SA LRT Disease

Question 1

Why do we see respiratory problems?

Answer 1

• URT obstruction
  
  • Something in the middle of it that is blocking it.
• Loss of thoracic capacity
  
  • Structure of airway: pleural space or mediastinum gets blocked and crushing lungs.
• Pulmonary parenchymal disease
• Non-CRS conditions
  
  • Metabolic/physiologic

Question 2

What can cause airway obstruction and what signs to we often see?

Answer 2

Causes

• F.B.
  
  • Acute
• Neoplasia
• Trauma/haemorrhage etc
  
  • Acute
• Laryngeal paralysis/trauma/granuloma
• BOAS - long soft palate, stenotic nares, larynx collapse etc
  
  • Not classically acute, but if have laryngeal collapse, can be.
• Tracheal or bronchial collapse
• Extra-luminal mass lesions - thyroid, abscess, lymphoma
• Asthma/bronchospasm (cat)
• Nasopharyngeal polyp (cat)
  
  • Chronic

Often see cough, cyanosis and noise

Question 3

Causes of loss of throacic capacity?

Answer 3

• Not always acute.
• Have changes in ability of chest.
• Pleural effusion
  
  • blood, pus, chyle, true/modified transudate
• Pneumothorax
• Neoplasia - pleural or mediastinal
• Ruptured diaphragm
  
  • Cats RTA
• Abdominal abnormality - severe ascites/mass
• Gross cardiomegaly
  
  • Animals that have pericardial effusions.

Question 4

Clinical signs of pulmonary parenchymal disease

Answer 4

• Usually increased inspiratory and expiratory effort
• Some interstitial lung diseases however limit compliance and so inspiratory effort predominates
• Cannot breathe in because cannot expand lungs – they are stiff due to fibrous tissue.
• Cough may or may not be present
  
  • As disease process may be too deep for cough receptors to be activated.
• Can see less frequently hemoptysis, collapse/syncope or cyanosis
  
  • Cyanoses with parenchymal disease = very severe.
• Occasionally minimal signs of respiratory disease are noted even with severe pathology
  
  • Particularly in cats

Question 5

What are you looking for on physical exam if you suspect pulmonary parenchymal disease?

Answer 5

• Are there other signs of systemic disease?
  
  • Pyrexia, lymphadenopathy, lameness
• Cyanosis
• Crackles
• Increased/decreased bronchovesicular sounds
• If patient is in respiratory distress immediate oxygen therapy is indicated
  
  • Regardless of underlying cause.

Question 6

Explain aspiration pneumonia

Answer 6

• Inhalation of material into the lower airway
  
  • Stomach contents with variable amounts of particulate matter
    
    • Acid, fluid +/- bits of food.
• Care with nursing recumbent patients
  
  • Esp. feeding recumbent patients – don’t tube or syringe feed them as will increase risk of this.
• Outcome depends on nature and amount of aspiration
  
  • pH, bacterial contents, volume, particle size
    
    • Chemical aspiration – pneumonitis
    • Large volumes of fluid – drowning event
    • PEG fluids (bowel prep) – pulls interstitial fluid into the lungs
  • Primary infection due to aspiration is less common
    
    • This usually occurs as a secondary event due to damage to the lungs.

Question 7

Signs of aspiration pneumonia

Answer 7

• cough, harsh/reduced (dull) lung sounds, tachypnoea, pyrexia
• Pyrexia is a tell-tale sign.
• Check oxygenation – serial evaluation

Question 8

Diagnosis of Aspiration pneumonia

Answer 8

• Radiographs alveolar infiltrate (patchy/focal)
  
  • Most common affected lobes are right middle, right cranial and left cranial
• BAL to confirm diagnosis
  
  • In human’s pepsin used in BAL fluid

Question 9

Treatment of aspiration pneumonia

Answer 9

• Supportive – oxygen therapy, antibiotics
  
  • Care with oxidative damage to already fragile lung
• Treat any underlying cause
  
  • E.g. laryngeal paralysis, mega-oesophagus
• Consider anti-acid medication if frequent occurrence
  
  • May increase gastric bacterial load therefore caution…
• Metoclopramide to improve motilty and increase LOS (lower oesophageal sphincter) tone

Question 10

Explain Pulmonary oedema

Answer 10

• Consequence of various conditions: stuff/ fluid etc. gets into the lungs.
  
  • Increased hydrostatic pressure
  • Reduced oncotic pressure
  • Increased vascular permeability
    
    • Seen with inflammation.
  • Impaired lymphatic drainage
    
    • Seen with lymphatic obstructions.
• This leads to fluid accumulation in the interstitium of lung (where transfer occurs) and subsequently it gets into the alveoli at a rate that exceeds removal.
  
  • Ventilation perfusion mismatching and hypoxaemia
    
    • Blood supply is going wrong – get hypoxaemia.

Question 11

Cardiogenic vs. non cardiogenic pulmonary pneumonia

Answer 11

• Main difference is type of fluid
• Cardiogenic oedema is low protein due to increased hydrostatic pressure without increased vascular permeability.
  
  • Due to increased hydrostatic pressure, so fluid is low protein, a lot more watery.
• Non-cardiogenic is the result of lung damage which increases vascular permeability
  
  • Associated with damage to lung, leading to increased permeability, so not just fluid – higher protein, so have much greater problem. Increase interstitial pressure, get compression of airways because fluid accumulates and get much more severe hypoxia.
  • If have damage to epithelial cell surface due to lung injury, process of removing fluid means non-cardiogenic oedema is harder to treat as lung damage needs to be addressed. Cardiogenic – they respond well to diuretics.
  • This leads to a higher protein fluid in the pulmonary parenchyma
  • This alters fluid dynamics and the resultant increase in interstitial pressure also alters perfusion causing ventilation perfusion mismatch
  • Alveolar fluid accumulation, reduced compliance, airway compression all increase pulmonary vascular resistance
  • This all contributes to the hypoxaemia
  • Removal of the fluid requires active transport of sodium and chloride from the luminal surface across epithelial cell to the basal surface
  • This is an active process – if the epithelium is damaged this cannot occur
  • So the damage to the epithelium leads to fluid accumulation and reduced the ability to remove the fluid which makes non-cardiogenic oedema more refractory to therapy than cardiogenic oedema

Question 12

Non-cardiogenic causes of pulmonary oedema?

Answer 12

• Importantly hypoalbuminaemia rarely causes pulmonary oedema due to efficient pulmonary lymphatics
• Lymphatic damage is more likely to cause a chylous effusion (chylothorax) rather than pulmonary oedema
• Neurogenic form (along with electric shock) – pathophysiology unclear but thought to be due to intense pulmonary vasoconstriction and inflammation both increase vascular permeability
• Most common cause is pulmonary epithelial injury
• Hypoalbuminaemia can exacerbate fluid accumulation if vascular permeability is compromised
• End up with either acute lung injury or ARDS. The severity is what differentiates the two and it is to do with oxygen concentration.

Question 13

Clinical signs of pulmonary oedema?

Answer 13

• Signs may be delayed after insult for up to 72 hours – so don’t say to O they are going to be fine!
• Clinical signs:
  
  • Moist cough (may produce froth), orthopnoea, cyanosis
  • Harsh BV lung sounds with crackles are typical
  • Radiographs – unstructured interstitial pattern and peri-bronchial can progress to alveolar, often caudo-dorsal.

Question 14

Treatment of Pulmonary oedema?

Answer 14

• Address underlying cause, treat ARDS/ALI
• Oxygen supplementation
• Sedation may be required (caution with resp depression)
• To keep them calm.
• May need active cooling as they cannot thermoregulate
• Support – keep affected lung dependent
• Diuretics less effective for non-cardiogenic oedema but still indicated.

Question 15

Explain physical lung injury

Answer 15

• Thoracic trauma
  
  • Pulmonary contusion - ventilation perfusion mismatch
  • Chest wall damage and pain
  • RTAs, dog fights etc.
• Thoracic radiographs to evaluate all thoracic structures
  
  • Lag phase
• Supportive care with supplemental oxygen ASAP
  
  • Other treatment as required – e.g. stabilisation of the thoracic wall, analgesia

Question 16

Explain drowning

Answer 16

• Aspiration of liquid (similar principle of aspiration pneumonia)
  
  • Immediate consequences result from hypoxaemia
    
    • Alveoli fill with fluid causing hypoxia.
    • As you dilute the surfactant, you cause alveolar collapse, leading to ventilation/perfusion mismatch.
  • Alveoli fill with fluid – dilutes surfactant and leads to alveolar collapse and intrapulmonary vascular shunting leading to V-Q mismatching
    
    • Disrupted oxygen passage and then the perfusion at the places were you need it aren’t receiving it.
  • Reduced compliance and inflammation leads to ARDS (acute respiratory distress syndrome) worsening hypoxaemia
    
    • Systemic complications of lactic acidosis and hypercapnia
  • More common in dogs than cats
    
    • Underlying cause laryngeal disease, seizure whilst swimming
    • Unable to exit water

Question 17

How will an animal present that has suffered from a drowning incident?

Answer 17

• Resp. distress, arrest, cough, unconscious
• Auscultation – increased or decreased lung sounds
• Radiographs varied but interstitial to alveolar pattern
  
  • This can progress to ARDS and so the appearance may underestimate the extent of the pathology
  • Sand bronchograms are a negative prognostic indicator
    
    • Radio-opaque material in the airways are negative prognostic indicator.
    • Oxygen therapy, may need ventilation if unable to keep saturation PaO2>60mmHg with FiO2 >50%.
• ARDS can occur despite patient appearing stable therefore continual monitoring is important
• Care with fluid therapy – over perfusion in the face of lung injury
• No evidence for antibiotics or corticosteroids improving outcomes

Question 18

Explain Eosinophilic lung disease

Answer 18

• EBN is more common in dogs, with reactive eosinophilic airway disease occurring in cats
  
  • Typically young adults? Huskies/malamutes and Rottweilers??
  • Acute or chronic presentation – usually coughing
  • Can also see weight loss
    
    • As inflammatory problem.
  • Radiographs show diffuse bronchointerstitial pattern although can see alveolar patterns (can be dense infiltrates)
  • Horrible puss like liquid in airways – stuffed full of eosinophils.
  • Circulating eosinophilia in ~50% dogs – some will have hypereosinophilic syndrome
    
    • Knowing whether they have this is really important as they might have parasitic disease.

Question 19

Diangosis and treatment of eosinophilic lung disease?

Answer 19

Diagnosis: BAL

Treatment: Prednisolone (1-2mg/kg daily)

Outcome: often very good, unless other organs involved - then prognosis is guarded.

Question 20

What would you find in the history and clicinal exam of a patient suffering with interstitial pulmonary fibrosis (IPF)

Answer 20

• Typically WHWT and other terriers (Staffordshire BT)
• Middle aged to older dogs
• History
  
  • Insidious onset
  • Chronic breathlessness which is slowly progressive
  • Coughing can be a feature
  • Exercise intolerance
  • Owner may notice cyanosis
  • Can cause syncope
• Clinical examination
  
  • Crackles throughout the lung fields
    
    • Dry diffuse crackles.
  • Prolonged expiratory phase with expiratory effort (fibrotic lungs – cannot compress them).

Question 21

Diagnosis of IPF?

Answer 21

• Suggestive clinical signs
  
  • Diffuse crackles on auscultation, dyspnoea, coughing
• Thoracic radiographs
  
  • Generalised interstitial lung pattern
  • +/- right sided cardiomegaly, +/- pulmonary hypertension due to fibrotic nature of lung.
• CT – method of choice in humans
  
  • Typical ground glass appearance – diffuse increase opacity without loss appearance of blood vessels.
• Bronchoscopy
  
  • BAL samples are either normal or show low cellularity
  • Rules out other inflammatory conditions – primarily Chronic bronchitis.
• Lung biopsy is the only method of definitive diagnosis
  
  • Relatively poorly understood compared with human fibrotic lung diseases
  • In absence of biopsies, efficacy of treatment difficult to determine
• Lung pattern generally reflects severity

Question 22

Treatment of IPF?

Answer 22

• Can’t do very much
• Success of therapy depends largely on whether active inflammation present (depends on whether it is inflammatory or non- inflammatory process).
• Symptomatic treatment
  
  • Avoid collars, harness only, avoid smoke inhalation
  • Avoid trauma to the airways
• Inhaled therapy
  
  • Bronchodilator, corticosteroids
    
    • Only if secondary airway spasm use bronchodilators.
• Oral therapy
  
  • Bronchodilators - especially if concurrent airway collapse
  • Corticosteroids
• Additional immunosuppressive medication
  
  • Azathioprine and cyclosporin
  • No evidence of clinical efficacy
• Antibiotics as necessary
  
  • They are not sterile, so chronically infected airways can get concurrent infections.
• Anti-fibrotics (e.g. colchicine)
  
  • Theoretically slows collagen deposition and reduces production of profibrotic cytokines
  • No evidence for efficacy of these in veterinary patients
  • No evidence of improved outcomes in humans either
• Management of pulmonary hypertension
  
  • Phosphodiesterase inhibitors
    
    • Sidenafil, tadalafil
    • Pimonbendan

Question 23

Prognosis of IPF?

Answer 23

• Guarded as this is a progressive disease
• Long-term palliation of clinical signs may be possible with combination therapy
• Reports in dogs suggest around 15 ½ months median survival times

Question 24

Signs of A. vasorum infestation?

Answer 24

• Coagulopathies
  
  • Clinically - anaemia, subcutaneoushaematomas, internal haemorrhages, prolonged bleeding fromwounds or after surgery
  • Thrombocytopenia, prolonged APTT and OSPT, elevated D-dimer (previously measurement of FDPs was used) –via consumptive coagulopathy – chronic DIC
    
    • Studies have shown deposition of immunoglobulins, complement and fibrinogen in pulmonary vessels
  • Also causes immune mediated thrombocytopaenia
  • Similar pathophysiology can lead to thrombopathia
  • Parasite releases – or stimulates host to release – factors that modulate blood clotting?
• Neurologicaldysfunction
  
  • Paresis, depression, seizures, spinalpain, behavioural changes, ataxia and loss of vision have beendescribed
  • Associated with aberrant nematode migrationor subdural haemorrhage secondary to coagulopathies

Question 25

Diagnosis of A. vasorum?

Answer 25

SNAP test PCR –on BAL fluid or pharynx swabs

Question 26

Management of A. vasorum?

Answer 26

* Over recent years products have become licensed * Previously no licensed products available in UK * Licensed products: * Advocate (Bayer), Prinovox (Virbac) spot on - (Imidacloprid and Moxidectin) – licensed * 2.5mg/kg spot on as a single dose * Milquantel (MSD), Milbemax (Elanco), Milbactor (Ceva) –milbemycin oxime and praziquantel –licensed * 0.5mg/kg milbemax orally * Given 4 times at weekly intervals * Studies have also used 2 doses a month apart in the pre-patent period * Unlicensed products: * Fenbendazole – effective but unlicensedused at 25-50mg/kg orally for 7-21 days, some people suggest treating at weekly intervals every 3 weeks for 3 treatments * Some clinicians start with a low dose to reduce the complications of acute treatment deterioration from massive worm death and liberation of worm Ag – 20mg/kg orally * Cow’s can get parasitic bronchopneumonia – farmers treat them and all dead the next day due to massive anaphylaxis as worms died in the lungs. We can see the same things in dogs – dogs that have severe lung worm infestation, when you start treatment, they can get severe worsening of the clinical signs and they might die. Hence, need to be careful when we start treatment and warn owner’s that they might die. * Levamisole and ivermectin also effective but unlicensed * alternative products are equally effective and licensed with fewer potential side effects * Studies on efficacy of treatment for naturally occurring infections are sparse and limited to a small number of case reports * The therapy of choice therefore remains relatively open

Question 27

Treatment of A.vasourm?

Answer 27

* Need to counsel owners about the risks of beginning therapy for Angiostrongylus * Considerations for supportive treatment in addition to anthelminthics with infections that have been identified * Bronchodilators * Aid with airway hyperresponsiveness * Corticosteroids * May reduce tendency for acute deterioration after beginning anthelminthic therapy * Phosphodiesterase inhibitors – for ongoing PH * Cage rest and possible oxygen therapy * if dyspnoea present * Keep rested for a few days after treatment. Don’t push them. * Considerations for haematological dyscrasias * May be ongoing despite therapy for angiostrongylus

Question 28

Prevention of A. vasorum?

Answer 28

* Limited licensed products for prevention * Advocate and Prinovox (moxidectin and imidacloprid) * Evidence suggests treatment in pre-patent period with Milbemycin oxime or moxidectin decreases or prevents establishment of adult parasites * Unclear to what extent dogs are protected from reinfection by persistence of macrocyclic lactones nor how severity of disease relates to level or stage of infection * Dogs in endemic areas treated every 3 months with milbemycin are half as likely to test positive for angiostronglyus as those treated with fenbendazole or untreated * Important to have an idea of local epidemiology * Difficult to control slugs and snails but can reduce time dogs are in contact by more active exercise regimes

Question 29

Explain pulmonary thromboembolism

Answer 29

* Acute onset dyspnoea * Few radiographic signs * Hypercoagulable states * Trauma/surgery * Sepsis/DIC * HAC/exogenous corticosteroids * HypoT4 * IMHA * Glomerulonephropathies * Pulmonary hypertension