Dog and Cat 9 Flashcards
Diagnostic investigation round 1 for nasal discharge
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
Diagnostic investigation round 2 for nasal discharge what achieves and the techniques
- 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
Diagnostic investigation round 3 and round 4 for nasal discharge what techniques done
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
nasal foreign body clinical signs and diagnosis/removal
- 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
Feline upper respiratory tract infection which cats occur in and presentation
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
Feline upper respiratory tract infection what are the 4 main causes, transmission, signs
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
Feline upper respiratory tract infection does it matter the cause, treatment and diagnosis
- Usually not! ○ Self-limiting ○ Lack of specific therapy ○ Mixed infections - Treatment generally symptomatic and supportive - Diagnosis usually presumptive
Feline upper respiratory tract infection general treatment
- 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
Feline upper respiratory tract infection treatment for herpesvirus, calicivirus and chlamydia
- 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
Feline upper respiratory tract infection prevention
1. Avoid exposure ○ Housing ○ Hygiene and disinfection ○ Limit overcrowding ○ Isolate new arrivals ○ Isolate kittening queens ○ Early weaning ○ Early vaccination 2. Strengthen specific immunity ○ Vaccination
Bacterial rhinitis what is important about it and treatment
- 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!
canine nasal mites transmission, signs, treatment
- 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
Allergic rhinitis causes, signs, findings and management
- 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)
The nose imaging what is involved
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
Radiographic changes for nasal cavity diseases
- 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
What are 5 main general patterns with nasal disease and causes
- 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
Altered trachea diameter how to measure and differences in size, what is normal
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
Positioning for good quality thoracic radiograph, how position and how know it is rotated
- 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
what do you need 3 views of the thorax and what is the main thing you are looking for
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
List the 4 main patterns and 5 main distributions for lung radiographs and describe the patterns
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
List differentials for lesions in cranioventral and diffuse area of lung
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
List differentials for lesions in the caudodorsal area of the lung
- Non cardiogenic pulmonary oedema ○ Upper airway obstruction, head trauma etc. - Cardiogenic pulmonary oedema - dog most common ○ Not in cat - Haemorrhage - Pneumonia - Neoplasia - Bronchitis - Fibrosis
What are the main causes of blood, pus, water and cells and another cause of increased lung opacity
- 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)
Bronchial pattern what are the 3 most common differentials
1) feline asthma
2) lungworm
3) neoplasia
commonly bronchointerstitial pattern
Interstitial pattern multifocal and solitary list differentials
Multifocal: - Pulmonary metastases - Granulomatous disease - Haemorrhage Solitary: - CHANG - Cyst - Haematoma - Abscess - Neoplasia (primary lung tumour) - Granuloma
What are the 4 important things to avoid getting confused with nodules on lung radiograph
- End on vessels
- Close to & same size as longitudinal vessels
- More opaque
- ↓ size and number towards the periphery - Calcified plaques “pulmonary osteomas”
- Diffuse
- Irregularly margined - don’t tapper towards periphery (vessels)
- Mineralised (2-4mm) - Nipples -> markers you can use and place on the
nipples - Subcutaneous masses
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
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
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
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
What are the 4 main techniques for ultrasounding the thorax
- TFAST3
= Thoracic Focused Assessment with Sonography for Trauma, Triage and Tracking
a. Used to detect pneumothorax and pleural effusion
b. Also assess pulmonary parenchyma - AFAST3
= Abdominal Focused Assessment with Sonography for Trauma, Triage and Tracking - CFAST3
=Combo FAST3:both AFAST3and TFAST3 - Vet blue
- Put probe on patient in 4 different sites
Caudodorsal lung, perihilar, Middle lung, cranial lung
TFAST3 ultrasound examination how to perform
- Patient right lateral recumbency
- Ultrasound probe longitudinal plane dorsally
- Watch pulmonary parenchyma moving backwards and forwards - Then move ventrally to the PCS (pericardial centesis site)
- Then move to the DH (diaphragmatic site)
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
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
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
What are the 5 main locations on the mediastinum and what structures often affected there
- Cranioventral - where most commonly see changes
○ Lymph nodes and thymus within -> diseases here - Craniodorsal
○ Rare often related to oesophagus - Perihilar/hilar
○ Related to the oesophagus -> where foreign bodies will stop - Caudodorsal
○ Often oesophagus - Caudoventral
○ Rare and often related to the diaphragm
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
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)
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
Diffusion of gases across the respiratory mechanisms what are the 5 main factors that affect diffusion and what else is it a factor or
- Respiratory Membrane Thickness
- Surface Area for Gas Exchange
- Diffusion Coefficient for Gas
- Alveolar to Venous Pressure Gradient
(Pulmonary Capillary Transit Time) - fasting blood moving less time for gas exchange
SAME AS UPTAKE OF ANAESTHESTICS
