced salt solution and should be reimplanted as soon as possible
b. Soft tissue repair and management of fractured alveolar bone
c. Semi-rigid fixation of tooth with wire and acrylic splint
- If dodgy owners - recommend tooth extraction
64
Peritoneum what is it and divided into
- Transverse fascia; covering of mesothelial cells
- Divided into two
○ Parietal: lines cavities
○ Visceral: overlaps organs
- Peritoneal cavity:
○ Develops from mesoderm
○ Contains scant non inflammatory fluid
65
What is a hernia and the 3 parts and what classifications are there
- Protrusion of an organ through an anatomical or pathological defect
- Three parts to a hernia
○ Hernia ring
○ Hernia sac
○Hernia contents
CLASSIFICATION
- congenital vs acquired
- true vs false
- reducible vs incarcerated
- strangulated
- location
66
what is involved in a congenital vs acquired, true vs false
- “Congenital” vs “acquired”
○ Congenital- failure of appropriate embryogenesis development
○ Acquired: traumatic or incisional
- “True” vs “false”
○ True hernia:
§ Through normal anatomical structure.
§ Hernia sac consists of a peritoneal lining or out pouch.
○ False hernia
§ No peritoneal lining of the hernia sac.
67
What is involved in a reducible vs incarcerated and strangulated
```
- “Reducible” vs “incarcerated”
○ Reducible
§ Contents can be manipulated back into normal anatomical cavity
○ Incarceration/non reducible
§ Contents are unable to be reduced.
□ Obstruction of a hollow viscous
□ Compromise of blood supply
- “Strangulated”
○ Compromise of bloody supply
§ Necrosis and perforation
Swelling, congestion
```
68
What are the 9 different locations of hernias
Different locations of hernias
1. Paracostal
2. Dorsal lateral
3. Inguinal
4. Prepubic rupture
5. Femoral
6. Umbilical
7. Ventral/subxiphoid
8. Scrotal
9. Perineal
69
What are the main clinical signs in hernias
- Variable on type, locations, incarcerated, strangulated?
- Swelling
- Pain
○ Uncomplicated hernias will not be painful - congenital inguinal hernia for example
70
herniorrhaphy what is it, what is involved and what is the main complication and how to prevent
surgery to fix hernia
- Basic concepts of Herniorrhaphy:
○ Return viable contents to normal location
§ Resection?
○ Secure and close hernia ring
○ Obliterate redundant tissue in sac -> reduce dead space to reduce serosal formation
Tension free closure
complication
- Loss of domain (abdominal compartment syndrome, no longer limited by intraabdominal pressure so enlarge -> increase pressure in abdomen onto viscera and diaphragm -> need special closure techniques to reduce this) chronic hernias
71
What are the 4 main congenital and 2 main acquired hernias
1) umbilical hernias
2) femoral hernias
3) inguinal hernias
4) scrotal hernias
Acquired
1) abdominal hernias
- traumatic
- incisional
2) diaphragmatic hernias
72
Umbilical hernias how common, cause, when occur and redicuble vs non-reducible in terms of treatment
○ Most common form of hernia
○ Congenital
○ These hernias can spontaneously close up to 6 months after birth
§ Repair at time of desexing generally
○ Inherited and heritable
§ Other inherited defects? Cryptorchidism
○ Reducible vs non?
§ Reducible risk of strangulation of intestines so want to fix quickly
§ Non-reducible - wait 6 months for spontaneously closure and if don't then fix at desexing
73
Femoral hernias how common, where move through and the 2 main causes
○ Rare
○ Hard to distinguish prior to surgery from inguinal
○ Through the femoral canal or vascular/muscular lacunae
○ Causes:
§ blunt trauma - pubic or inguinal ligament avulsion
§ iatrogenic transection
74
Inguinal hernias what are the 2 main things can go through and direct vs indirect
○ Anatomy:
§ Internal inguinal ring- a hole in the aponeurosis of the external abdominal oblique muscle)
§ External inguinal ring
○ direct” or “indirect”
§ A direct hernia is passage through the normal invagination;
an indirect herniation is passage adjacent to the normal invagination. Eg Scrotal hernias in males
75
Inguinal hernias congenital vs acquired what generally occur in and assicated with what other hernias
§ Congenital:
□ Young male dogs
□ Cavalier king Charles spaniel, cocker spaniel, dachshund,
□ Associated with umbilical hernias, left sided
§ Acquired:
□ Older entire females
□ Obesity predisposes
□ Associated with perineal hernias in intact males
76
Inguinal hernia diagnosis, repair and complications
○ Diagnosis: palpation may be sufficient, Radiography, US
○ Repair:
§ Ventrolateral incision +/- midline
§ Desexing recommended
□ Increase risk of testicular cancer
□ Neutered females at lower risk of recurrence
○ Complications; haematoma/seroma and subsequent infection/dehiscence, fat necrosis (cats)
77
Scrotal hernias what are they, most common cause of, treatment and prognosis
○ Indirect inguinal hernias.
○ Scrotal hernias account for most of the cases of strangulated bowel in young male dogs.
○ Castration recommended time of surgery for scrotal hernias
§ Amputation of the whole hernia sac
○ Non-entrapped or non-strangulated scrotal hernias carry a good prognosis
78
traumatic Abdominal hernias main causes, what lead to
§ Blunt traumas, bite wounds
§ MVA - motor vehicle accidents
§ Lack of true peritoneal sac
□ Risk of Adhesions
§ Blunt force trauma- at region of abdominal wall attachment
□ Paracostal, prepubic
§ Sharp lacerating trauma can occur anywhere
79
Trumatic abdominal hernias what are important considerations besides the hernia
§ Concurrent injuries as most are traumatic
§ Prominent swelling- doesn’t relate to size of body wall defect
□ Often present due to signs relating to traumatic incident
§ Musculoskeletal injuries, shock?
□ Require stabilization
80
Abdominal hernias diagnosis and treatment
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Diagnosis:
§ Radiographs
□ Free intra-abdominal gas
□ Abdominal wall contour?
□ Or size alterations?
□ Include thoracic radiographs
§ Ultrasound if concern for perforation
Treatment
§ Treat shock and stabilize first
§ Acute traumatic
□ midline celiotomy
abdominal exploration, intra-abdominal repair
§ Chronic?
□ Incision over hernia contents
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81
Incisional hernias when result from, how common, causes and treatment
Wound breakdown
§ Rare in small animals
Causes:
□ Fat entrapped in incision, inappropriate suture material or suture handling technique.
□ Weakening of wound edges (infection, chronic steroid us, excessive motion) or delayed healing (diabetes, cushings)
Treatment
□ Debridement only recommended if tissue edges are non viable as will only worsen the tension on the wound
□ Evisceration can occur if body wall and skin incision break down
□ Self mutilation common
82
Diaphragmatic hernias what is the most cmmon cause, why occur, types, what commonly affect and diagnosis
○ Traumatic most common (85%)
○ Sudden increase in intraabdominal pressure with the glottis open
○ Costal muscles; circumferential vs radial
○ Liver most commonly herniated
○ Diagnosis - radiographs
83
Diaphragmatic hernias repair and considerations
○ Repair: Ventral midline celiotomy +/- thoracotomy
○ Considerations:
§ Concurrent injuries and illness
§ Chronic- reperfusion injury, adhesions, abdominal compartment syndrome (as said before)
§ Liver herniation; congestion, necrosis, obstruction. Bacterial proliferation in devitalised tissue
§ Pleural effusion
84
Perineal hernias anatomy what muscles involved and pathophysiology
- Levator ani, external anal sphincter and coccygeus muscle.
- Weakening of this diaphragm (mainly levator ani)
Pathophysiology:
○ Older, entire male dogs
§ Breed predisposition (Pekingese, boston terrier, corgi, boxer, poodle, bouviers, old English sheepdogs)
○ Weakened perineal diaphragm mainly levator ani
§ Rectal dilation and deviation
○ If significant in size- allows displacement of the caudal abdominal organs through the diaphragm.
§ Caudal hernia: between the levator ani, internal obturator and external sphincter.
85
Perineal hernia complication and causes
- Complication -> Bladder retroflexion - bladder will lift and go into swelling -> cannot urinate
§ Acutely life-threatening -> hyperkalaemia -> heart arrythmias -> EMERGENCY SURGERY
- Causes?
○ Androgens - entire male dogs
○ Gender differences in muscle conformation
○ Relaxin - within females
○ Prostatic disease (chronic straining?)
○ Neurogenic atrophy
86
Perineal hernia clinical signs and diagnosis
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- Clinical signs:
○ Perineal swelling/bulging - generally nonpaingul
○ Straining to defaecate (tenesmus)
○ Constipation
○ Dysuria
○ Bladder retroflexion?
- Diagnosis can be confirmed by digital rectal exam - often sufficient
○ Contrast radiography
○ Ultrasonography
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87
Perineal hernias what are the 3 main treatment options and things within
1) conservative - not enough in the long term - medical manageemtn with frequent enemas, high fibre moisture diet and stool softeners
2) surgical
- traditional herniorraphy
- internal obturator muscle transposition - most common
- superficial gluteal transposition - not recommended
- semitendinosus - salvage
- prosthetic - mesh
3) castration - without there is a large chance of recurrence
88
What is involved with traditional herniorraphy for treatment of perineal hernias
□ Suturing levator ani and coccygeus muscle to the external anal sphincter.
▪ Care with excessive tension on external- incontinence
▪ If bilateral hernias are present then stage procedures 3-4 weeks apart to minimise tension
□ Sciatic nerve close to Sacrotuberous ligament and internal obturator -> don’t catch with suture
▪ Will know when animal wake up in extreme pain
□ Muscles atrophied, recurrence is likely
89
What is involved with the internal obturatory muscle transposition for treatment of perineal hernias
□ Provides vascular supply and reinforcement
□ Dorsomedial transposition -> Elevate and place dorsal to help support
□ Procedure of choice for more complex or bilateral hernia
90
Prosthetics in treatment for perineal hernias what is involved
□ Can be used alone or as an adjunct to other procedures
□ Suturing mesh to the coccygeus muscle dorsally and medially and Sacrotuberous ligament laterally and internal obturator muscle ventrally
□ Use to reinforce the area but if possible use internal obturator muscle
91
what are some complications of perineal hernia treatment
- Wound infection
- Faecal incontinence
- Tensesmus
- Rectal prolapse
- Urinary incontinence/bladder necrosis
- Sciatic nerve entrapment:
- Recurrence - OWNER EDUCATION
92
Metabolic alkalosis what worried about
OBSTRUCTION
93
With GDV what anaglesia given, common complication how overcome and what premedication to use
- Analgesia - methadone - NEED TO GO TO SURGERY
- Irregular pulses - ECG -> ventricular premature contractions probably - lidocaine infusion (helps with reperfusion injury, analgesia) - USE IN GDV
Premedication - comes in flat -> lower sedation needed
- ketamine + midazolam - moderate
- Ace and methadone -> sedation, analgesia - moderate
- Alpha-2 agonist - wouldn't use
94
What are some anaesthetic complications during GDV surgery
- Cardiac dysrhythmias - when derotate the stomach high risk, if bad give bolus of lidocaine
- Hypoventilation -> large stomach compressing diaphragm
- Painful -> is analgesia appropriate
- Hypotension
- Hypothermia - low temperature
- Hypoxaemia -> if aspiration pneumonia, if hypoventilation so severe - generally not an issue
Acidemia -> hyperlactatemia, compensatory increase RR
95
Erythropoietin what stimulate, synthesised by, when
- Erythrocyte production
(in bone marrow) stimulated by erythropoietin:
○ EPO synthesized by the kidneys
○ Synthesis of EPO increased by hypoxia
96
What are the 3 main causes of hyperbilirubinaemia, what occurs and what expect on biochemistry
1) Haemolytic (prehepatic)
§ Rapid destruction of RBC causes release of bilirubin into blood
§ Expect an increase in unconjugated (bilirubin)
§ Animal expected to be anaemic
§ Release of hepatic enzymes into blood (ALT, AST, GLDH, SDH)
2) Hepatocellular (hepatic)
§ Hepatic injury or dysfunction impairs uptake and conjugation of bilirubin
§ Expect an increase in unconjugated (bilirubin)
3) Post-hepatic (obstructive)
§ Obstruction of bile flow causes regurgitation (reflux) of bilirubin into the circulation -> cholestatic liver disease
§ Expect an increase in conjugated (bilirubin)
§ Reflux of enzymes lining biliary tract into bloodstream (GGT, alkaline phosphatase (AP or ALP - not as specific)
97
Anaemic patients what is it, what result in and what need to do to maintain oxygen delivery
- absolute reduction in RBC mass -> reduced haemoglobin concentration -> Decrease in bloods O2 carrying capacity
SHIFT CURVE TO THE RIGHT
- Easier to remove oxygen from the haemoglobin
- PO2 same but removed more oxygen within the venous system
- O2 EXTRACTION RATIO HAS INCREASED
THEREFORE
○ In order to maintain oxygen delivery = cardiac output x 02 content (this has decreased as said above)
SO INCREASE IN CARDIAC OUTPUT to compensate
98
What are the 3 main mechanisms of clinical signs of anaemia
- Signs of anaemia are caused by the body compensating for decreased O2 carrying capacity
1. Decreased haemoglobin affinity for 02
§ Increased production of 2,2-DPG
§ Allows tissues to more easily strip O2 from haemoglobin
2. Increased cardiac output to maintain tissue DO2
§ Increase in heart rate and/or stroke volume
3. Redistribution of blood flow
§ Selective vasoconstriction of blood vessels to "non-vital" tissue beds
99
what are the actual clinical signs of anaemia and what is important for the severity
○ exercise intolerance, lethargy, depression (dementia)
○ Tachycardia (increase in heart rate)
§ Increase tissue DO2
§ Systolic murmur - due to change in viscosity of blood
○ Tachypnoeic (increased respiratory rate)
§ Ensure complete arterial oxygenation
○ Cool extremities and weak peripheral pulses
§ Redistribution of blood to vital organs
○ Signs of shock (blood loss >30-40% of blood volume)
SEVERITY -> rate of development
100
Haemorrhage what are the main indications that this is occurring
§ Mucous membrane pallor
□ Icterus not usually a feature -> unless internal haemorrhage
§ Clinical signs of decrease D02
□ Tachycardia, tachypnoea etc
§ Hypovolaemic
§ Anaemia accompanied by hypoproteinaemia
□ PCV and (protein) normal acutely - lost all at the same rate
® Until blood is diluted through fluids or movement of fluids within the animal
□ Splenic contraction may obscure anaemia acutely in horses
Protein may be normal with haemorrhage into a body cavity
101
Haemolysis what are the main indications that this is occurring
§ Icteric/jaundice (hyperbilirubinaemia)
§ Signs of an inflammatory reaction - fever (intravascular causes inflammatory and could be secondary to infection), neutrophilia
§ Anaemia with a normal or slightly increase (protein)
§ Erythrocyte morphology can suggest etiology - heinz body
§ Hyperbilirubinaemia (unconjugated)
- Anti-RBC antibodies (cooms test or flow cytometry)
102
Bone marrow dysfunction what are the main indications that this is occurring
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□ HR and RR often fairly normal
□ Mucous membrane/scleral pallor
□ Icterus not usually a feature
® May be present in anorectic horses
□ Protein normal or increased
® Increased gamma-globulin concentration
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