Respiratory Flashcards
Brachycephalic dogs are predisposed to what type of airway disorder?
Obstructive disease- brachycephalic dogs often have stenotic nares, everted laryngeal saccules, elongated soft palates, and hypoplastic tracheas, all of which cause obstructions to airflow and increase the work of breathing
Increased FiO2 (fraction of inspired oxygen) can cause all of the following except which?
Decreased oxygen affinity for haemoglobin - FiO2 does not change oxygen affinity for haemoglobin (and we didn’t talk about this in lecture either)
Which of the following describes an expected effect of methadone administration?
Decreased RR (respiratory rate) - opioids all have the potential to decrease respiratory rate and tidal volume which causes hypoventilation
True or False: Watching the patient’s chest and reservior bag move can give you an accurate assessment of ventilation.
False - ventilation can only be accurately assessed by measuring either the CO2 in the blood (PaCO2) or in the expired gases (EtCO2).
The ABCs in an emergency patient?
Major Body Assessment
Resp rate, resp pattern, resp effort, pulmonary auscultation
Normal breathing– RR? Pattern? RE?
Normal RE: inspiration is active but effortless, expiration is passive
Pulmonary Auscultation
** If animal is breathing harder (exercise)– louder
Lung sounds
are generated by
turbulence
of air
within the airways: varies with flow rate
•
“Normal” depends on respiratory rate
•
Lung sounds are more harsh during tachypnoea
•
Distribution:
dorsoventral
, symmetry
Lung sounds
are generated by
turbulence
of air
within the airways: varies with flow rate
•
“Normal” depends on respiratory rate
•
Lung sounds are more harsh during tachypnoea
•
Distribution:
dorsoventral
, symmetry
Harsh, crackles, wheezes
Crackles caused by fluid or alveoli opening and closing
Wheezes caused by narrow airways
Absent lung sounds = pleural space disease; no flow
Signs of dyspnoea
Recognizing Dyspnoea
Tachypnoea
Increased abdominal movement
Paradoxical abdominal movement
Extended neck (orthopnoea)
Abducted elbows (orthopnoea)
Open mouth breathing
Cyanosis
Lateral recumbency
The possible anatomic origin of dyspnoea
If increased inspiratory effort think what? expiratory effort increased? Inspiratory and expiratory effort increased?
DDX upper airway problem in dogs and cats?
What will you notice in a dynamic v. fixed obstruction in the upper airway? Where is the problem with stertor? Stridor?
Paradoxical Abdominal Movement DDX
Small Airway Respiratory issues DDX
What would you hear with a pulmonary parenchyma problem?
DDX of pulmonary parenchyma
DDX for pleural space disease
What will you see with pleural space disease?
Chest wall and diaphragm DDX
Chest wall and diaphragm look alikes
Dyspnoea after trauma
Most dyspnoeic cats will have one of three things?
Pattern recognition with old toy and small-breed dogs? Brachycephalic breeds? Old large-breed dogs?
Pattern recognition with resp. puppies?
Diagnostics with respiratory problems
Risk vs. benefit analysis
Upper airway exam
Thoracic radiographs
Arterial blood gas analysis
CT scan
Tracheoscopy/bronchoscopy
Airway cytology
When should you quantify hypoxaemia? How do you? Cyanosis that is life threatening?
Arterial blood gas– normal? Venous blood gas– normal? O2 saturation of Hb?
Sampling of arterial blood gas
* Percutaneous: femoral, dorsal metatarsal, brachial, auricular arteries
* Catheter: dorsal metatarsal
* Pre-heparinized syringe: liquid sodium heparin, lyophilized lithium heparin, use minimum volumes of heparin (heparin reduces measured PCO2)
* Remove all air bubbles– exposure to air changes PO2/PCO2
* Cap with an airtight seal
* Place on ice– glycolysis produces CO2, aerobic metabolism reduces PO2
* Analyze within 2 hours
* May adjust for body temperature
Normal value of arterial blood gas? When it falls below <75 mmHg then what? < 55 mmHg, then what?
Pulse oximetry– normal? Acceptable?
Where do you put a pulse oximeter?
Summary of emergency response to respiratory issue
Oxygen delivery– what does it depend on?
What is the oxygen cascade?
Mechanisms of hypoxaemia
What is flow by oxygen?
Using an oxygen mask
Using nasal oxygen catheters?
Oxygen hood?
Use of an oxygen cage
How do you assess if oxygen supplementation is working?
- Assess for improvement of respiratory distress
- Pulse oximetry SpO2
What is going on in hypoventilation?
Causes of hypoventilation?
General Management of an Upper Airway Obstruction
Using sedation to manage US obstruction? Pros?
Using sedation to manage US obstruction? Precautions?
Management of a UA obstruction…. reduction of body temperature?
Intubation in the management of UA obstruction
Pulmonary gas exchange and mechanisms of impairment?
Saturating Hb with oxygen
What happens with pulmonary gas exchange with flooded or collapsed alveolus?
Causes of venous admixture
Management of respiratory presentation
What if this doesn’t work?
Intubation/ ventilation!
Intubation/ ventilation settings and modes?
What is pressure-controlled ventilation?
Volume controlled ventilation?
Intubation/ventilation start settings for volume controlled?
Start settings for pressure controlled?
What is dead space?
Neuromuscular inspiration v. expiration and nerves?
What does the parasympathetic supply do to the lungs? What does the sympathetic supply do to the lungs?
What is the normal percentage of dead space in a dog? What are the three parts of dead space?
Diffusion of gases across the respiratory membrane
* think of cystic fibrosis
** think of lung lobectomy = less surface area for gas exchange
* diffusion coefficient– can’t change it– why some gases diffuse better than others
** 150 mmHg of oxygen available because 21% * 760 mmHg (sea level)– why don’t we get that much? It is diluted out with other gases
* pulm. capillary transit time– does not effect diffusion but effected gas exchange– how long is the blood in contact… CO high = faster pumping past alveoli- less time for gas exchange to take place
Matching ventilation and perfusion
V = air
Q = blood
Perfect world 1:1 match– not the case due to regional differences in perfusion and oxygenation…
•
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
When does shunt happen?
Blood flies by– your patient aspirated a peanut and it is stuck in the bronchi– there is still blood coming past but not getting any oxygen
When does alveolar dead space occur? What is it?
Lots of air, but the blood doesn’t get there– HBC and haemorrhaged… embolism
How does gas move into the blood?
How is carbon dioxide carried in the blood?
How is ventilation controlled centrally under normal conditions?
Control of ventilation via peripheral methods?
Respiratory Anaesthesia Pharmacology– effects of Ace and Benzos? Alpha 2 agonists? Opioids? Thio, Alfaxan, Propofol? Ketamine? Inhalants? Anticholinergics?
Effects of anaesthesia on Respiratory Function
* 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
* Surgical technique can depress respiratory function
ex. Insufflation of Co2 into the abdomen for laproscopy
- reduced diaphragmatic excursion
* Restrictions of airflow
- endotracheal tube diameter < tracheal diameter increases resistance to air flow
- obstructions also increase resistance
- increased resistance = increased WORK of breathing
* Effects of 100% FiO2
- can improve O2 uptake in patients with decreased PAO2, respiratory membrane dysfunction, +/- increased shunt fraction (<30%) BUT may exacerbate chronic respiratory acidosis– absorption atelectasis– worsening of shunt fraction!…. Oxygen toxicity– oxygen free radical production
* Effects of PPV– 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
Dyspnoeic patient
Considerations with obstructive disorders in sedated or anaesthetised animals?
•
Obstructive Disorders
–
Lar
Par, Tracheal Collapse, Asthma, Bronchitis,
Space Occupying Masses
•
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
•
Patient may be exhausted which will be exacerbated by
muscle relaxation/anaesthesia
•
Pickwickian
Syndrome??
•
Recovery is the most dangerous time (always)
–
Airway obstruction/collapse
–
Regurgitation/aspiration
–
Providing analgesia but avoiding significant sedation
How do I anaesthetize an animal with obstructive airway disease?
–
No premedication
•
Most premeds have the potential to decrease laryngeal
function (
controversial topic!)
–
Propofol
slowly
to effect (theoretical gold standard)
•
Thiopental can also be used
•
Avoid apnea
–
Doxapram
(0.25 mg/kg) may be given to stimulate
respiration
if needed
Sedation/ Anaesthesia of Respiratory Patients
•
Restrictive Disorders
–
Anaesthesia Considerations:
•
PPV will be necessary
–
Higher PAP might be required
•
Inhalants and high FiO
2
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
How do I anaesthetize an animal with restrictive lung disease?
How do I sedate an animal for chest tube placement?
What is meant by combination disorder?
How do I anaesthetize an animal with a combination disorder?
Projections to evaluate nasal cavity
Mandible superimposed over the maxilla and nose– so limited use in nose
So we open the jaw!
Open Mouth Dorsoventral (or VD)
Rostrocaudal
frontal sinuses
Looking for nasal turbinates present and surrounded by air and not soft tissue… also look at the vomer bone, nasal septum is intact and straight
Best modality for nasal issues?
Why isn’t MRI as good?
* MRI isn’t as good with bone
Important to remember about radiographs and nasal cavity assessment?
* Non specific… meaning it likely will only help us narrow down differentials.. it won’t be diagnostic
What are the general patterns of nasal passage radiography?
DDX of the nasal cavity
Fluid or mass lesions within the frontal sinus– LEFT frontal sinus is abnormal
Masses often have abnormal surface– mass will light up with contrast, just exudate it will not
Increased soft tissue opacity
CT increased soft tissue and turbinate destruction
On the right loss of vomer bone.. aggressive lesion…
Extension of nasal
neoplasia into brain
Normal Trachea
Tracheal Displacement– the angle is not 40 degrees to the thoracic spine
And dramatic dip ventrally at the carina, the bifurcation
Altered tracheal diameter
Hypoplastic trachea
Collapsing Trachea
Grades of collapsing trachea
Oesophagus draped over trachea
Obtaining a good quality thoracic radiograph
Rotated Thorax
(prefer ventrodorsal can stretch them out better)
whenever a dog is in RLR, the lung underneath has less air in it (atelectasis)– less air = less contrast
LLR= looking at the right lung
RLR= looking at the left lung
Lung patterns vs. distribution
Cranioventral lung fields
Caudodorsal lung fields
Clinical signs of nasal disease
Clinical signs of nasopharyngeal disease
Unilateral nasal discharge DDX? Bilateral nasal discharge DDX? Either DDX?
Physical Exam for nasal discharge
When to investigate nasal discharge?
DDX for sneezing
DDX for discharge
DDX for Epistaxis
DDX for Destructive lesions
The “Rounds” of investigation
Round 1 Investigation General? Epistaxis?
Round 2 general investigation?
Round 3 and 4 investigation?
Acute nasal signs? Top 3 DDX?
Nasal FB signs and symptoms? Diagnosis? Removal options?
Feline URT infection– which cats? Where?
Presentation of Feline URT infection? How long does it take to resolve?
Feline URT DDX
Feline Herpes Virus
DDX?
FHV, Feline Calicivirus, Chlamydia felis, Bordatella bronchiseptica
Does nasal and ocular discharge in cats matter?
Treatment of cat presenting with ocular and nasal discharge
Address
hydration
:
–
SQ or parenteral fluids
Address nutrition:
–
warm, soft, fishy foods.
–
Appetite stimulants?
–
Oral care
–
Feeding
tube
Clear oculonasal
discharge:
–
Moist cotton balls
–
Humidification
–
Decongestants?
Treat
2
°
bacterial infections:
–
Doxycycline
–
Amoxicillin
–
Topical antibiotic ocular
therapy
What is bacterial rhinitis?
Found in a dog’s nose
Signs of allergic rhinitis? Findings? Management?
Key points in acute nasal disease
Signs of Feline nasopharyngeal polyps. Who are they seen in?
Diagnosis and treatment of feline nasopharyngeal polyps?
Dogs and cats nasal neoplasia– who do you see it in?
Signs of nasal neoplasia?
Nasal tumour diagnosis
Nasal tumours treatment
Minimal palliation in nasal tumours
Fungal rhinosinusitis in dogs and cats
Sinonasal aspergillosis (SNA)
SNA Clinical signs
Sinonasal aspergillosis (SNA)
SNA Diagnosis
SNA Treatment
Clotrimazole infusion
Treatment for SNA
Aspergillus terreus and A. felis?
Cryptococcosis
Dissemination of Cryptococcus in cats
Signalment?
Cryptococcosis in cats v. dogs
Diagnosis of Cryptococcosis
Cryptococcosis treatment and prognosis
Chronic idiopathic rhinitis cats v. dogs
Diagnosis of feline chronic rhinosinusitis
Management of feline chronic rhinosinusitis
Treat possible FHV or
Mycoplasma
spp. Infections:
–
Oral lysine trial 4
-
6 weeks
–
Oral famcyclovir trial
–
Doxycycline trial
Control secondary bacterial infection:
–
4
-
6 week antibiotic courses, choice as for URTI
–
Repeat as needed (some cats need ongoing)
If inadequate response, control inflammation (last!):
–
Antihistamines help some cats
–
CAUTIOUS anti
-
inflammatory glucocorticoids
–
Doxycycline or azithromycin
–
(Piroxicam, leukotriene inhibitors, omega
-
3 FA)
Presentation of canine chronic (lymphoplasmacytic) rhinitis
Management of canine idiopathic rhinitis
Nasal Tumour, SNA, and Chronic rhinitis– differentiating chronic nasal presentations in dogs
DDX
* Hypertension
* Coagulopathy
* Nasal neoplasia
* Nasal aspergillosis
Tests
- Measure systollic BP
- Check clotting times (BMBT, platelets and PT/APTT)
- Take nasal swab for cytology
- Take nasal swab for culture (+ fungus)
- Take blind biopsy of nasal cavity
Key Points
* Epistaxis should make you think fungal disease or tumour
* Fungal disease is more painful than tumour
* Nasal cytology is only useful for cryptococcosis
* Idiopathic chronic rhinitis and feline CRS are never cured
Clinical signs of lower respiratory tract disease
What do cats with lower respiratory tract NOT usually do that dogs do? What might they do that is different to dogs? DDX in a coughing cat?
Productive v. Non-productive cough?
Loud, harsh and paroxysmal cough?
Soft cough?
Exacerbated by neck pressure?
Goose honk?
Worse resting at night?
Worse after rest, with exercise or cold air?
Huge heart pressing on the airways, exercise tolerance would make you worry that she may have CHF… but not all signs point to that. So thinking bronchitis possible?
** Need to do more investigation to confirm problem
Signs of LRT if gas exchange impaired? Non-specific systemic signs ?
Haemoptysis DDX?
Approach to LRT
What would you see with URT or extrathoracic tracheal obstruction?
What would you see with intrathoracic airway obstruction? Small airway and lung disease?
Physical Exam LRT
Observe resp pattern, RR, RE
Physical exam– abnormal lung sounds… when decreased suspect? Increased/ harsh? Crackles? Wheezes? Snapping?
Cardiac vs. respiratory cough
Round 1 Diagnostic Eval of the LRT
Round 2 non-invasive LRT investigation? Round 3 more invasive LRT investigation?
Airway cytology
What is bronchoalveolar lavage?
Airway wash sample handling and interpretation?
Bronchoscopy indications
Trans-thoracic lung aspirate or biopsy indications? Risks? C/Is?
Other LRT diagnostics you might run when investigating
Relatively happy coughing patients DDX
CIRDC- Canine Infectious Respiratory Disease Complex aka Kennel Cough– Parainfluenza, adenovirus, canine resp coronavirus, canine herpesvirus, canine distemper virus, canine influenza virus… bordatella bronchiseptica, Mycoplasma spp., Streptococcus zooepidemicus
What is CIRDC? Which dogs? Transmission?
CIRDC- Canine Infectious Respiratory Disease Complex aka Kennel Cough– Parainfluenza, adenovirus, canine resp coronavirus, canine herpesvirus, canine distemper virus, canine influenza virus… bordatella bronchiseptica, Mycoplasma spp., Streptococcus zooepidemicus
CIRDC Pathogens
CIRDC- Clinical signs? Diagnosis?
CIRDC Treatment?
CIRDC Prevention
* Minimize exposure
- In shelter/ kennel environments:
- Isolate puppies and recently boarded dogs form other dogs
- disinfect cages, bowls, runs, etc, wash hands between handling dogs
- no nose- nose contact
- at least 10-15 air exchanges/ hour (good ventilation) and < 50% relative humidity
* Maintain good general health
- Good nutrition, regular deworming, limit stress
Key Points LRT
Interpretation of radiographs of lung disease
Simplified DDX for increased lung opacity
Pattern of lung disease algorithm
Question you ask to start algorithm for interpretation of lung disease on radiographs
What pattern?
Alveolar filled with blood pus water or cells
What pattern?
Alveolar Pattern VD
Alveolar filled with blood pus water or cells
CT of airbronchograms
* blood pus water or cells
Right cranial lung lobe, when we see this line it tells us we have severe disease– because it is white and air filled lung behind. Distinct line tells us we have a severe alveolar opacity
First differential?
Aspiration pneumonia
What do you look at when you look at the size of the lung lobes?
Mediastinal shift towards the lesion
Heart is the main structure– supported by the air filled . If a lung lobe has a decreased volume (atelectasis) won’t support the heart in the normal position in the midline
Recumbent Atelectasis
Put them in sternal recumbency, ventilate them… when anaesthetized they are in sternal recumbency so we don’t get this
DDX?
Metastatic neoplasia or fungal granulomas (not in AUS)
DDX Nodular Interstitial Pattern
Things not to confuse with nodules
Mineral- not round unlike metastatic neoplastic lesions
Cranioventral
What are you doing here?
Checking to see if they are lesions or nipples using wire on the nipples
Perihilar is BS– actually just a big left atrium
Caudodorsal
Multifocal to diffuse– haemorrhage high on the differential list depending on history, neoplasia, pneumonia
Ways to read lungs
Making a diagnosis
Signalment- young dog, caught by collar, was completley normal before incident… blood? pus? Water? Cells?
** Caudodorsal distribution
DDX: Non cardiogenic pulmonary oedema, cardiogenic pulmonary oedema, haemorrhage, neoplasia, bronchitis, fibrosis
History: upper airway obstruction
Sudden change– haemorrhage is non patchy
Non cardiogenic pulm oedema– treated for it and got better
Case 2: Signalment
:
•
11
wo
F Mastiff
•
Soft cough for 2 weeks
•
Presented with
inappetance
and dyspnoea
Abnormal cranioventral and caudodorsal as well.
Mixed pattern
Ddx: non
cardiogenic
pulmonary
oedema,
cardiogenic
pulmonary
oedema,
haemorrhage,
pneumonia,
neoplasia
,
bronchitis,
fibrosis
** Ranked DDX: Pneumonia, haemorrhage, non cardiogenic pulmonary oedema… What do we do next? Take some cells. Suppurative
Treat empirically, BAL, (Coag profile)
** It was pneumonia– had been vaccinated 2 weeks previously. C&S– Pure heavy growth of Bordetella bronchiseptica sensitive to Clavulox and enroflaxicin
Pathogenesis of collapsing trachea/ TBM
Signalment of collapsing trachea/TBM
Collapsing trachea/ TBM exacerbating or triggering factors
What could a goose honk cough mean?
Collapsing trachea/TBM
Clinical presentation– history and PE of collapsing trachea/TBM
Diagnosis of collapsing trachea/ TBM
Collapsing trachea/ TBM treatment
Chronic management of collapsing trachea/TBM
What is Canine Chronic Bronchitis?
Complications of CCB
CCB presentation
PE of CCB
Diagnosis of CCB
CCB Management
CCB Medications
For some cases:
Antitussives (opiates)
- cough incessant, exhausting, ineffective
- lowest effective dose
- strategic timing
- avoid in v. productive cough
- avoid in bronchiectiasis (nebulisation & coupage)
Intermittently: Antibiotics
- inhaled oropharyngeal flora (gram negatives)
- C&S best
- +/- mycoplasmas
- need to penetrate airways and respiratory secretions (doxycycline)
- At least 3-4 weeks
Feline Bronchial disease (FBD)
FBD DDX
Idiopathic FBD presentation
FBD Physical examination
FBD Diagnostics
Terbutaline = bronchodilator
* too unstable for airway wash so just started steroids
Chronic management of idiopathic FBD
Possible allergy?
−
Eliminate allergen
–
Consider
all canned
food
Idiopathic?
Many
cats improve with improved
air quality
–
Eliminate smoke, aerosols and perfumed products
–
Trial sand or plain clay litter
–
Reduce dust, mould and mildew
•
clean carpets, furnishings, bedding,
drapes
–
Clean heating units/ducts, change air filters
regularly
–
Use a vacuum with a HEPA filter
–
Use an air purifier
Ongoing signs or
Intermittent flare
-
ups
Bronchodilators
•
Inhaled salbutamol
(
Ventolin
®
)
−
Best for intermittent use
−
Prior to inhaled fluticasone
•
Oral aminophylline
or
terbutaline PO
Refractory cases
•
Cyclosporin
–
experimental
•
Cyproheptadine
–
mild bronchodilation
•
Leukotriene inhibitors
–
no evidence
•
No antihistamines!
Idiopathic FBD prognosis
Key points in tracheal collapse, CCB, and FBD
Signs of parenchymal disease & non-resp ddx look alikes
Bacterial pneumonia routes
Bacterial pneumonia in adult dogs and cats
Bacterial pneumonia predisposing causes
Diagnosis of bacterial pneumonia
Bacterial pneumonia
-Diagnosis
Clinical signs
•Cough (soft, productive)
–Dogs!
•Bilateral mucopurulent nasal
discharge
- Exercise intolerance
- Respiratory distress
- Lethargy, anorexia, fever and
weight loss
Physical exam
- Fever (50%)
- Tachypnoea or hyperpnoea
- Nasal discharge
- Focal crackles, +/- expiratory wheeze (auscultation)
Less common
- +/-sinus arrhythmia
- +/- cyanosis (hypoxia)
Treatment of bacterial pneumonia
GCs are contraindicated!!! NO ANTITUSSIVES no matter how much they are coughing– we need to clear the bugs out of the airways
Bronchodilators: cats, and in dogs with expiratory effort or wheeze (monitor)
Oxygen therapy: clinical signs, SpO2 < 94%, PaO2 (blood gas) < 80 mmHg
(Mucolytics)
Should improve within 48-72 hours
Monitor:
* clinical signs frequently
* haematology and thoracic radiographs
- q 24-72 hours initially
- 1 week after DC
- then q 2-4 weeks after DC
* Prognosis usually good
Aspiration pneumonia
Diagnosis of aspiration pneumonia
Predisposing causes of aspiration pneumonia
Treatment of aspiration pneumonia
Do not lavage and do not anaesthetise!!
Can suction the airways if the animal is unconscious
Pulmonary hypertension (PHT)
Diagnosis of pulmonary hypertension
What is idiopathic pulmonary fibrosis?
Pure collagen deposition throughout the interstitium of the lung– do not know why this happens
Radiographs are relatively boring in this condition, but you will hear really loud crackles
IPF management and prognosis
What is eosinophilic bronchopneumopathy (EB)?
EB presentation
EB Management
Metastatic v. Multicentric pulmonary neoplasia
Primary pulmonary neoplasia
Treatment and prognosis of pulmonary neoplasia
Presentation of pulmonary thromboembolism? What is Virchow’s triad?
PTE associated diseases and risk factors?
PTE Treatment
Pathogenesis of pulmonary oedema
Non- cardiogenic pulmonary oedema (NCPO)
Non- cardiogenic pulmonary oedema (NCPO) Treatment and prognosis
Difficult to shift fluid with diarrhetics unless it is due to CNS injury or electrocution
The unhappy coughing patient- pulmonary parenchymal disease
Neat trick when looking for rib fractures
Turn the RG 90 degrees
Pleural space
Interlobar fissures
RG changes seen in pulmonary disease
When there is fluid in the pleural space, the pressure of the fluid means the lungs will be reduced in volume- this will appear as mild atelectasis. You will also see opacity between the lungs and the thoracic wall
what is a TFAST?
TFAST
3
•
Thoracic Focused Assessment with Sonology for
Trauma, Triage and Tracking
•
Used
to detect pneumothorax and concurrent
thoracic
injury, pleural effusion and pericardial
effusion
•
5
point TFAST in
dogs
–
CTS (bilateral) (chest tube site)
–
PCS (bilateral) (pericardiocentesis?)
–
AFAST DH (diaphragmatic hepatic site)
Diagnosis of pneumothorax using TFAST and its Chest Tube Sites (CTS)
Slide sign- if you don’t see it, suspect pneumothorax
Cardiac silhouette is separated from the sternum– not elevated
Patient hit by a car, blood is the opacity
Life threatening
Normal in fat animals
Mediastinal shifting
Anything that reduces lung volume causes shift towards the reduction.
If it is a mediastinal mass, it won’t
Locations of mediastinal masses
Cranioventral- lymphoma, lipoma
Perihilar- second most common– tracheobronchial lymphadenomegaly
Pneumomediastinum
Causes of a pneumomediastinum
Pneumomediastinum
Pneumothorax
* can see Cranial vena cava, can see oesophagus– can’t normally see them but highlighted by the air
Heart disease v. Heart failure
Considerations for RG appearance of the normal heart
Problem with the VHS
* make the lines in the wrong places
* breed specific
* lots of dogs and cats have normal hearts outside of the parameters
** Could use it to track what is normal in that dog over time!!
5th to 7th rib rule
Cranio to caudal dimension of the heart should not be any greater than that line
** old cats hearts can flop forward (is this a sign of hypertension? NO. (because it is in people))
Changes with cardiac disease
Radiographic features of cardiomegaly
•
Ventrodorsal (dorsoventral projection)
–
Increased transverse diameter (width) of heart
–
Cardiac width on a DV view is usually 60
-
65% of the thoracic width and
no more than two
-
thirds of the thoracic width at the widest point of the
cardiac silhouette on a VD view
–
Increased rounding and elongation of heart borders
–
Bulging of left heart border due to increased size of left auricle
–
Caudal and leftward displacement of cardiac apex
–
Cat “Valentine Shaped” heart
Big heart- how can you tell?
•
Ventrodorsal (dorsoventral projection)
–
Increased transverse diameter (width) of heart
–
Cardiac width on a DV view is usually 60
-
65% of the thoracic width and
no more than two
-
thirds of the thoracic width at the widest point of the
cardiac silhouette on a VD view
–
Increased rounding and elongation of heart borders
–
Bulging of left heart border due to increased size of left auricle
–
Caudal and leftward displacement of cardiac apex
–
Cat “Valentine Shaped” heart
Where are the cardiac veins?
What are we considering when looking at the cardiac vessels?
Should be about the same size
Enlarged pulmonary veins DDX
Why won’t you always see enlarged pulmonary veins in the left sided heart failure even though pathophysiology would suggest otherwise?
Caudo dorsal in dogs– opacity in cardiogenic heart failure (unless it is really bad)
Anywhere in cats
Enlarged pulmonary arteries DDX
Enlarged pulmonary arteries and veins DDX
Small pulmonary vessels DDX
Haemabdomen– we see a small heart, the blood is all in the abdomen
(also microcardia with GDV)
Mitral valve endocardiosis– small dogs
DCM– big dogs
Globoid heart, soccer ball
Wider than the 5th to 7th rib rule, valentine appearance
Increased opacity on the lungs
Take home messages cardiac radiographic assessment
•
Use the “checklist” to assess the cardiac
silhouette
•
Do not use the VHS alone
•
Cardiac enlargement alone does not mean the
patient is in heart failure
•
Assess for radiographic evidence of heart
failure
Might see oesophagus, left subclavian, brachiocephalic trunk branching off rostrally
Cardiac disease v. cardiac failure
Differential Diagnosis
Chronic Bronchitis (chronic form of “Feline Asthma”)
Etiology: initially allergic
Secondary bacterial infections common
Infectious Tracheobronchitis
Virus,bacteria,mycoplasma, chlamydia
Parasitic Disease
Aelurostrongylus abstrusus
Capillaria aerophilia
Toxoplasma gondii
Inhalation of Toxins
Atypical Pulmonary Edema
Bronchogenic Carcinoma (early)
Bullae (air bubbles)- aka emphysema or air trapping
Animals it typically occurs secondary to a primary obstructive pulmonary disease process. Pathogenesis not fully understood 1) an imbalance between protease secreted by neutrophils and macrophages, and antiprotease activity results in destruction of alveolar walls and interstitial matrix; 2) inappropriate maintenance of lung structure and repair follows injury; and 3) the condition develops secondary to obstruction of airways on expiration due to chronic bronchitis/bronchiolitis or congenital abnormality of the airway wall. This creates a “check valve” lesion, in which air is able to enter alveoli on inspiration or through collateral ventilation but is unable to leave freely and causes air trapping.
Treatment
Emphysema is an irreversible lung lesion; however, therapy directed toward the primary disease process may result in significant improvement of clinical signs, especially by targeting airway obstruction with administration of bronchodilator and anti-inflammatory drugs.
Diaphragmatic hernia with the stomach pushed through crushing the left lung
Rabbit unique respiratory tract features
What is Pasteurellosis in rabbits?
Rhinitis in rabbits
Picture- worried about bilateral dental disease
Pneumonia in the rabbit carries a poor prognosis as most infections are chronic and
clinical signs are not often apparent until the disease has progressed significantly.
Widespread lung involvement is usually present due to the thin pleura and lack of
septa diving the lung lobes in the rabbit, whereas pneumonia in other mammals may
be more localised.
When pneumonia is suspected or diagnosed on thoracic radiographs, check for signs
of concurrent upper respiratory tract disease via radiographs of the neck and head.
Obtaining a culture and sensitivity from the respiratory tract is recommended, as
identification of the causative organism(s) and selecting appropriate antibiotics will
increase the chance of successful treatment. The bacteria causing the pneumonia
may difficult to culture and a ‘no growth’ result is not uncommon. A fine needle
aspirate (FNA) from the chest is often the safest method to obtain a sample for
culture and sensitivity or cytology and is surprising well tolerated by rabbits
Bronchoalveolar lavage is more difficult and carries a higher risk in the rabbit
compared with many other species
.
Myxomatosis rabbits can present with upper respiratory tract signs initially, and often
die from a fulminating pneumonia
Typical radiographic features of pulmonary metastases are the presence of multiple
interstitial nodular densities within the thoracic cavity. These may be well defined or
ill-defined and coalesce merging with neighbouring densities, obscuring the heart in
some cases. Elevation of the trachea can also be present.
An example of metastatic disease in the rabbit is
uterine adenocarcinoma
.
Adenocarcinoma of the uterus is the most commonly reported neoplasm of the
female rabbit.
The incidence increases with age and pulmonary metastases carry a
grave prognosis.
Thoracic radiography is advisable in all rabbits with suspected
uterine abnormalities to assess the prognosis before considering surgery
.
Ovariohysterectomy is curative if metastasis has not occurred. Metastases may not
be visible at the time of surgery or on survey thoracic radiographs so regular repeat
thoracic and abdominal survey radiographs, at least every 6 months, may be taken in
any suspect cases after neutering is performed.
Bilateral exopthalmus in a rabbit?
Cardiac disease in rabbits
Clinical signs
include those of cardiac disease, seizures and/or chronic renal failure (polydypsia,
weight loss)
Mineralization of aorta
Mineralization of the aorta may be seen on thoracic radiographs. Clinical signs
include those of cardiac disease, seizures and/or chronic renal failure (polydypsia,
weight loss).
In pet rabbits, mineralisation of the aorta is usually associated with
chronic renal disease
(Harcourt-Brown, 2007) and is often linked with
E. cuniculi
infection. Calcium metabolism in rabbits is regulated by renal excretion rather than
intestinal uptake so advanced renal disease impairs calcium (and phosphorus)
excretion, which can result in high blood calcium and phosphorus values and ectopic
mineralisation of tissues, especially the aorta and skeleton.
Unique GP traits respiratory and cardiac disease
•
heart occupies relatively large percentage of thoracic space
•
left lung has 3 lobes, right lung 4 lobes
•
middle or inner ear infections occasionally accompany respiratory disease in
guinea pigs
•
additional symptoms in these cases include incoordination, torticollis (twisting
of the neck), circling, and rolling
GP
* Clinical signs are variable
* Radiographs
* FNA from chest- BAL?
* Prognosis guarded in many cases
*Prolonged treatment
GP neoplasia, cardiac disease
Ferret unique traits of thorax
- lungs relatively long
- right side has 4 lobes, left side 2 or 3 lobes (number varies with references)
- large lung volume in relation to body weight
- auscultation of heart: lies more caudal than expected
- situated between 6th-8th ribs
- sinus bradycardia is normal
- tip of heart attached to sternum by cardiodiaphragmatic ligament, often contains fat
Moist dermatitis around chin & lips & inguinal area in a ferret
Cardiac disease in ferrets
Cardiac disease therapy
•
Frusemide 1-2 mg/kg bid to tid
•
Pimobendin 0.5 mg/kg bid
•
ACE-inhibitor 0.25 - 0.5 mg/kg sid to bid
Heartworm in ferrets, diagnosis? Treatment?
Chronic respiratory disease in rats and mice
CRD
•
Clinical signs variable
•
Dyspnoea
•
Sniffles, snuffles, nasal discharge
•
Weight loss, unkempt coat
•
Red tears
•
Progression to severe pneumonia or
bronchopneumonia
CRD in rats and mice Control
Don’t use mucolytics in rats and mice! Don’t use corticosteroids in them.
•
Subacute Chronic Bronchitis (SACB) results in chronic inflammation and
respiratory tract epithelial dysfunction
•
Nebulisation
•
Hypertonic saline
•
Particle size 2-5 um required
•
Bronchodilators
•
Aminylline (theophylline) 10-20 mg/kg bid to tid
•
Fluoquinolones increase serum concentration: decrease dosage by 30%
•
Avoid using corticosteroids
•
May live for several months
Unique attributes to the Cardiovascular system
Unique respiratory system traits in reptiles
•
Lungs single chambered in snakes, some
lizards
•
Multi-chambered in chelonians,
crocodilians, monitor lizards
•
Most snakes: One functional lung (right)
•
Pythons/boas 2 lungs
General respiratory disease in reptiles and chelonia
Diagnosis of respiratory disease in reptiles? Treatment?
What is Sunshine virus?
Sunshine Virus
Novel paramyxovirus
•
Diagnosis
•
Sudden outbreak, clinical signs
•
PCR test developed by Tim Hyndman in WA
•
Not commercially available
•
No treatment
•
Outbreaks
reported in Victoria
•
‘hot’ virus?
•
Outbreak, sudden death
•
Some exposed may recover, resistant
•
Carriers?
•
Transmission?
What is Ferlavirus?
Clinically it may be difficult to distinguish paramyxovirus infections (Ferlavirus and
Sunshine virus) from Arenavirus infection (pInclusion Body Disease (IBD), another
viral disease of pythons. All three conditions may present with neurological signs.
Pythons with IBD do not usually show respiratory signs
Cardiac disease in reptiles
Cardiac Disease in
Reptiles
Most pet reptiles presented with cardiac problems are in an advanced state
of disease; the prognosis is very poor and treatment usually unrewarding
Clinical exam/ presentation cardiac cases in reptiles
Treatment options of cardiac disease
3 presentations with cardiac murmurs and approach?
Normal = Growing puppies up until 16 weeks and older cats
Anaemic patient= due to low viscosity
Patient that is coughing + heart murmur (common in small breed dogs) = work out resp disease? cardiac disease? Both?
Patient present dyspnoeic and has a murmur= congestive heart failure?
** signalment, history, where the murmur is, type of murmur
Myxomatous mitral valve disease?
Present from birth and slowly progressive with age
myxomatous= Myxomatous degeneration refers to a pathological weakening of connective tissue.
Signalment of dogs with MMVD
•
Uncommon in large breeds
–
GSD
–
Dalmatian
–
Dobermann
•
Earlier onset and
progression
•
Major ddx dilated
cardiomyopathy
•
Worse prognosis
Pathology and pathogenesis of MMVD
Pathophysiology of MMVD, early disease mild-moderate, severe?
Left heart volume overload in MMVD? Late and acute complications?
Clinical signs- early/mild disease– when you first pick it up?
SNS activation in MMVD
RAAS role in MMVD
Eccentric hypertrophy with MMVD
Eccentric- heart enlarges to accomodate larger blood volume
* SNS and RAAS activation at this point– high HR
Arrows- bronchial compression
Heart is big but not in CHF
Pathophysiology of heart failure
Clinical signs of CHF
* Early: decreased exercise tolerance (due to oedema developing); cough or tachypnoea with exertion
Then: coughting- night, morning, activity; elevated resting RR
Finally: dyspnoea, +/- moist cough, lethargy, anorexia
** Many dogs with significant pulmonary oedema do not cough– they are focused on breathing
Less common signs:
* Ascites: RSCHF
* Cardiac cachexia
Physical exam- LSCHF
CHF (wet):
•Usually high
-grademurmur (4-6/6), loud S1. (so if it was soft, ask is it related? as atypical presentation)
- Tachycardia– trying to maintain CO (SNS maximally activated)
- Tachypnoea, dyspnoea
- +/- crackles, wheezes
- Brisk pulses
- Pale MM (hypoxia)
- Cyanosis (severe hypoxia)
Physical examination RSCHF
Some will even have jugular pulses at rest just visually
Lily: “cough for past 4 weeks, less keen on
exercise”
–
LSCHF or respiratory disease?
Coughing
–
CHF or respiratory disease?
At least not LSCHF
Yes, CHF will need management
MMVD Diagnosis
Echocardiography
* Confirm diagnosis
* Assess contractility
* Assess severity
* Complications
* Pulmonary hypertension
* NOT pulmonary oedema
* Valve appearance; valve prolapse
* LA size:
- correlates with severity
- except acute CT rupture!
Fractional shortening
MMVD diagnosis in large breed dogs
Laboratory testing in MMVD
ISACHC classification of heart failure
Treatment guidelines preclinical MMVD? Stage I?
* geriatric diet, slightly salt restricted, don’t let them get overweight
Treatment guidelines Stage II MMVD?
started to get signs of CHF, sleeping RR starting to go up at home
* take your time starting all the different drugs
* Pimobendan + ACE inhibitor= prolongs survival big time
Treatment guidelines MMVD Stage IIIb
severe heart failure, need to be in hospital
+/- viagra
* hills makes a cardiac diet with low salt, but many don’t like to eat it
Complications in treatment of MMVD? Monitoring?
Prognosis of MMVD
Key points of MMVD
What are primary cardiomyopathies? Diagnosis?
Secondary cardiomyopathies? Treatment?
DCM aetiology?
DCM presentation?
DCM dog breed differences
DCM pathogenesis
DCM
Highest prevalence of DCM in what breed?
Prognosis of DCM in Doberman pinschers?
Preclinical screening in Doberman pinschers for ?? What do you do?
Boxer cardiomyopathy is??
Boxer ARVC categories?
Cocker spaniel DCM?
Irish wolfhounds- 2 presentations of DCM
Portuguese water dogs DCM
What are you looking at to diagnose?
Echocardiography diagnosis of DCM
Diagnosis of DCM with ECG
Labwork diagnosis of DCM
DCM Treatment
DCM differences from MMVD?
DCM differences from MMVD?
DCM prognosis?
Feline primary cardiomyopathies
Primary Feline cardiomyopathies presentations?
Feline dilated cardiomyopathy causes?
HCM in cats, what do you need to work out?
Primary or secondary?
HCM pathogenesis
HCM clinical presentation
Clinical (CHF)
* Usually acute, precipitating event commone (50%)- corticosteroids
Signs
* tachypnoea, dyspnoea, panting (with activity), lethargy, murmur, strong pulses, +/- cough/ vomit, +/- pulmonary crackles
Aortic thromboembolism in HCM
HCM diagnosis
Cardiac or respiratory disease?
HCM treatment
HCM treatment CHF
Prognosis of HCM
Key points in DCM, HCM and cats with pleural effusion with LSCHF
Heart Failure Classification
Practical pointers in cardiac disease
What is warm & dry? Dry & cold? warm & wet? cold & wet?
Warm & dry?
warm & wet?
dry and cold?
cold & wet?
Treatment aims acute CHF
Is that it?
Oxygen
Sedation if distressed
Frusemide
IV bolus (1
-4 mg/kg) to start
Swap to oral as soon as RR decreases
If RR still high 4 hours after bolus then start a CRI
(0. 5
- 2.0 mg/kg/hour), titrating down as quickly as
possible.
Decrease systemic pressure (> 100 mm Hg)
Pimobendan, nitrates, hydralazine, amlodipine
Treatment aims of chronic CHF
But…
* Treatment causes decreased perfusion of the kidneys
* disease causes decreased GFR
* may have pre-existing renal disease
What do you do because chronic CHF treatment….?
But…
* Treatment causes decreased perfusion of the kidneys
* disease causes decreased GFR
* may have pre-existing renal disease
The pulmonary oedema will kill the animal before the azotaemia, so first priority so don’t give Pimobendan straight away… wait two weeks and check bloods and then add on.
** BUT DON’T add water!
* These dogs are usually hypervolaemic
* Reduce diuretic dosage and vasodilate
* If dehydration or azotaemia is going to kill dog before oedema then give 0.45% saline, preferably SC
Balance hydration with heart disease
* Correct fluids because dehydration would kill it first!!!
*But monitor more carefully and administer slower vs. normal dog
* Pre screening blood test– urea, creatinine + USG…. maybe a PCV. If azotaemia would benefit from fluids before the anaesthetic but 1.5 x maintenance (not dramatic fluids)… imp. to retain renal perfusion during anaesthetic!!! Otherwise make the azotaemia a lot worse.
* Often the owner will say it has this heart murmur so I can’t do its teeth
* know this dog has heart disease because it has a murmur
* Is this dog in CHF– Look at VD– LOOK AT BLOOD VESSEL SIZE (oedema so can’t see often).. in this case no venus congestion. This dog is coughing for another reason… this dog has dynamic airway collapse– tracheal collapse
Treatment?
Enalapril no effect according to studies
** initially tracheal disease but her huge left atrium told us at some point she would go into CHF
** 4 months later–
* RR at rest 50 breaths/minute
* Crackles on auscultation
* HR 160 beats/minute, murmur as previously
NOW warm & wet meaning?
- Relieve congestion
- Preserve perfusion
- Decrease mortality
** Now she has pulmonary oedema & gasping for air so aerophagia
* Drug categories: Diuretics, vasodilators, positive inotropes, beta blockers, calcium channel blockers, adjunctive, emergency
What are loop diuretics?
Frusemide-
Pharmacokinetics
•
IV administration
–
Onset of action 5 minutes
–
Peak effects 30 minutes
–
Duration of effect 2
-3 hours
•
Oral administration
–
Onset of action 60 minutes
–
Peak effects 1
-2 hours
–
Duration of effect 6 hours
Frusemide side effects? When to use?
Pre-renal azotaemia
* Hypokalaemia
* Dehydration
Thiazide diuretics?
ACE inhibitors?
ACE inhibitors
•
Definitely improved quality of life & survival
times in dogs with DCM
•
Prolonged development of CHF and improved
survival times in Dobermans with occult DCM
•
MVD improvement seen in mild and moderate
CHF
•
Benefit shown in cats with HCM
•
Eventually get production of ATII by other
mechanisms
–
Tissue chymase pathways
•
Aldosterone escape
•
Therefore in progressive CHF may need
additional neurohormonal suppression
•
All similar
•
Benazapril (Fortekor)
–
Once daily
–
50:50 urine:bile dogs (80:20 cats)
•
Enalapril (Enalfor)
–
Dogs 1-
2 times daily, cats q 24
-48 hours
•
Ramipril (Vasotop)
–
Once daily
What is Pimobendan (Vetmedin)?
Studies on Pimobendan ?
Need to know about Pimobendan
CHF what to do?
Amlodipine
Nitrates
Digoxin?
Which drug to add in CHF?
Monitoring MVD
Myocardial diseases of dogs = ?
Treatment?
= systolic dysfunction
*Be careful with vasodilation- avoid negative inotropes if possible
* Treat arrhythmias
* Need pimobendan
O2 transport with cell and alveolus and vein and artery side of a capillary
Venous side with high CO2 and low O2 and opp. on the arterial side
Blood gas analyzer
paO2 = 85- 100 mmHg
paCO2 = 34-42 mmHg
(dog, breathing room air)
Acid Base Status
How hard is the animal breathing to get to that point or are you supplementing???
PaO2 4-5 times FiO2
PaO2/FiO2 ratio- 476 normal
Abnormal- breathing more oxygen to get to that point (0.4)
PF ratio can be used to assess oxygenation in animals who are receiving supplemental oxygen
Left mildy hypoxic (85-100 normal)
Right– normal at 85
** FiO2 differs 21% in one; 100% in the other
PF ratio 77.1/0.21 = 367 (400-500)
PF ratio 185/1.0= 185 (normal 400-500)
Patient 2 more serious gas exchange abnormality than the westie
1st dog pCo2 34.1 (FiO2 constant breathing room air)
2nd pCO230 hyperventilation more to get to the same marginal PaO2
Marked inspiratory dyspnoea (stridor) dog A paO261.9, 62 (paCO2)– hypoventilating because paCO2 is above normal range– difference CO2 risen from O2 has fallen, about a 1:1 (+22 and -22 above and below normal)
** dog B– PCO2 constant … paO2 quite a bit lower… paO2 50.4, paCO2 62 …. flail chest. Inspiration the flail segment goes in and creates pleural space defect and pain all causing hypoventilation. PaO2 even more decreased then can be explained by all this alone… probably also pulmonary contusion interfering with gas exchange.
Key points on blood gas analysis
12 yo MN shih tzu
Loud, harsh cough intermittently for 6 months
Terminal retch and swallow, slowing down on walks
Eating and drinking ok
* General appearance- BAR, normal temp, normal RR RE
Coarse crackles and occasional expiratory wheeze, coughs on tracheal palpation, productive
Low heart rate, II/VI left apical systolic cadiac murmur, pulses normal
BCS 7/9
Chronic canine bronchitis
BAL: inflammatory cells, some RBCs
Higher WCC, neutrophilia, eosinophilia, monocytosis, increased TS
Blood gas: PaO2 - 90 mm Hg; PaCO2- 40 mmHg (NORMAL)
Treatment:
* Anti-inflammatory GCs, methylxanthine bronchodilator, consider antitussives, manage allergens, irritants and air quality and humidity of the home, treat infection if present, weight loss, limit stress/ excitement, consider nebulisation and coupage, can be treated but not cured, long term prognosis guarded
12 yr old MN shih tzu, heavy breathing, not eating, weight loss
Last 24 hours breathing heavily, dull lethargic, starting to slow down on walks, several soft infrequent cough
Quiet, alert, responsive, normal temperature,
RR = 60 with moderate increase in effort
Diffuse soft crackles
162 HR, grade V/VI left apical systolic murmur, pulses normal
BCS 3/9
Left sided congestive heart failure
* high ALT, ALP, neutrophilia, lymphopenia
Blood gases: PaO2- 60 mmHg, PaCO2- 25 mmHg
Treatment
* Supplemental oxygen and minimal stress
* 2-4 mg/kg frusemide IV q 1-2 hours until RR
* consider venodilator or systemic vasodilator if frusemide alone is not effective
* MOnitor RR/ effort, potassium concentration, PCV/TP and renal parameters
* Can be treated but not cured, long term prognosis guarded
6 yr FS westie, heavy breathing, bringing food/ water up
* Breathing heavily last 24 hours
* Dull, lethargic, Brought up intact biscuits covered in clear fluid soon after eating
* Drank and brought the water straight back up
* General appearance- quiet, alert, responsive
* Temp 40 C
* Resp 60 with moderate increase in effort, MM hyperaemic, diffusely harsh lung sounds with crackles cranioventrally on the right
CVS- HR 162 MMs hyperaemic, CRT 0.5 seconds, no murmur, pulses tall and wide
BCS 4.5/9
Aspiration pneumonia with megaoesophagus
Leukocytosis, bands, neutrophilia, monocytosis, inc. TS, inc. TP, Moderate toxic change
Blood gas: PaO2- 60 mmHg, PaCO2- 25 mmHg
Treatment:
* Supplemental oxygen and minimal stress
* Broad spectrum antibiotics
* BAL or blind BAL for culture and susceptibility testing
* Restrictive IV fluid therapy
* Nebulisation and coupage
* Consider bronchodilator if acutely dyspnoeic and bronchospasm suspected
* Prognosis for resp disease is good but must carry out investigation for underlying cause when stable
12 yr FS westie, heavy breathing, coughing and slowing down over the last few months, weight loss
* Loud, harsh cough intermittently for 6 months, breathing heavily, coughed up white foamy material with trace of blood this mornign, starting to slow down on walks, decreased appetite, weight loss
* quiet, alert, responsive, normal temp, RR 60 with mod increase in effort, pale pink MMs, diffusely harsh lung sounds, HR 162, grade II/VI left systolic cardiac murmur
BCS 3/9
Metastatic Pulmonary Neoplasia
Anaemia, high platelets, leukocytosis, neutrophilia, monocytosis, increased TS, increased TP, increased ALT, ALP, AST, hypoglycaemic, hypercalcaemia
Mild toxic change
Blood gases: PaO2- 60 mmHg, PaCO2- 25 mmHg
Treatment:
* Supplemental oxygen as needed (clinical signs + SpO2 or arterial blood gas to determine)
* Chemotherapy likely little impact
* Palliation with NSAIDs or corticosteroids, antitussives
* Treat secondary infections
* Consider appetite stimulants
* Pain management as needed
* Long term prognosis is poor
3 yr ME Jack Russel, heavy breathing, collapsed, protracted seizure and now heavy breathing, is sometimes dull after eating, small compared to littermates, general appearance- laterally recumbent, mentally altered, hypersalivating
* high temp 40C
* RR 60, MM cyanotic, marked increase in effort, diffusely harsh lung sounds and generalised crackles
CVS- HR 180, MM cyanotic, tacky, CRT 2.5 seconds, pulses short and narrow
Neuro- pupils responsive, no menace, normal spinal reflexes, non-ambulatory
BCS 4.5/9
Non Cardiogenic pulmonary oedema
Anaemic, neutrophilia, lymphopenia, decreased urea, hypoglycaemia, low cholesterol, increased AST, increased CK, increased PT, increased APTT
Mild microcytosis, WBC morphology unremarkable
Blood gases: PaO2- 60 mmHg; PaCO2- 25 mmHg
Treatment
* Supplemental oxygen and minimal stress
* Furosemide can be considered
* Positive pressure ventilation with PEEP as needed (clinical signs + SpO2 or arterial blood gas to determine)
* Investigate/ manage primary cuase
* May worsen before it improves, likely to recover over 48-72 hours, long term prognosis for resp disease is good but must carry out investigation for underlying cause when stable
3 yr ME Jack Russel, heavy breathing, white gums, coughed up pink foamy material with frank blood, not eating/ drinking, normally very active farm dog, works in the paddocks during the day, kennelled overnight, toxins or trauma?
* Weakly standing but orthopnoeic, quiet but responsive, normal temp
RR 60, MM pale, pattern is rapid and shallow with paradoxical movement, reduced breath sounds ventrally with crackles dorsally, mild right epistaxis noted
CVS- HR 180, MM tacky, unable to assess CRT, regular rhythm, pulses short and narrow, BCS 4.5/9
Vitamin K antagonist rodenticide toxicity
Anaemic, neutrophilia, lymphopaenia, decreased TS, increased urea, hypoalbuinaemia, extremely high PT, high APTT
PaO2- 60 mmHg (decreased), PaCO2- 50 mmHg (slightly elevated)
Treatment:
* Supplemental oxygen and minimal stress
*PPV with PEEP as needed (clinical signs + SpO2 or arterial blood gas to determine)
* 15-20 ml/kg FFP (or whole blood if very anemic)
* Vit K1 5 mg/kg initially then 2.5 mg/kg BID (duration, dependent on agent)
* Return for recheck PT 48 hours after vit K1 supplementation is completed
* Monitor RR/effort, PCV/TP, BP, PT/aPTT
* Long term prognosis is excellent
3 yr ME Jack Russell struggling to breathe, collapsed, found collapsed in the yard, weak with rapid breathing, normally very active, works in the paddocks during the day, kennelled overnight, possible access to toxins/ trauma
* Laterally recumbent, dyspnoeic, appears panicked, profoundly weak, normal temp, RR 60 with minimal chest movement, then agonal just after presentation, MM cyanotic, lung sounds were quiet prior to respiratory arrest
CVS- HR 180, regular moist unable to assess CRT, pulses tall and wide
Neuro- dilated pupils, depressed spinal reflexes, non-ambulatory, profoundly weak
BCS 4.5/9
Low platelets, leukocytosis, neutrophilia, lymphopenia, monocytosis, increased phosphate, increased urea, increased creatinine, hyperglycaemic, increased ALT, increased AST, off the charts CK, off the charts PT and APTT
Blood gas- PaO2- 52 mmHg, PaCO2- 78 mmHg
Treatment
* supplemental oxygen, minimal stress
* Immediate intubation and PPV required
* Tiger snake antiserum, repeated vials until anti-venom detection kit shows negative resulto n blood
* Fluid therapy and nursing support
* monitor coagulation times, CK, renal function
* Long term prognosis is good
Visualize the capillary (systemic circulation), interstitium, parietal pleura, viscercal pleura, interstitium and capillary (pulmonary circulation). Where do the lymphatics fit in?
Oncotic pressure and hydrostatic pressure?
Where does the pleural fluid go from the pleural space?
Paradoxical breathing– inward movement of the abdomen with inspiration
Clinical presentation of pleural space disease
What do you do to stabilise a patient with pleural space disease?
Historical clues causative of pleural space disease
Algorithm with suspicion of pleural space disease
Performing a thoracocentesis for pleural space disease
Categories of pleural effusions… < 25 Total Protein (g/L) & Total nucleated count < 1.5 x 10^ 9 /L… Causes?
What does transudate cause?
Hypoalbuminaemia & Right congestive heart failure
Categories of pleural effusions… 25-75 Total Protein (g/L) & Total nucleated count 1-7 x 10^ 9 /L… Causes?
Categories of pleural effusions… >30 Total Protein (g/L) & Total nucleated count > 7 x 10^ 9 /L… Causes?
Specific pleural space occupiers
Chylothorax aetiology
diagnostic approach of chylothorax
ECG for heart failure in cats
Treatment of chylothorax
Causes of haemothorax
Diagnostic approach to haemothorax
Haemothorax treatment
Presentation/signalment of pyothorax
Aetiology of pyothorax
Diagnostic approach to pyothorax
Pyothorax organisms
Pyothorax therapy
* Medical treatment vs. surgery
* When is surgery indicated?
- Dogs- always
- Cats- if have pulmonary abscessation or migrating FB
- Both species
– if have been treated medically–> ongoing fluid and infection
– lack of clinical improvement after 3-7 days
– evidence of foreign material, pulmonary or mediastinal lesions, isolation of actinomyces
** consider referral after stabilization
Neoplastic exudates
Fluid analysis from the thorax summary
Types of pneumothorax
Causes of pneumothorax
Pneumothorax
Pneumothorax: Diagnostic and therapeutic approach
Subacute pneumothorax
Diaphragmatic hernia causes? Resp dysfunction? Acute signs? Chronic signs?
Diaphragmatic hernia
Treatment of diaphragmatic hernia
Rib tumours? Clinical signs? Tests? Treatment? Prognosis?
What alerts us to mediastinal disease?
Mediastinal disease causes?
Mediastinal diagnostic approach
Limits of the thoracic cavity
Name the thoracic lung lobes
Pleural disease
Thoracocentesis
* Diagnostic and/or therapeutic
* Obtain samples for clinical pathology and to provide therapeutic drainage of air or fluid
* Needles or over the needle catheter (14-22 G), 3 way taps, syringes, extension tubing, clinical pathology sample containers
* Conscious or sedation/ anaesthesia
* Pre-oxygenate and O2 supplementation during procedure
* Patient position variable- sternal preferred if conscious animal
* Clip both sides of the thorax and aseptically prepare skin
* Local anaesthetic infiltration at site
* Enter needle perpendicular to the thoracic wall off cranial edge of rib (7-9 ICS)
* Withdraw fluid or air with syringe attached to needle
Thoracostomy tube placement
Indications for thoracotomy
Thoracotomy approaches
+ equipment
Left intercostal thoracotomy- indications?
Right intercostal thoracotomy indications
Medial sternotomy approach indications
Transdiaphragmatic thoracotomy approach indications
Different intercostal spaces for different conditions
Most common ICS for intercostal thoracotomy? Anatomic landmarks?
The layers you cut through for an intercostal thoracotomy left 4th or 5th ICS
Thoracoscopy indications
What might herniate into the thoracic cavity with a diaphragmatic hernia? What is the congenital condition?
Diaphgragmatic hernia clinical signs
Diaphragmatic hernia diagnosis
Indications and C/I for D-hernia surgery
Anaesthetic management in D-hernia surgery
D-hernia surgery–approach? two types of tear?
D-hernia surgery suture method? When do freshen edges? What else?
PPDH
Flail chest causes? Treatment?
Rib tumours approach
Prognosis of two main types of rib tumours
Primary lung neoplasia in cats and dogs
Summary of thoracic surgeries
Summary
•
Thoracocentesis and thoracic tube placement
are important skills that will be used in
general practice for diagnostic and
therapeutic indications
•
Minimize stress and handling of animals with
pleural space disease
•
Thorough knowledge of anatomy and
cardiorespiratory physiology required for
thoracic surgery
URT Anatomy? How do you know that is where the problem is?
Stertor v. stridor– both associated with what?
Common conditions that affect the upper airway
BOAS signalment? Clinical signs?
Pathophysiology of BOAS
Increased airway resistance by narrowed airway causes increase in intraluminal pressure gradient during inspiration.
Leads to mucosal inflammation and swelling of airways.
Concurrent conditions seen with BOAS
BOAS initial management
BOAS Surgical correction
Surgical correction:
Nares – wedge resection (images and video)
Soft palate – landmarks, sharp incision and suturing versus harmonic scalpel, laser, ligasure
Everted laryngeal saccules
Role of cortoicosteroids, acepromazine, oxygen supplementation, temporary tracheostomy in post op period.
minimal hemorrhage, swelling, and signs of postoperative pain and potential bactericidal properties of laser ablation. The laser coagulates small vessels as it cuts, seals lymphatic vessels, minimizes tissue handling and subsequent swelling, and decreases signs of postoperative pain by sealing nerve endings.14 Use of the laser reduces the duration of surgeries by more than half
BOAS Laryngeal collapse stages?
BOAS Post op care
BOAS Prognosis
Types of laryngeal paralysis
Laryngeal paralysis
Signalment, clinical signs (voice change, exercise intolerance, heat stress), diagnosis [insert video of lar par exam here]
Mention congenital lar par here as well – Bouvier de Flandres
Concurrent conditions, (megaoesophagus, aspiration pneumonia, polyneuropathy, hypothyroidism)
Most commonly idiopathic.
Equipment required for sedated laryngeal exam (laryngoscope, IV catheter access, oxygen, ET tubes ready (variety of sizes) sedation agents to use and those to avoid). Light plane of anaesthesia.
Clinical signs of Lar Par
Lar par diagnosis
- Medial displacement of vocal folds or no movement during inspiration → Laryngeal paralysis
- Assistant to monitor phase of respiration and note inspiration so evaluator can assess vocal fold movement
- Paradoxical vocal fold movement during expiration passively moves vocal folds laterally simulating abduction
- Doxapram will increase respiratory effort and intrinsic laryngeal motion (Doxapram hydrochloride is a respiratory stimulant. Administered intravenously, doxapram stimulates an increase in tidal volume, and respiratory rate)
Laryngeal paralysis treatment
Treatment – unilateral arytenoid lateralization, moderate tension.
Surgical anatomy unfamiliar for most as we do not do surgery here regularly. Important to stress need for appropriate aftercare of these patients. ICU 24 hour monitoring required with oxygen source.
[Image of pre and post adducted arytenoid]
Post op complications – life long risk of aspiration pneumonia
Larynx anatomy- tx for lar par
Prognosis of Lar par
Indications for tracheostomy
Permanent Tracheostomy Indications? Risks?
Permanent tracheostomy how to
Neoplasia of the upper airway– Types? diagnosis? Treatment?
Laryngeal and tracheal neoplasia
BOAS Summary
Lar par summary
