Dog and Cat 9 Flashcards
1
Q
Diagnostic investigation round 1 for nasal discharge
A
1. Cytology/culture - NOT HELPFUL ○ Except if cryptosporidium (uncommon) 2. FNA ○ Facial swellings ○ SM lymph nodes 3. Haematology/biochemistry 4. Aspergillus titres (dogs) - screen for fungal infections 5. LCAT (cats) 6. Thoracic radiographs 7. +/-PCR for feline URTI pathogens
2
Q
Diagnostic investigation round 2 for nasal discharge what achieves and the techniques
A
- Requires anaesthesia
- Required for definitive diagnosis in most cases
1. Oral cavity exam
○ Probe tooth roots
2. Imaging - GOOD
○ Nasal radiography
○ CT scan or MRI
3. Rhinoscopy - GOOD
○ antegrade (rigid) and retrograde (flexible)
○ +/-sinusotomy and sinusoscopy
○ Limited as can only go into the main air passages -> should pair with imaging
4. Biopsies
○ histopathology and
○ bacterial and fungal culture
○ Swabs for viral isolation/PCR (CATS)
If don’t get specific diagnosis -> just inflammatory
3
Q
Diagnostic investigation round 3 and round 4 for nasal discharge what techniques done
A
Round 3 - Advanced imaging, if not done initially. - + repeat rhinoscopy and sampling. - + include frontal sinus (if involved). - Wait 1-2 months and repeat testing. Round 4 - Exploratory rhinotomy - +/-sinusotomy - +/-turbinectomy - generally don't do - RARE ○ Remove the normal physiological
4
Q
nasal foreign body clinical signs and diagnosis/removal
A
- Acute paroxysmal sneezing ○ Subsides with time - Gag/retch (cats) - Unilateral nasal discharge ○ Serous > MP +/-blood Diagnose/remove: - Otoscope cone + spey hook/dental mirror -> to see around the back of the nose -> occurs commonly in cats - Flush - Rhinoscopy - Advanced imaging/rhinoscopy -> if more chronic foreign body if buried within mucous or tissue
5
Q
Feline upper respiratory tract infection which cats occur in and presentation
A
Which cats? - Young - Stressed - Immunosuppressed -> Breeding/boarding catteries, shelters Presentation: - acute sneezing - serous to MP oculonasal discharge - differentiate from foreign body - conjunctivitis - hypersalivation (oral ulceration) - fever - anorexia - dehydration
6
Q
Feline upper respiratory tract infection what are the 4 main causes, transmission, signs
A
1) feline herpes virus - carrier state, relapse with stress - kittening transmit this dsease, ulcerative keratitis, eosinophilic facial dermatitis, major shelter pathogen
2) feline calicivirus - carrier state, shed continuously, more oral involvement - ulcers on nose, tongue, lips, predominates in stable multicat environments
3) chlamydia felis - conjunctivitis, URT
4) bordetella bronchiseptica - purulent rhinitis, cough, pneumonia
7
Q
Feline upper respiratory tract infection does it matter the cause, treatment and diagnosis
A
- Usually not! ○ Self-limiting ○ Lack of specific therapy ○ Mixed infections - Treatment generally symptomatic and supportive - Diagnosis usually presumptive
8
Q
Feline upper respiratory tract infection general treatment
A
- Address hydration: ○ SQ or parenteral fluids - Address nutrition: - rare ○ warm, soft, fishy foods. ○ Appetite stimulants? ○ Oral care ○ Feeding tube - Clear oculonasal discharge: ○ Moist cotton balls ○ Humidification ○ Decongestants? - don't use - Treat 2°bacterial infections: ○ Doxycycline ○ Amoxicillin ○ Topical antibiotic ocular therapy
9
Q
Feline upper respiratory tract infection treatment for herpesvirus, calicivirus and chlamydia
A
- Herpesvirus
○ Oral famcyclovir - possible to reduced severity of clinical signs
○ Topical (ocular) antivirals - Calicivirus
○ Recombinant feline IFN-ωfor chronic gingivostomatitis
○ Nothing for acute upper respiratory tract infection - Chlamydia
○ Treat ALL in contact cats
○ Doxycycline at least 4 weeks - 1-2 weeks treatment beyond clincial signs resolving
○ Topical (ocular) tetracycline
10
Q
Feline upper respiratory tract infection prevention
A
1. Avoid exposure ○ Housing ○ Hygiene and disinfection ○ Limit overcrowding ○ Isolate new arrivals ○ Isolate kittening queens ○ Early weaning ○ Early vaccination 2. Strengthen specific immunity ○ Vaccination
11
Q
Bacterial rhinitis what is important about it and treatment
A
- NOT a primary condition! - NEED TO IDENTIFY AND TREAT PRIMARY DISEASE
○ COMMON secondary to primary nasal diseases (most chronic)
§ 7-10 d empiric antibiotic course acutely -> if also treating the primary disease
(amoxicillin, clindamycin, TMS, doxycycline)
DO NOT use multiple or prolonged antibiotic courses without investigating the nasal disease!
12
Q
canine nasal mites transmission, signs, treatment
A
- Pneumonyssoides caninum
- 1 mm, white
- Direct transmission
- Frontal sinuses, caudal nose
- Acute rhinitis signs
- Ivermectin, milbemycin or selamectin 2-3 x
- Treat in-contact dogs
13
Q
Allergic rhinitis causes, signs, findings and management
A
- Poorly characterised
- Hypersensitivity to inhaled nasal allergens?
- +/-food allergens
- Reaction to local nasal allergens
- Irritant vs. allergen?
Signs - Acute or chronic
- Sneezing
- Serous to MP bilateral DC
Findings - Eosinophilic to mixed inflammation
- Not destructive!
Management - Remove allergen
- Antihistamines
- Anti-inflammatory glucocorticoids (inhaled - not systemic)
14
Q
The nose imaging what is involved
A
1) radiograph
- lateral
- open mouth dorsoventral - good
- (Dorsoventral/ventrodorsal) -> superimposition of mandible over the nose - not as useful
- Rostrocaudal frontal sinuses
2) computed tomography
3) MRI
15
Q
Radiographic changes for nasal cavity diseases
A
- Assess location of change
a. Uni vs bilateral
b. Rostral vs caudal - Alterations in opacity
○ Addition of soft tissue opacity or:
○ Bony destruction (vs proliferation)
○ Combination
16
Q
What are 5 main general patterns with nasal disease and causes
A
- Normal radiographic appearance of both nasal passages - foreign body, rhinitis
- Areas of increased soft tissue opacity superimposed over normal turbinate pattern - rhinitis, foreign body
- Areas of increased soft tissue opacity superimposed over areas of turbinate destruction - typically aspergillosis - MOST COMMON
- Areas of decreased opacity due to turbinate destruction without accompanying soft tissue opacity - after treatment of aspergillosis
- Mixed pattern of turbinate destruction and superimposed soft tissue opacity interspersed with areas of turbinate destruction alone
○ Most common in aspergillosis or neoplasia
17
Q
Altered trachea diameter how to measure and differences in size, what is normal
A
Normal size as ratio at thoracic inlet: -> if large fine but if small BAD - ≥0.2 Normal non brachycephalic breeds - 0.16 Normal non bulldog brachycephalic - 0.13 Normal bulldog ○ Tracheal hypoplasia common in
18
Q
Positioning for good quality thoracic radiograph, how position and how know it is rotated
A
- Pull the forelimbs forward with sand bags or ropes so triceps muscle and forelimb aren’t superimposed on the chest
- Thorax rotates if lie on side sternum flops down - heart looks like cardiomegaly
- Wedge under the sternum so the thorax is parallel with the cassette
Know rotated
1. Costochondral junctions straight - level
2. Forelimbs pulled forward so not superimposed
3. All pulmonary parenchyma lung fields
19
Q
what do you need 3 views of the thorax and what is the main thing you are looking for
A
About how lungs respond to compression
- Need air around the soft tissue opacity -> maximum amount of air around the abnormalities
○ Left lateral recumbency - atelectasis of dependent lung lobes (ones laying down)
§ Will see lesions within the right side (air filled as facing upwards) but not on the left side (atelectasis as laying on the table and being compressed)
And vice versa -> Right lateral recumbent will see the left lung fields
What are we looking for?
- Change in opacity - MOST IMPORTANT
○ Can you see the blood vessels (surrounded by air) -> if not possibly surrounded by fluid or soft tissue - as they are the same opacity - NO CONTRAST
20
Q
List the 4 main patterns and 5 main distributions for lung radiographs and describe the patterns
A
PATTERN
1. Interstitial - Vessels are harder to see - Can look if artefacts - such as expiration
2. Alveolar - Black tubes on a white background (airbronchograms)
- Soft tissue opacity within the lung and displaces the air and so alveolar soft tissue opacity and only air is the air within the bronchi
3. Bronchial - - Change at the level of the bronchial wall - thickening
- Tram track (longitudinal) or donuts (transversely cut)
4. Vascular
DISTRIBUTION - MOST IMPORTANT (not pattern)
1. Cranioventral
2. Caudodorsal
3. Diffuse
4. Focal
5. Multifocal
21
Q
List differentials for lesions in cranioventral and diffuse area of lung
A
Cranioventral - Aspiration pneumonia (alveolar pattern)- most common - Haemorrhage - Neoplasia - Bronchitis Diffuse/multifocal - Cardiogenic pulmonary oedema - Haemorrhage - Pneumonia - Neoplasia - pulmonary metastasis (well defined margins need to be greater than 0.5-1cm in diameter - Bronchitis - Fibrosis
22
Q
List differentials for lesions in the caudodorsal area of the lung
A
- Non cardiogenic pulmonary oedema ○ Upper airway obstruction, head trauma etc. - Cardiogenic pulmonary oedema - dog most common ○ Not in cat - Haemorrhage - Pneumonia - Neoplasia - Bronchitis - Fibrosis
23
Q
What are the main causes of blood, pus, water and cells and another cause of increased lung opacity
A
- Blood - (Trauma, Coagulopathy)
- Pus - (Pneumonia-aspiration, bronchopneumonia-bacterial viral, mycoplasmal, fungal; parasitic; lipid; inhalation)
- Water - (Cardiogenic & Non Cardiogenic Pulmonary Oedema)
- Cells - (Neoplasia, Inflammatory, Fibrosis, eosinophilic bronchopneumopathyetc)
- (Atelectasis)
24
Q
Bronchial pattern what are the 3 most common differentials
A
1) feline asthma
2) lungworm
3) neoplasia
commonly bronchointerstitial pattern
25
Interstitial pattern multifocal and solitary list differentials
```
Multifocal:
- Pulmonary metastases
- Granulomatous disease
- Haemorrhage
Solitary: - CHANG
- Cyst
- Haematoma
- Abscess
- Neoplasia (primary lung tumour)
- Granuloma
```
26
What are the 4 important things to avoid getting confused with nodules on lung radiograph
1. End on vessels
- Close to & same size as longitudinal vessels
- More opaque
- ↓ size and number towards the periphery
2. Calcified plaques “pulmonary osteomas”
- Diffuse
- Irregularly margined - don't tapper towards periphery (vessels)
- Mineralised (2-4mm)
3. Nipples -> markers you can use and place on the
nipples
4. Subcutaneous masses
27
Border effacement/obliteration or "silhouette sign" what is it, how associated with lungs and when occurs
- If two or more (or more) structures of the similar radiopacity are in direct contact with each other they will be projected as one merged silhouette on a radiograph leading to the disappearance of the individual silhouettes
- Normal thorax can see the heart as surrounded by the air filled lungs
Effusion -> won't be able to see the outline of the heart or diaphragm
28
Leafing on chest radiograph what does it result from and what other information can it tell you
- When there is fluid in the pleural space get atelectasis as well as retracting of the lung from the thoracic wall -> due to soft tissue opacity between lung and thoracic wall
- Particularly can see in the ventrodorsal projection
- Need to assess the margins of the lung lobes -> if sharp more acute, if rounded more chronic
29
pleural effusion what are the 3 signs on radiograph
1) boarder effacement "silhouette sign"
2) leafing
3) fissure lines - fluid moves up the fissure lines between the lung lobes - fat animals can have fat that looks like this as well
30
What occurs with pleural fluid in sternal and dorsal recumbency and how to determine type of fluid and if fluid or air
Sternal recumbency
- Fluid around the cardiac silhouette
Dorsal recumbency
- Heart sits up out of the fluid, can see the margins better
- Small volume due ventrodorsal -> best
Which fluid - need to sample - thorcocentesis
Ultrasound examination
- Able to differentiate between the fluid - cellular or non-cellular
- Pneumothorax - need to confirm with thoracic radiograph anyway
31
What are the 4 main techniques for ultrasounding the thorax
1. TFAST3
= Thoracic Focused Assessment with Sonography for Trauma, Triage and Tracking
a. Used to detect pneumothorax and pleural effusion
b. Also assess pulmonary parenchyma
2. AFAST3
= Abdominal Focused Assessment with Sonography for Trauma, Triage and Tracking
3. CFAST3
=Combo FAST3:both AFAST3and TFAST3
4. Vet blue
- Put probe on patient in 4 different sites
Caudodorsal lung, perihilar, Middle lung, cranial lung
32
TFAST3 ultrasound examination how to perform
1. Patient right lateral recumbency
2. Ultrasound probe longitudinal plane dorsally
- Watch pulmonary parenchyma moving backwards and forwards
3. Then move ventrally to the PCS (pericardial centesis site)
4. Then move to the DH (diaphragmatic site)
33
In terms of pleural effusion or pneumothorax what 3 things on ultrasound can help differentiate
- Look for “slide sign” of normal pulmonary-pleural interface moving with respiration - will be absent
- Presence of comet tail artefacts that move with inspiration and expiration rule out PTX
- If lung not air filled then the sound will be transmitted into the lung -> won't have the reverberation artefact
○ Pleural fluid
○ Pericardial fluid
34
pneumothorax what are the main radiographic findings
- Increased radiolucency within the pleural space
- Retraction of the lung lobes from thoracic wall but air between the lung and thoracic wall this time 0 leafing with air
- Heart drops into thorax and shifts away from the sternum - Projects the separation as a gap -> isn't ELEVATED just displaced from the sternum
35
How to tell when there is mediastinal widening and what occurs with a mediastinal (heart) shift
Width - Should be <2 x width of the vertebral column
Mediastinal shift (heart shift (main structure within the mediastinum))
- Mass shift is AWAY from lesions
- Loss of volume shift is TOWARDS the lesion
36
What are the 5 main locations on the mediastinum and what structures often affected there
1. Cranioventral - where most commonly see changes
○ Lymph nodes and thymus within -> diseases here
2. Craniodorsal
○ Rare often related to oesophagus
3. Perihilar/hilar
○ Related to the oesophagus -> where foreign bodies will stop
4. Caudodorsal
○ Often oesophagus
5. Caudoventral
○ Rare and often related to the diaphragm
37
Pneumomediastinum what is it, when visible , what may progress to and causes
- Air in the mediastinum
- Individual mediastinal structures visible
- Air may extend to fascia of neck +/-retroperitoneum
- Most visible on lateral projection
- May progress to pneumothorax and dyspnoea
Causes
- Escape of air from bronchi or alveoli
- Extension from fascial planes of neck
- Cranial extension from retroperitoneum
- Gas producing organisms - bacteria
38
Respiratory neuromuscular anatomy what works with inspiration, expiration and what does parasympathetic and sympathetic
○ Inspiration - ACTIVE
§ Diaphragm – innervated by phrenic n.
§ External Intercostals – innervated by intercostal nn.
○ Expiration - PASSIVE (dogs, cats, humans) (muscles when process becomes active - horses)
§ Internal Intercostals – innervated by intercostal nn.
§ Abdominal Muscles
○ Parasympathetic
§ Bronchoconstriction
§ Pulmonary Vasodilation
§ Increased Respiratory Secretions
○ Sympathetic
§ Bronchodilation
§ Decreased Respiratory Secretions
§ α – VC (vasoconstriction) ; β - VD (vasodilation)
39
dead space what are the 3 parts and what is the percentage of tidal volume that is dead space and therefore how much is available for gas exchange
§ 3 parts of dead space
□ 1. anatomic - trachea
□ 2. alveoli - alveoli that have gas without blood supply
□ 3. mechanical - added when anaesthetised
§ Dead space = 35% of tidal volume in normal awake dogs
○ Therefore: 65% of each breathe is available for gas exchange
40
Diffusion of gases across the respiratory mechanisms what are the 5 main factors that affect diffusion and what else is it a factor or
1. Respiratory Membrane Thickness
2. Surface Area for Gas Exchange
3. Diffusion Coefficient for Gas
4. Alveolar to Venous Pressure Gradient
(Pulmonary Capillary Transit Time) - fasting blood moving less time for gas exchange
SAME AS UPTAKE OF ANAESTHESTICS
41
Matching ventilation and perfusion what is ideal and what occurs in the acutal body
- Ideally blood would flow to every alveoli with air and vice versa…..but that is not always the case
- Due to regional differences in perfusion and ventilation, there is some degree of mismatching
○ An ideal ratio of V/Q = 1 but the normal ratio for our species is V/Q = 0.8
○ Differ depending on the individual and species, anatomic positioning of the legs
§ 3 different situations
42
What are the 3 main different situations for matching ventilation and perfusion within the lungs
1. Alveoli without air -> due to mucous plug or something obstructing air movement -> movement of air alveoli into others further down doesn't flow
- Can't pick up O2 and get rid of CO2
- Increase in V/Q mismatch and shunt fraction
2. Perfect
3. Alveoli full of air BUT not much blood going passed due to obstruction of blood -> gas in that alveoli is wasted HOWEVER gas can move into other spaces for gas exchange -> INCREASE in alveolar dead space
V/Q>1
43
What is a shunt, what is a normal shunt fraction, what increases this shunt fraction
- Measure of the mixing of deoxygenated blood with oxygenated blood in the left heart
- Some is normal = Physiologic Shunting
○ Ex – Bronchopulmonary Veins, Thebesian Vessels (drain myocardial blood (Deoxygenated blood) into heart chamber)
○ Normal Shunt Fraction = 1-5% = 1-5% of blood been mixed
- Low V/Q ratio increases the shunt fraction
- Anatomic R->L Shunts also increase the shunt fraction
○ Ex – Reverse PDA, Tetralogy of Fallot
44
Alveolar dead space what does it indicate, what increases this dead space and how estimated
- Indicates gas that reaches the alveoli but does not participate in gas exchange d/t reduced or lacking blood supply-
- High V/Q ratio increases alveolar dead space
○ Ex – Pulmonary Thromboembolism, ↓ Cardiac Output (Decrease blood flow) - decrease end tidal volume of CO2
- Can be estimated by comparing PaCO2 to EtCO2 (end tidal CO2)
45
Control of ventilation where occurs and the chemoreceptors and what sensitive to
- Ventilation is normally controlled in the CNS (medulla)
○ Central chemoreceptors are sensitive to changes in CSF [H+]
§ CSF [H+] changes with PaCO2
- Peripheral chemoreceptors (aortic and carotid bodies)
○ Minimal influence under normal conditions
○ Sensitive to extremely low PaO2 >50-60
○ Send signals to medulla that override input from central chemoreceptors
§ PaCO2 may be very low with hyperventilation
46
What are the respiratory affects of the following anaesthesia agents - ace, benzo, alpha-2, opioids, thio, alfax, pop and ketamine
- Ace and Benzos: minimal effects
- Alpha-2 Agonists: varying but typically minimal
- Opioids: CNS depression → ↓RR and VT (tidal volume) (hypoventilation)
- Thio, Alfaxan, Propofol: CNS depression → hypoventilation; apnoea
- Ketamine: ↑RR - CNS stimulant
47
What are the respiratory affects of inhalants and anticholinergics
- Inhalants: CNS depression → hypoventilation; Blocks HPV (hypoxic pulmonary vasoconstriction -> prevents shunting by locally vasoconstricting blood vessels in alveoli without air
○ Occurs in the foetus -> pulmonary artery to the aorta -> vasoconstriction of the pulmonary vessels
- Anticholinergics (parasympathetic): bronchodilation; ↑ viscosity of airway secretions (decrease watery saliva part)
Don’t forget: Inhalant anesthetics RELY on respiratory function for both uptake and elimination!
48
What are the 5 surgical affects on respiratory function
1. Patient positioning can depress respiratory function
2. Surgical technique can depress respiratory function
3. Restrictions of Airflow
4. Effects of 100% FiO2
5. Effects of Positive Pressure Ventilation
49
How does patient posioning and restriction of airflow during surgery effect respiratory function
1. Patient positioning can depress respiratory function
○ Ex. Horses in lateral or dorsal recumbency
○ Atelectasis, abdominal contents pushing on diaphragm
§ Decreased FRC and Tidal Volume
§ Hypoventilation and V/Q mismatch
3. Restrictions of Airflow
○ Endotracheal tube diameter < tracheal diameter
§ increases resistance to air flow
○ Obstructions also increase resistance
○ Increased resistance = Increased WORK of breathing
50
How does 100% inspired O2 and positive pressure ventilation during surgery effect respiratory function
4. Effects of 100% FiO2
○ Can improve O2 uptake in patients with decreased PAO2, respiratory membrane dysfunction, +/- increased shunt fraction (<30%)
○ May exacerbate chronic respiratory acidosis
§ Absorption atelectasis
□ Worsening of shunt fraction!
§ Oxygen toxicity - free-radical production
5. Effects of Positive Pressure Ventilation
○ May help prevent/correct atelectasis
○ Beneficial in the patient with NM weakness/exhaustion or increased compliance
§ Makes inhalation a passive event for the animal
○ Improves ventilation in patients with decreased compliance
○ BUT
• ↑ intrathoracic pressure = ↓ venous return
• ↑ alveolar/small airway pressure = compression of pulmonary capillaries = ↑alveolar dead space
51
Sedation/anaesthesia of dyspnoic patients what to do
1. Don’t be afraid of a sedative or anxiolytic and “hands off” until animal is calm!
2. Sometimes your only option is to rapidly induce and intubate the animal to gain control over ventilation!
○ When extending the neck -> real issue
52
Obstructive disorders what predisposed to and anaesthesia considerations
- Lar Par animals predisposed to aspiration
§ Cause increased “work” of inspiration - Patient can become exhausted
§ Expiration may be “active”
§ Can cause hypoxemia and/or hypoventilation if severe
□ Increased shunt fraction (low V/Q mismatch)
Anaesthesia considerations:
§ If obstructive disorder is at a lower point in airway than tracheal tube, intubation will not “fix” it
□ If upper airway -> tube will fix temporarily
§ Patient may be exhausted which will be exacerbated by muscle relaxation/anaesthesia
§ Recovery is the most dangerous time (always) - Regurgitation/aspiration
□ Providing analgesia but avoiding significant sedation
53
In terms of an animal with obstructive airway disease what premed, induction, maintenance and recovey used
• Premedication – Opioid of choice (based on expected pain of procedures) +/- acepromazine
• Induction – Propofol (or alfaxalone) to effect (short acting)
○ Can give midazolam before to decrease propofol requirements
• Maintenance – Inhalants or Propofol based TIVA (if indicated)
○ Don’t forget the benefits of local/regional anaesthesia in reducing maintenance requirements and providing analgesia in the recovery period
• Recovery – Buprenorphine analgesia unless severe pain expected then fentanyl CRI
54
How do you anaesthetize an animal for an airway function exam
- No premedication
○ Most premeds have the potential to decrease laryngeal function (controversial topic!)
- Propofol slowly to effect (theoretical gold standard) - effect (open mouth as not to be bitten but still can breathe)
○ Thiopental or alfaxalone can also be used
○ Avoid apnoea
- Doxapram (central CNS stimulant) (0.25 mg/kg) may be given to stimulate respiration if needed
55
Restrictive lung disorders list some and what is the pathogenesis of what it leads to
- Pulmonary fibrosis, air or fluid in pleural space, diaphragmatic hernia, bloat, pregnancy
○ Anything that causes pleural space pressure to become less negative, decreases the elasticity of the lung parynchema, or physically restricts the movement of the diaphragm or chest wall
○ ↑ muscular work of breathing
○ ↓ tidal volume, ↓ decreased FRC
» Patient prone to hypoxemia and hypoventilation
○ Atelectasis likely
» Increased shunt fraction!
56
Restrictive lung disease anaesthesia considerations
- PPV will be necessary
○ Higher PAP (positive airway pressure) might be required
- Inhalants and high FiO2 will reverse HPV
○ Leads to increased shunt fraction and may also increase alveolar dead space ventilation
- Depending on duration of atelectasis, slow “reinflation” may be warranted
○ Reexpansion Pulmonary Edema -> release of toxic substances that could lead to shock
57
What premedication, induction, maintenance and recovery used to anaesthetise an animal with restrictive lung disease
- Premedication – Opioid of choice (based on expected pain); avoid excessive sedation
- Induction – Any choice is appropriate
- Maintenance – Inhalants or propofol based TIVA
○ Local analgesia!!!!!
- Recovery – Watch ventilation/oxygenation after animal is extubated; avoid excessive sedation
58
How do you sedate an animal for chest tube placement, when done and what else need to provide
- Only do this under sedation if animal is eupnic!! (not stressed)
○ Be prepared to induce and intubate if necessary
- Sedate with butorphanol +/- medetomidine
○ Reverse medetomidine at end
- Provide local analgesia
○ Paravertebral blocks, inverted L, intercostal blocks
○ Consider locals into tube (depending on disease)
59
What is the most common signs of LRT and some differentials
```
- Cough is the most common sign of LRT disease:
○ Lower respiratory tract
○ Cardiac
○ Pleural space disease
○ Gastro-oesophageal reflux
○ Post-nasal drip
```
60
Feline nasopharyngeal polyps where arise and signs
```
- Arise auditory canal or middle ear
Signs:
- Stertor - into the mouth
- Serous to MP nasal DC
- Head tilt, nystagmus, Horner’s syndrome - middle ear involvement
- Otitis externa - external ear canal
```
61
Feline nasopharyngeal diagnosis and treatment
Diagnosis:
- Exam under GA
○ Spey hook/mirror
○ Otoscopy
- CT or radiography
Treatment:
- Traction - pull out with mosquitoes
○ Short course anti-inflammatory prednisolone
○ 90% success if no middle ear involvement
- Surgery (bulla osteotomy)
Better prognosis with middle ear involvement
62
Nasal neoplasia in dogs and cats what age, breed, type and character
```
Dogs
- Older (median 10 y)
- Dolichocephalic, medium to large breeds
- Adenocarcinoma, SCC, undifferentiated carcinoma > sarcoma
- Caudal 1/3 nasal cavity
- May involve sinuses
- Late metastasis (lungs, LN)
Cats
- Older (9-10 y)
- No breed predisposition
- Lymphoma, adenocarcinoma
Benign tumours are very rare in both species
```
63
Nasal neoplasia signs and those with chronicity and uncommon
```
- Nasal discharge
○ Any type, epistaxis common
○ Unilateral> bilateral, lateralised
- Stridor/stertor (obstruction)
- Sneezing
With chronicity….
○ Facial deformity +/-discomfort
○ Exopthalmos/hard to retropulse eye
○ Epiphora
Uncommon
○ Anorexia, weight loss.
○ Malaena (swallowing blood)
○ Neurologic signs
§ Behaviour change, seizures, abnormal mentation
```
64
Nasal neoplasia what are the 5 main diagnostic techniques and the most common one
1. Advanced imaging - identify tumour - most common
2. Rhinoscopy - can miss 25-30%
3. FNA/tru-cut external masses
4. Pinch biopsy - to determine the type of tumour
○ Scope/image-guided
○ Deep, large, multiple!
○ Check platelets/coagsprior
○ Control bleeding
○ Interpret path with caution
5. Staging - if considering
65
Nasal neoplasia for dog and cat with is estimated survival time with different treatments
```
Dog
- MST 12 months
- Better with radiosensitiser
- Better with surgery AFTER
Cat
- Nasal lymphoma 20.8 mo MST +/- chem
- Carcinoma/sarcomas 12 mo
Chemotherapy
- dog - less effective, variable response
- cat - nasal lymphoma MST 12 months with chem
```
66
Nasal enoplasia what are some minimal palliation options for carcinomas, lymphomas and other tumours and prognosis
```
○ Carcinomas:
§ Piroxicam (COX inhibition)
□ COX inhibitor
□ Anti-tumour, analgesia
□ MST 8 mo
□ GI/renal toxicity - keep an eye on blood work
○ Lymphoma:
§ Prednisolone
○ Other tumours:
§ NSAID or anti-inflammatory prednisolone
○ Prognosis:
§ MST 2-5 mo with no treatment - can be quite painful
§ Euthanasia due to poor QOL (quality of life)
□ Severe/persistent epistaxis
□ URT obstruction
□ Anorexia, weight loss
□ Neuro signs
```
67
Fungal rhinosinusitis what leads to and main cause in dog and cat
- Destruction of bone - epistaxis -> painful
Dog - aspergillus fumigatus - most common
Cat - cryptococcus neoformans - most common
68
Sinonasal aspergillosis what caused by, most susceptable in, uncommon in and main clinical signs
```
- A. fumigatus
○ Environmental, filamentous
- Most susceptible
○ Young-middle aged dogs
○ Mesaticephalic-dolicocephalic - longer nose breeds
○ GSD and Rottweilers
- Uncommon in cats
○ Usually immunocompromised
Clinical signs
- Nasal discharge
○ mucoid –MP +/-haemorrhage
○ Unilateral> bilateral, may progress
○ Pure epistaxis common
- Facial pain/sensitivity
- Depigmentation/ulceration
- sneezing
- Systemic signs (uncommon)
- Facial deformity (uncommon)
- CNS signs (uncommon/late)
```
69
Sinonasal aspergillosis what are the 3 main diagnosis techniques
```
1. Imaging -> radiograph, CT, MRI
○ Radiograph - insensitive with turbinate bones
○ CT - the BEST
2. Rhinoscopy
○ Turbinate destruction
○ +/-white-green fungal plaques
○ Trephine frontal sinuses to access
○ Multiple pinch biopsies
§ histopathology
○ fungal culture
3. Serology:
○ AGID (agar gel immunodiffusion) sensitivity 67% , specificity 98%
§ Adds weight to diagnosis
```
70
Sinonasal aspergillosis treatment which better and when to use which
- Topical vs. oral
○ Topical: 84-94% efficacy - BETTER THAN SYSTEMIC
○ Oral itraconazole 3-6 months: 60% efficacy
○ Clotrimazole infusion
- Nasal discharge resolves within 2 weeks of successful treatment
- Occasional permanent turbinate/mucosal damage
§ Chronic inflammation
§ Chronic secondary bacterial infections
- When to use oral
○ CNS involvement
§ Cribriform plate breached -> topical will get through this SO DON’T USE
§ Orbit breached
○ Extensive bone involvement (+/-topical)
○ Soft tissue invasion -> See cats!
71
Sinus aspergillus terreus and a. felis what animal present in and how disseminate and prognosis
```
A. terreusand other spp.
- Usually disseminate
○ mucosal immune defect (GSD)
○ Immunocompromised dogs or cats
- Disease advanced at presentation
○ Pulmonary, renal, uveitis, discospondylitis etc
- Grave prognosis
A. felis
- Sino-orbital aspergillosis
- Immunocompetent cats
- Highly drug resistant
- Multiagent systemic therapy recommended
○ Amphotericin B
○ Terbinafine
○ Posaconazole
- Poor prognosis (even with surgical debridement)
```
72
Sinus cryptococcosis what common in, characteristic, 2 main forms and what cats generally affect
```
8 times more common in cats than dogs
- Environmental ‘niche’ yeast
- Large polysaccharide capsule that makes it hard to immune system to kill
- C. neoformans
○ 70% infections SE Aus.
○ Immunocompetent cats.
○ Immunocompromised dogs, people.
- C. gattii
○ Remaining SE cases.
○ Up to 50% feline cases WA.
○ Immunocompetent hosts.
```
73
Cryptococcosis within the nasal cavity pathogenesis and signalment
1) nasal cavity can tehn disseminate in most dogs and few cats to lung -> haematogenous dissemination to eye brain, mandibular LN, skin bone etc
Signalement - young adults, Check FIV/FeLV status- Poor prognosis is FeLV +
74
Cryptococcosis within the nasal cavity what are the 2 main ways to diagnosis and ways within
```
1) Demonstrate organisms (75%)
○ Nasal discharge
○ Exudative skin lesions
○ FNA of granulomas
○ (CSF, bronchoalveolar lavage fluid)
○ Histopathology
2) Latex cryptococcal antigen agglutination test (LCAT)
○ Highly sensitive
§ serum (URT)
§ Urine or CSF (neuro)
```
75
Treatment and prognosis for cryptococcosis standard nasal case and severe/disseminated
Standard nasal case:
- Oral fluconazole (eye/CNS) or itraconazole
- 1-2 mo beyond negative LCAT
- Monitor LCAT q 3-6 mo long term
Severe/disseminated:
- Systemic Amphotericin B + flucytosine(14d) + oral fluconazole
76
Cryptococcous outcome in cats and dogs
```
Outcome cats:
- Successful in 75%
- 15-20% relapse
- Palliative only if FeLV+
- Guarded prognosis if CNS
signs or disseminated
Outcome dogs:
- Systemic therapy - as generally more severe and disseminated
- Successful in up to 55%
- Prognosis always guarded
```
77
Feline chronic rhinosinusitis signs and diagnosis
- Bilateral (usually) chronic mucoid-MP (mucopurulent) nasal discharge +/-traces of blood
- +/-sneezing
- Obstruction uncommon
- Systemic signs uncommon
Diagnosis -> Nasal investigation:
- Mild turbinate destruction
- Mucosal inflammation
- Increased mucus
- +/-epithelial hyperplasia, fibrosis
- Secondary bacterial or Mycoplasmaspp. infection common
78
Feline chronic rhinosinusitis what are the 5 main management options and what aim
1) facilitate clearnace of nasal discharge - nasaflush under GA, vaporiser
2) control environmental irritatns - air filters, smoke, clean bedding
3) treat possible FHV or mycoplasma infection
4) control secondary bacterial infection
5) if inadequate response control inflammation
GOAL - Increase the quality of life via these management processes
79
What is involved with treating possible FHV or mycoplasma and secondary bacterial infections in feline chronic rhinosinusitis
3. Treat possible FHV or Mycoplasmaspp. Infections:
○ Oral lysine trial 4-6 weeks - if significant improvement then continue on
○ Oral famcyclovir trial
○ Doxycycline trial - for secondary infections and immunomodulating
§ If relapse after stopping then need to continue treatment
80
Why in feline chronic rhinosinusitis cases controlling inflammation only occurs if inadequate response to others and what use
○ Antihistamines help some cats
○ CAUTIOUS anti-inflammatory glucocorticoids - don't want to suppress immune system
○ Doxycycline or azithromycin
81
Canine chronic (lymphoplasmacytic) rhinitis signs and diagnosis
- Bilateral (usually) chronic mucoid-MPnasal discharge +/-traces of blood
- +/-sneezing
- +/-obstruction (oedema, mucous)
- +/-epistaxis - sometimes - tumour or fungal?
- Systemic signs uncommon
Diagnosis - Nasal investigation:
- Imaging may be normal
- Occasional turbinate destruction and sinus involvement
- Mucosal oedema and inflammation
○ Lymphoplasmacytic and/or suppurative +/-low numbers of eosinophils
82
Canine chronic (lymphoplasmacytic) rhinitis management strategies and goal
○ Encourage mucous clearance
○ Reduce environmental irritants
○ Manage secondary bacterial infection
- ADDITIONALLY -> Usually need anti-inflammatories or immunosuppressives:
○ Immunosuppressive prednisolone (2 mg/kg/d) 2-4 weeks, taper.
○ Piroxicam + immunomodulatory antibiotic (doxycycline or azithromycin) at least 6 months.
○ Itraconazole 3-6 months.
○ Azathioprine or cyclosporine if refractory.
○ Most cases manageable with chronic therapy.
○ 50% good response
Again - management increase quality of life NO CURE
83
What is different with cats a cough and the 3 most common causes
- Cats with many lower respiratory tract disease DO NOT COUGH
- (cats with heart disease often vomit)
Most common cause of cough in cats
1. Feline bronchial disease (feline asthma)
2. Pulmonary parasites
3. Heartworm disease
84
What are the 2 main types of cough and differentials for each
Productive
- Mucus, exudate, oedema, blood
- Usually swallowed - so hard for owners to recognise
○ inflammation or infection (airways or alveoli)
○ pulmonary oedema (congestive heart failure)
Non-productive (dry)
- Airway disease
- Some interstitial disease
- Pleural space
85
Cough intensity and timing what disease represent: loud, harsh, paroxysmal, soft, exacerbated by neck pressure, goose honk, at night, worse after rest, excercise or cold air
- Loud, harsh and paroxysmal: airway
- Soft: pneumonia, pulmonary oedema (parenchyma)
- Exacerbated by neck pressure: tracheal disease
- Goose honk: collapsing trachea
- At night: cardiogenic pulmonary oedema -> worse due to gravity and lying down -> fluid moving caudally
- Worse after rest, with exercise or cold air: bronchitis
86
Ontop of coughing what are some other clinical signs of LRT disease
```
If gas exchange is impaired: - lung involvement
- respiratory distress
○ Tachypnoea
○ Hyperpnoea
○ Orthopnoeicstance
○ Open-mouth breathing
- exercise intolerance
- Weakness
- Cyanosis and/or
- Syncope
Non-specific systemic signs
- fever
- anorexia
- weight loss
- depression
Cats with obvious chest wall excursions or open-mouth breathing are severely dyspnoeic
```
87
Haemoptysis define and the main 2 differentials and diifferentials below
(coughing up blood) Differential diagnosis
- Heartworm disease - common
- Pulmonary neoplasia - common
- Fungal infection
- Foreign body
- Severe LSCHF
- Thromboembolic disease
- Pulmonary contusions
- Lung-lobe torsion
- Pulmonary infiltrates with eosinophils
- Systemic coagulopathy
88
What are the 6 steps in diagnosing LRT disease (coughing)
oach
1. Signalment
2. History
○ Type, timing, duration and progression of cough signs
3. physical examination - RR, pattern and effort, MM, HR, rhythm, pulses, palpate trachea, thoracic auscultation
4. diagnostic evaluation - non-invasive round 1
5. non-invasive round 2 - CT, ultrasound, Scintigraphy
6. more invasive round 3 - tracheal wash, bronchoalveolar lavage, bronchoscopy
89
Observe respiratory rate, pattern and effort for examining a cough case what occurs with URT or tracheal obstruction, intrathoracic obstruction and small airway lung disease
```
1. URT or extrathoracic tracheal obstruction
□ Prolonged, laboured inspiration
□ +/-stridor
2. Intrathoracic airway obstruction
□ Prolonged, laboured expiration
□ +/-expiratory sounds (gross or auscultation)
3. Small airway and lung disease
□ Rapid, shallow respiration
□ Inspiratory, expiratory OR BOTH
□ Abnormal lung sounds common
```
90
What are the clinical signs of a cardiac vs respiratory cough
```
Cardiac
- Compression mainstem bronchi (large heart)
○ Loud, harsh cough
- CHF (congestive heart failure)
○ +/-soft cough
○ tachypnoea, tachycardia
○ exercise intolerance
○ harsh lung sounds +/-crackles
- +/-other signs - poor airways
Airway
- Loud, harsh cough
○ dry or productive
- Often relatively bradycardic
- +/-respiratory sinus arrhythmia
○ High vagal tone
- harsh lung sounds - wheezes and crackles
- +/-other abnormal respiratory sounds
```
91
Abnormal lung sounds what are the causes of decreased, increased "harsh", crackles, wheezes and snapping
- Decreased:
○ pleural space disease
- Increased/’harsh’:
○ Non-specific - from lungs of alveoli
○ pulmonary oedema or pneumonia
- Crackles:
○ oedema or exudate within the alveoli and airways
○ some interstitial diseases (especially pulmonary fibrosis)
- Wheezes:
○ airway narrowing
○ increased luminal content, mural changes or external compression
- Snapping
○ end expiration, some intrathoracic collapsing tracheas
92
For every coughing patient what diagnostic evaluation (non-invasive round 1) do you need to perform
```
○ Thoracic radiography
§ Every coughing patient!
§ +/-Include the neck
§ Localise: cardiac, pulmonary, pleural or mediastinal
§ For pulmonary changes:
- alveolar, bronchial, interstitial or vascular?
- Distribution?
○ Haematology and biochemistry
§ Not very sensitive or specific
```
93
What are the 2 main ways to get airway cytology, differences in terms of conscious or GA, contaminated and animals used for
1. Transtracheal (TTW)
- conscious
- Avoids oropharyngeal contamination
- Tolerated in moderate dyspnoea
2. Endotracheal (ETW) wash
- GA required
- Cats and small dogs
- Risk of oropharyngeal contamination
94
Bronchoalveolar lavage (BAL) what are the 2 techniques, what both require, what gain and risk
```
- Bronchoscopic
○ Visual guidance
○ Sample specific sites
- Non-bronchoscopic
○ Blind technique
- Both require GA
- Lavage a large wedge of lung
- Small airway, alveolar and interstitial disease
- More risk of hypoxaemia
```
95
Airway wash sample handling/interpretation what need to do, what tests and diagnostic for how many cases
- Delicate samples-chill fluid, process quickly:
- Direct smears fresh
○ fluid and mucus (cytology)
- ETDA (cytology) and plain tubes (culture)
○ Lab cytology +/-cell counts
- Swabs of fluid
○ Bacterial culture
○ +/-fungal culture
○ +/-Mycoplasma culture/PCR
- Diagnostic 25% cases
○ infectious or overt malignancy
- Supportive 50% cases - major process may need more information for a specific diagnosis
96
Bronchoscopy what looking for
- Tracheal collapse
- Airway masses
- Airways tears or strictures
- Mucosal appearance
- Lung lobe torsion
- Bronchiectasis
- Bronchial collapse/compression
- Foreign body or parasites
- Mucus, blood, exudate
97
Trans-thoracic lung aspirate or biopsy when done, risk and contraindications
```
- Focal (solid) lesions
○ Imaging guidance
○ Low risk if against pleura
- Interstitial disease
○ More risk pneumo
○ BAL safer?
○ May need biopsy
Risks - chest tube might be needed -> referral maybe?
- Pneumothorax
- Haemothorax
- Pulmonary haemorrhage
Contraindications
- Cysts
- Abscesses
- Pulmonary hypertension
- Coagulopathy
```
98
What are 3 otherLRT diagnostics that are uncommonly used and what used for
1. Thoracotomy or thoracoscopy and lung biopsy
- Larger samples: impression smear, histopathology, special stains and cultures
- Sampling of local lymph nodes
- Lobectomy: neoplasia, abscess, cyst, FB, torsion
2. Arterial blood gas analysis
- most accurate was to assess for hypoxaemia
3. Pulmonary function testing (spirometry)
- uncommonly performed, certain institutions only
99
What are the 4 main tracheal and bronchial diseases
Major conditions
1. CIRDC (canine infectious respiratory disease complex) - KENNEL COUGH
2. Tracheobronchomalacia
3. Canine chronic bronchitis
4. Feline bronchial disease
100
Canine infectious respiratory disease complex character, spread, location, generla treatment and pathogens involved
- Lots of pathogens - canine adenovirus 2, canine parainfluenza virus, bordetella bronchiseptica
- Acute, highly contagious
- Nose-nose transmission
- Confined to airways - tracheitis
○ Pneumonia rare
- Usually self-limiting (2 wks)
○ Antibiotics rarely indicated!
- Which dogs?
○ High risk where dogs of mixed ages/susceptibility congregate
