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SMALL ANIMAL > 1.1.4: Coughing in small animals > Flashcards

1.1.4: Coughing in small animals Flashcards

1
Q

Acute coughing ddx in dogs

A
  • Tracheobronchitis (kennel cough)
  • Irritation by smoke/dust/chemicals/medicines
  • Airway FB
  • Pulmonary haemorrhage
  • Acute pneumonia e.g. aspiration
  • Acute oedema (can be cardiogenic/non-cardiogenic)
  • Airway trauma e.g. choke chains, bites
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2
Q

From this list of acute coughing ddx, which ones are often accompanied by dyspnoea, and why is this?

  • Tracheobronchitis (kennel cough)
  • Irritation by smoke/dust/chemicals/medicines
  • Airway FB
  • Pulmonary haemorrhage
  • Acute pneumonia e.g. aspiration
  • Acute oedema (can be cardiogenic/non-cardiogenic)
  • Airway trauma e.g. choke chains, bites
A
  • Tracheobronchitis (kennel cough)
  • Irritation by smoke/dust/chemicals/medicines
  • Airway FB
  • Pulmonary haemorrhage
  • Acute pneumonia e.g. aspiration
  • Acute oedema (can be cardiogenic/non-cardiogenic)
  • Airway trauma e.g. choke chains, bites

With these causes, there is alveolar disease, hence the dyspnoea. Sometimes it spills over into/affects airways too, hence the acute onset coughing.

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3
Q

What are some differential diagnoses for chronic coughing in the dog?

A
  • Chronic bronchitis
  • L-sided heart failure
  • Oslerus/aelurostrongylus/angiostrongylus infestation
  • Tracheal collapse
  • Airway FB
  • Bronchopneumonia
  • Pulmonary neoplasia
  • Extra-luminal mass lesions
  • Eosinophilic disease
  • Pulmonary fibrosis
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4
Q

Where are cough receptors located?

A
  • Larynx
  • Trachea
  • Carina
  • Bronchi

Coughing is a reflex designed to protect the lower respiratory tract and the alveoli

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5
Q

What is infectious tracheobronchitis, what can cause it and how do you prevent this?

A

Infectious tracheobronchitis: infectious disease of canine URT.

Causative agents:
* Canine parainfluenza - live vaccine, injection
* Canine adenovirus-2 - live vaccine, injection
* Bordetella bronchiseptica - live vaccine, intranasal

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6
Q

What is the typical recovery time for infectious tracheobronchitis and when might further treatment be needed?

A
  • Spontaneous recovery tends to occur within 7-10 days
  • May need further treatment if pyrexic, systemically unwell, mucopurulent nasal discharge etc.
  • Could consider NSAIDs ± antibiotics if indicated
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7
Q

Signalment and history associated with Canine Chronic Bronchitis

A
  • Daily coughing over >2 months duration
  • Harsh cough with attempts at production (usually clear / frothy; yellow would suggest infection)
  • Worse on excitement
  • Typically seen in small/ toy breeds but can be any age/ breed
  • Dogs are usually externally well, often obese. May pant exvessively.
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8
Q

Pathology of Canine Chronic Bronchitis

A
  • Neutrophilic / eosinophilic infiltration of mucosa and thickening of smooth muscle
  • Fibrosis and scarring of the lamina propria
  • Increased goblet and glandular cell size and number
  • Oxidative damage and inflammatory products damage cells -> leads to mucus hypersecretion
  • Loss of ciliated epithelial cells and failure of mucociliary clearance and debris
  • More mucus which is more sticky

Combination of these events leads to thickening of bronchial trees (donuts and tramlines), overproduction of airway mucus and narrowing of airways (esp terminal bronchi)

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9
Q

Complications of Canine Chronic Bronchitis

A
  • Bronchoectasis (widening of airways)
  • Bronchomalacia (weakness of airways)

This combination can lead to dilation and then collapse of airways due to wall weakness.

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10
Q

Aetiology of Canine Chronic Bronchitis

A

Cause unknown; may be seen secondary to underlying conditions:
* Tracheal collapse
* Chronic barking
* FB
* Previous infections or inhalant toxins
* Environmental factors
* Chronic smoke inhalation / noxious gas

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11
Q

Clinical exam findings of dog with Canine Chronic Bronchitis

A
  • Tracheal pinch positive - animal will cough when you palpate
  • Marked sinus arrhythmia
  • Often very little to find on exam
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12
Q

Diagnosis of Canine Chronic Bronchitis

A
  • History and clinical exam findings
  • Thoracic radiographs: increased bronchial pattern (this is often subtle)
  • Bronchoscopy and BAL
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13
Q

What would BAL of a dog with Canine Chronic Bronchitis show?

A
  • Increased mucus
  • Non-degenerate neutrophils, eosinophils, macrophages
  • Cushmann’s spirals (airway mucus casts)
  • Presence of bacteria / particulate matter are less common and would suggest an underlying cause somewhere
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14
Q

Management of Canine Chronic Bronchitis

A
  • General: weight control, use harness rather than collar/ lead, avoid irritants/ smoking environment
  • Mucus is easier to shift if hydrated: avoid v dry environments, use steamy bathrooms and coupage to encourage coughing mucus up
  • Warn owener that these animals will always cough (the damage is irreversible)
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15
Q

What lung pattern and radiographic changes are shown in the circle?

A

Bronchial pattern - images from a dog with Canine Chronic Bronchitis
* We can see tramlines
* Airways are dilated (they should taper)

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16
Q

What radiographic changes can be seen in this circle?

A
  • There is bronchoectasis (dilated and weak airways)
  • The hilus of the lungs is a good place to look for this
  • This image is from a dog with Canine Chronic Bronchitis
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17
Q

How would Canine Chronic Bronchitis appear on bronchoscopy?

A
  • Airways may look pale, scarred, fibrotic
  • There is mucus stuck to the airway walls
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18
Q

True/false: in a dog with Canine Chronic Bronchitis you would not expect to see donuts or tramlines on thoracic radiographs

A

False
You WOULD expect to see these findings but they may be subtle

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19
Q

What disease is shown on the right? Describe the changes visible.

A

Canine Chronic Bronchitis
* Chronic, permanent change in the airway walls with increased numbers of goblet cells (mucus metaplasia)
* There is more mucus than usual
* Ciliary loss affecting the airways, which is now overlain by stratified squamous epithelium (squamous metaplasia)

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20
Q

Medical managament of Canine Chronic Bronchitis

A
  • Glucocorticoids (oral and inhaled)
  • Bronchodilator therapy often prescribed but damaged resp tract may not be able to respond ;theophyline, beta agonists (terbutaline, salbutamol, salmeterol)
  • The purpose of inhaled medications is to reduce side effects of the disease not cure it
  • Coupage
  • AVOID using cough suppressants unless absolutely necessary (mucus will just build up)
  • ONLY use antimicrobials if there is evidence of need
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21
Q

Describe how you would determine if antimicrobial therapy was needed in a dog with Canine Chronic Bronchitis

A
  • Infection is rare in these dogs; should only use antimicrobials if evidence of infection
  • Evidence of infection: intracellular, growth from BAL, neutrophilic inflammation on cytology
  • Remember that URT and larger airways will have commensal bacteria and numbers will increase if the mucociliary escalator is damaged
  • Can request a quantitative culture (rare in vet med but common in humans)
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22
Q

What are the problems with diagnosing infection based on culture from BAL?

A
  • There is risk of contamination from URT - might conclude there is an infection present when there is not
  • Equally, in vet med, BAL is often perfomed after antibiotic therapy has failed, but antibiotics remain in the lung for sufficient quantities for 7+ days - might conclude there is no infection when in fact there is
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23
Q

What are the broad treatment options for lower airway disease?

A
  • Inhaled medications: corticosteroids, bronchodilators, nebulisers
  • Oral therapy: anti-inflammatories (e.g. corticosteroids, NSAIDs, anti-leukotrienes), bronchodilators (terbutaline, theophylline), antibiotics & anthelmintics as indicated, mucolytics (N-acetyl cysteine)
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24
Q

What are the benefits of inhaled over oral medications?

A

✅ Useful in management of chronic airway disease
✅ Minimal absorption into systemic circulation -> less side effects esp with steroids
✅ Faster onset of action compared to oral meds

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25
Q

What is salbutamol and when might you use it?

A

Salbutamol = beta 2 agonist, can be delivered by inhalation
* Fast onset of action
* Lasts >3 hrs
* Metabolised and cleared renally
* Side effects: tachycardia, arrhythmias, tremors

Used in cats with asthma

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26
Q

What is the difference between salbutamol and salmeterol?

A

Salmeterol is longer acting

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27
Q

What drugs might you use to treat a dog with CCB?

A
  • Corticosteroids e.g. fluticasone propionate, beclomethasone
  • Cromolyn sodium / sodium cromoglicate -> to inhibit mast cell degranulation
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28
Q

Characteristics of fluticasone propionate for treatment of CCB

A
  • Slowly absorbed from lungs (long dwell time)
  • Rapid first pass metabolism in the liver -> less systemic side effects
  • Long half life
  • Least bioavailable
  • Side effects: oral infections due to immune response suppression e.g. candidiasis, coughing, wheezing
  • (The above may hold true for all inhaled glucocorticoids)
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29
Q

Why are inhaled glucocorticoids useful?

A
  • Inhaled version valuable in reduced systemic exposure and side effects
  • Effective in acute situations
  • Very useful in asthmatic cats
30
Q

Benefits of glucocorticoids on the airways

A

✅ Bronchodilatory
✅ Anti-inflammatory -> inhibit both prostaglandin and leukotriene synthesis
✅ Potentiate beta-2 adrenergic activity
✅ Reduce leukocyte accumulation
✅ Reverse increased vascular permeability
✅ Inhibit fibroblast growth
✅ Modulate the immune system

Remember they do have side effects so limited the dose is important!

31
Q

Benefits of bronchodilators on the airway

A

✅ Reduce spasm of lower airways
✅ Decrease intrathoracic pressres
✅ Decrease tendency of large airways to collapse
✅ Improve diaphragmatic function
✅ Improve mucociliary clearance
✅ Inhibit mast cell granulation -> reduced released of mediators of bronchoconstriction
Possibly also: improve pulmonary circulation, improved cardiac function, reduced respiratory effort but not always.

32
Q

Disadvantages of inhaled medications

A

❌ Expensive
❌ Time-consuming
❌ Owner compliance
❌ Patient compliance

33
Q

What should you bear in mind if considering antibiotic use for chronic bronchitis?

A
  • Most chronic bronchitis cases do not have bacterial infection as a causal agent. If there is a secondary infection, this requires immediate therapy due to compromised resistance mechanism.
  • Antibiotics are indicated if: C&S positive, or intracellular bacteria found on BAL
  • Tale care re fluoroquinolones and theophylline -> they inhibit metabolism of theophylline meaning conc increased and risk of toxicity
34
Q

Prognosis of Canine Chronic Bronchitis

A
  • Long-term control is possible; cure is not. The dog will always cough.
  • Major goal is to prevent sequelae e.g. secondary pneumonia, bronchiectasis / bronchomalacia, emphysema
35
Q

What are the other names for feline bronchial disease? What causes it and who is predisposed?

A

Feline bronchial disease = feline asthma, feline allergic airway disease, etc.
* There is a continuum between acute asthma and chronic bronchitis and cough
* Type 1 hypersensitivity reaction to inhaled allergens e.g. smoke, feathers, aerosol inhalation, dust, cat litters, sometimes seasonality
* Suspected genetic predisposition as some breeds (e.g. Siamese) more commonly affected

36
Q

True/false: bacterial bronchopneumonia (primary infection) is common in dogs and cats.

A

False.
Primary infections are rare in healthy dogs and cats.
If present, look for an underlying cause!

37
Q

If you found a dog with a primary bacterial bronchopneumonia?

A
  • Bordetella bronchiseptica
  • Streptococcus equi subsp zooepidemicus
  • Mycobacteria

Many infections are mixed

38
Q

Characteristics and clinical signs of Strep equi subsp zooepidemicus infection?

A
  • New causative organisms recognised with increasing frequency
  • Often associated with outbreaks
  • Has been linked to acute fatal haemorrhagic pneumonia
  • Highly contagious
  • Sudden onset
  • Clinical signs: pyrexia, dyspnoea, haemorrhagic nasal discharge, haemoptysis
39
Q

Factors predisposing to bacterial bronchopneumonia

A
  • Debilitation
  • Prolonged recumbency
  • Systemic immunosuppression (e.g. HAC, chemo, preds)
  • Immunodeficiency states
  • Defective respiratory defences
  • Damaged respiratory epithelium
  • Aspiration
  • Airway obstruction
  • Bronchiectasis
  • Systemic sepsis
40
Q

Clinical signs of bronchopneumonia

A
  • Variable; occasionally only minor clinical signs
  • Cough
  • Respiratory distress
  • Exercise intolerance
  • More severe infections may produce hyperthermia
  • Anorexia and lethargy
  • Increased / decreased lung sounds (depending on how consolidated the lung is; might be so thick you can’t hear, or may hear crackles)
  • Respiratory distress and cyanosis may develop in severe cases
41
Q

Diagnosis of bronchopneumonia

A
  • CBC, biochemistry, UA, faecal sample
  • Thoracic radiographs: would see alveolar pattern with variable distribution. Early disease may show only interstitial pattern.
  • Airway sampling helpful: TTW / BAL; culture and cytology on fluid (integration of inflammation and bacterial culture)
42
Q

In aspiration pnuemonia, which lung pattern would you expect and with what distribution?

A
  • Alveolar pattern with cranio-ventral distribution
43
Q

Treatment of bronchopneumonia

A
  • Broad spectrum antibiotics
  • Humidified oxygen
  • IVFT -> must keep hydrated and high RR / panting means much water loss; want to keep mucus wet and easy to cough up
  • Anti-inflammatories
  • Bronchodilators
  • Mucolytics
  • Physio
  • Nebulisation
  • Surgery if localised disease very difficult to move
44
Q

History associated with bronchial foreign bodies

A
  • High frequency in working dogs / dogs in rural environments
  • Often signs after exercising in agricultural fields
  • May see good initial response to antibiotics (as some localised pnuemonia) but will not resolve without foreign body removal
45
Q

Clinical signs of bronchial foreign bodies

A
  • Sudden onset coughing and gagging
  • Halitosis may be present and progressive due to rotting material in lungs
  • May see weight loss if significant infection associated with FB
  • More substantial resp signs may suggest progression to pleural disease (i.e. FB working way out of lung into pleural space -> causing secondary pyothorax)
46
Q

Diagnosis of bronchial foreign body

A
  • Thoracic radiographs (check if lobar or diffuse disease, and for signs of pleural involvement)
  • Bronchoscopy: visualisation and removal of object, BAL and culture for antibiotic therapy (may need to refer for bronchoscopy)
47
Q

In which lung lobe do most inhaled FBs end up?

A
  • Right diaphragmatic lobe bronchus (this is the most straight direction if you look down the airway)
48
Q

Which are more common: primary or secondary lung neoplasias?

A

Secondary (i.e. metastases) far more common than primary tumours.
Common metastases that end up in lungs:
* Oral melanoma
* Thyroid carcinoma
* Osteosarcoma
* Haemangiosarcoma
* Mammary carcinoma

49
Q

What is the most common primary lung tumour and what clinical signs does it cause?

A

Bronchogenic carcinomas
* Signalment: older dogs (median age 11yrs)
* Often found in right caudal lobe
* Causes non-productive cough or exercise intolerance
* May see hypertrophic osteopathy as a rare paraneoplastic disease (=proliferation of periosteum in limbs)

50
Q
A

Secondary pulmonary neoplasia (metastatic disease)
Interstitial disease
Presents with breathlessness

51
Q
A

Primary pulmonary neoplasia
* Presents with cough
* Often found in R caudal lobe
* >50% of these masses are solitary

52
Q
A

Primary pulmonary neoplasia
Presents with cough

53
Q
A

Primary pulmonary neoplasia
Presents with cough

54
Q
A

Secondary pulmonary neoplasia (metastasis)
Interstitial disease
Presents with breathlessness

55
Q

Diagnosis of primary pulmonary neoplasia

A
  • Ultrasound-guided transthoracic FNA (don’t do this if the animal can’t clot, the lesion is full of air, or infection is suspected)
  • Fluoroscopy / CT can also guide
  • BAL rarely helpful
56
Q

Contraindications for transthoracic FNA

A
  • Pulmonary bullae or cysts
  • Coagulopathies
  • Pulmonary hypertension
  • Pre-existing pneumothorax
  • Suspected infectious process
57
Q

Potential complications of transthoracic FNA

A
  • Pneumothorax
  • Empyema
  • Bleeding
  • Implantation
  • Seeding of neoplasia through body wall
58
Q

Treatment and prognosis of primary lung neoplasia

A
  • Depends on size, location (resectability) and spread
  • Adjunctive chemo often little use
  • Best case scenario = adenocarcinoma, has better survival than SqCC
59
Q

How does secondary pulmonary neoplasia (a.k.a. metastatic disease) present?

A
  • Interstitial disease -> presents with breathlessness
60
Q

Which lungworms affect dogs?

A
  • Oslerus osleri
  • Filaroides spp.
  • Crenosoma vulpis
  • Angiostrongylus vasorum
  • Capilaria aerophilia
61
Q

Which lungworms affect cats?

A
  • Aelurostrongylus abstrusus
  • Capilaria aerophilia
62
Q

Characteristics and epidemiology of Oslerus osleri

A
  • Prevalent in UK; rarer now due to routine worming of dogs
  • More common in greyhounds and kennelled dogs
  • PPP: 10-18 weeks
  • Worms live in trachea, immune response causes worm to encapsulate in trachea and bronchus
  • Nodules in which worms live appear 2 months from infection
63
Q

Clinical signs of Oslerus osleri

A
  • May include chronic cough: dry rasping, particular after exercise
  • This is most notable in young (6-12 month old) dogs
64
Q

Diagnosis of Oslerus osleri

A
  • Bronchoscopy -> visualisation of nodules, sampling of tracheal mucus to identify eggs and larvae
  • BAL: can see L1s and eosinophils
  • Faecal sample: L1 count unreliable due to variable shedding; requires experienced parasitologist
65
Q
A

Oslerus osleri nodule in trachea

66
Q
A

Oslerus osleri nodules

67
Q

Treatment of Oslerus osleri

A
  • Can be hard as nodules may remain and calcify
  • Cough may persist
  • Fenbendazole (e.g. panacur) at 50 mg/kg daily for 10 days. Often need to repeat 4 weeks later.
68
Q

Presentation, diagnosis and treatment of Filaroides hirthi

A
  • Life cycle same as Oslerus osleri but F. hirthi not considered pathogenic
  • Originally found in breeding colonies of beagles
  • Infection generally asymptomatic; usually diagnosed at PM
  • Worms live in alveoli
  • Radiographs show diffuse broncho-interstitial patterns, rarely alveolar pattern
  • Treatment rarely indicated; if needed, fenbendazole for 10 days, then repeate 4 weeks later (same as O. osleri)
69
Q

Epidemiology and life cycle of Crenosoma vulpis

A
  • Found in UK, occasionally seen in practice
  • Usually affects foxes and wolves, occasionally dogs 🦊🐺🐶
  • Indirect life cycke: slugs and snails = intermediate hosts; paratenic hosts eat slugs and snails and are infective
  • PPP 3 weeks
  • Highest incidence in autumn due to summer infection (seasonality of snail host)
  • Larvae visible to naked eye unlike other lungworm
70
Q

Clinical presentation, diagnosis and treatment of Crenosoma vulpis

A
  • Adults live in bronchi and bronchioles where they cause bronchitis; do not form nodules
  • Leads to chronic bronchopulmonary disease and productive cough
  • Diagnosis: bronchoscopy, BAL, thoracic rads
  • Treatment: fenbendazole 10 days then 4 weeks later; often rapid response cf O. osleri
71
Q

Diagnostic plan for investigation of coughing in the dog and what each would detect

A

Radiography
* If bronchial pattern, consider Chronic Bronchitis, EBP
* If cardiac enlargement, consider left-sided heart failure
* May suggest foreign body
Radiography / CT very useful for airway disease investigation.

Endoscopy / bronchoscopy
* Good for foreign bodies

Other options: TTW, tracheal wash, BAL, haematology.
BAL and faecal exam
* Useful for parasites.

72
Q

What are some anti-tussives and when should you use them?

A

Anti-tussives e.g. butorphanol, codeine
* Only use when absolutely necessary - they suppress cough, and in most cases coughing is protective
* Useful in anatomical airway disease e.g. tracheal collapse
* Useful in non-productive pathological cough e.g. neoplasia, heart failure that is receiving treatment but cough not resolving

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