SA Airway Disease

Question 1

What can cause pulmonary parenchymal disease?

Answer 1

• Aspiration pneumonia
• Pulmonary oedema (cardio vs. non-cardiogenic oedema)
• Drowning
• Eosinophilic lung disease
• Idiopathic pulmonary fibrosis
• (Pulmonary parasites)
• (Pulmonary neoplasia – primary/metastatic)
• (infectious pneumonias)
• Many more occur and are part of the SDLs

–Ensure awareness of additional common pathologies including

• Pulmonary haemorrhage
• Lung lobe torsions
• Pulmonary thromboemboli
• Congenital airway diseases
• Bullous pulmonary diseases
• Lipid pneumonias
• Smoke inhalation
• Paraquat poisoning

Question 2

What are some reasons why we would see respiratory problems?

Answer 2

1.URT obstruction

•Something blocking it

2.Loss of thoracic capacity

•Structure of airway, pleural space or mediastinum becomes occupied

3.Pulmonary parenchymal disease

•Bit where oxygen is transferred

4.Non-CRS conditions

•Metabolic/physiologic

Question 3

Name some things that can cause airway obstruction?

Answer 3

• F.B.
• Neoplasia
• Trauma/haemorrhage etc
• Laryngeal paralysis/trauma/granuloma

–typical sounds

• BOAS - long soft palate, stenotic nares, larynx collapse etc
• Tracheal or bronchial collapse

–Typical sounds

• Extra-luminal mass lesions - thyroid, abscess, lymphoma
• Asthma/bronchospasm (cat)
• Nasopharyngeal polyp (cat)

Question 4

What are some things that can casue loss of thoracic capacity?

Answer 4

• Pleural effusion

• blood, pus, chyle, true/modified transudate
• Pneumothorax
• Neoplasia - pleural or mediastinal

–Compressing large parts of the chest space, cranial lung fields are just squashed out of the way

• Ruptured diaphragm
• Abdominal abnormality - severe ascites/mass
• Gross cardiomegaly

–particularly animals that have things like pericardial effusion

Question 5

What are some clinical signs of pulmonary parenchymal disease?

Answer 5

–Usually increased inspiratory and expiratory effort

–Some interstitial lung diseases however limit compliance and so inspiratory effort predominates

–Cough may or may not be present

•Don’t exclude possibility of this just because they aren’t coughing!!

–Can see less frequently hemoptysis, collapse/syncope or cyanosis

•Cynaosis with parenchymal disease shows very severe disease

–Occasionally minimal signs of respiratory disease are noted even with severe pathology

•Particularly in cats – don’t overlook the situation

Question 6

What should you look for on a clinical exam in a patient with pulmonary parenchymal disease?

Answer 6

•Physical examination is important

–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

–Struggle getting oxygen into airstream, supplemental oxygen can make a big difference no matter the underlying cause

Question 7

What is a big risk for nursing recumbent patients?

Answer 7

•Aspiration pneumonia – big risk for nursing recumbent patients, especially recumbent patients. Recumbent patients shouldn’t be tube fed as increases the risk of AP

–Inhalation of material into the lower airway

• Stomach contents with variable amounts of particulate matter
• Care with nursing recumbent patients

Question 8

What does the outcome depend on with regards to aspiration pneumonia?

Answer 8

–Outcome depends on nature and amount of aspiration

•pH, bacterial contents, volume, particle size

–Chemical aspiration – pneumonitis – acidic fluid that causes the majority of the problems

–Large volumes of fluid – drowning event

–PEG fluids (bowel prep) – pulls interstitial fluid into the lungs

Question 9

What are some signs of aspiration pneumonia?

Answer 9

–Signs – cough, harsh/reduced lung sounds, tachypnoea, pyrexia

•Check oxygenation – serial evaluation

Question 10

How can you diagnose aspiration pneumonia?

Answer 10

–Radiographs alveolar infiltrate (patchy/focal)

•Most common affected lobes are right middle, right cranial and left cranial

–BAL to confirm diagnosis

•In humans pepsin used in BAL fluid

Question 11

What is the treatment for aspiration pneumonia?

Answer 11

•Supportive – oxygen therapy, antibiotics

–Care with oxidative damage to already fragile lung

• Treat any underlying cause – some may have laryngeal paralysis, may have megaesophagus – need to treat or identify those or it will otherwise keep happening
• Consider anti-acid medication if frequent occurrence

–May increase gastric bacterial load therefore caution…

•Metoclopramide to improve motilty and increase Lower Oesophageal Shincter tone

Question 12

What is arrowed here?

Answer 12

• Abnormality
• Lung lobe commonly affected - right middle lung lobe involvement. Major suspicion of aspiration pneumonia
• A lot of supportive evidence comes from acute onset and findings

Question 13

Pulmonary oedema can be an important presenting abnormality of pulmonary parenchymal disease.

What can cause pulmonary oedema? (the mechanisms that could be responsible)

What do these mechanisms lead to?

Answer 13

• Increased hydrostatic pressure
• Reduced oncotic pressure
• Increased vascular permeability
• Impaired lymphatic drainage – get with lymphatic obstructions

–This leads to fluid accumulation in the interstitium of the lung (where gas transfer occurs) and subsequently in the alveoli at a rate that exceeds removal

•Ventilation perfusion mismatching and hypoxaemia – blood supply and ability to aerate the blood is going wrong

Question 14

How can pulmonary oedema be classified?

Answer 14

Cardiogenic and non-cardiogenic

Question 15

What is cardiogenic oedema?

What causes it?

Answer 15

•Cardiogenic oedema is low protein due to increased hydrostatic pressure without increased vascular permeability

–The process that forms this oedema is pulmonary hypertension, increased hydrostatic pressure.

–A lot more watery, less protein

Question 16

What is non-cardiogenic oedema?

What causes it?

Answer 16

•Non-cardiogenic is the result of lung damage which increases vascular permeability

–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

-Associated with some kind of damage to the lung

Question 17

What are some of the causes of pulmonary oedema?

Answer 17

•Pulmonary oedema

–NC causes are numerous

• Importantly hypoalbuminaemia rarely causes pulmonary oedema due to efficient pulmonary lymphatics – these lymphatics are very good
• Lymphatic damage is more likely to cause a chylous effusion(chylothorax for example) rather than pulmonary oedema
• Neurogenic form (along with electric shock) – pathophys. 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

Question 18

How does pulmonary oedema present?

Answer 18

–Presentation – signs may be delayed after insult for up to 72 hours

• 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 19

What is the therapy for pulmonary oedema?

Answer 19

–Therapy – caution as animals clinically fragile

• Address underlying cause, treat ARDS/ALI
• Oxygen supplementation
• Sedation may be required (caution with resp depression)
• Support – keep affected lung dependent
• Diuretics less effective for non-cardiogenic oedema but still indicated
• They might need cooling

Question 20

What can cause thoracic lung injury?

How should you diagnose and how should you support?

Answer 20

•Physical lung injury – not that common, but things like RTAs or dog bites

–Thoracic trauma

• Pulmonary contusion - ventilation perfusion mismatch
• Chest wall damage and pain – can change how the animals are breathing

–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 21

What happens with drowning after the aspiration of liquid?

Answer 21

• Immediate consequences result from hypoxaemia
• Alveoli fill with fluid – dilutes surfactant and leads to alveolar collapse and intrapulmonary vascular shunting leading to V-Q mismatching
• Reduced compliance and inflammation leads to ARDS 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 22

How does drowing present?

Answer 22

• 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

»Oxygen therapy, may need ventilation if unable to keep saturation PaO2>60mmHg with FiO2 >50%.

»These are often referral cases – see stuff in their airway that shouldn’t be there, definitely speak to owners about referring

–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 23

What is eosinophilic lung disease?

Answer 23

–Various names – eosinophilic bronchopneumopathy*, pulmonary infiltrate with eosinophils (PIE), eosinophilic pneumonitis – basically, inflammatory disease based on eosinophils

–EBN is more common in dogs, with reactive eosinophilic airway disease occurring in cats

Question 24

How does eosinophilic lung disease present?

What is the treatment?

Answer 24

• Typically young adults ?huskies/malamutes and Rottweilers??
• Acute or chronic presentation – usually coughing, may lose weight because its an inflammatory problem

–Can also see weight loss

–Radiographs show diffuse bronchointerstitial pattern although can see alveolar patterns (can be dense infiltrates)

–Circulating eosinophilia in ~50% dogs – some will have hypereosinophilic syndrome – if going to anaesthetise the patient, knowing whether it has a circulation eosinophilia before you start is important – make sure you have worked it up enough to know that you need a bronchoscopy.

–BAL for diagnosis – caution to look for parasites, neoplasia and fungal disease

•Treatment – prednisolone 1-2mg/kg daily

–Outcome often very good unless other organs involved in which case prognosis guarded

Question 25

Describe the lung pattern here

Answer 25

Lung pattern – bronchial pattern, can see tramlines and doughnuts on both sides

Also looks like a bit of an interstitial component also as not as black as it should be.

Exudate within lumen, inflammatory process

Question 26

What breeds is interstitial pulmonary fibrosis seen in?

What is often their history?

Answer 26

•Interstitial pulmonary Fibrosis (IPF) – once you have heard one, you don’t forget it!

–Typically in WHWT and other terriers (Staffordshire BT)

–Middle aged to older dogs

–History

• Insidious onset – chronic onset, similar picture of humans with chronic emphysema
• Chronic breathlessness which is slowly progressive
• Coughing can be a feature
• Exercise intolerance
• Owner may notice cyanosis
• Can cause syncope

Question 27

What do you see on clinical exam with interstitial pulmonary fibrosis?

Answer 27

–Clinical examination

• Crackles throughout the lung fields – diffuse and dry
• Prolonged expiratory phase with expiratory effort.

Question 28

What is the diagnosis of interstitial pulmonary fibrosis?

Answer 28

–Suggestive clinical signs

•Diffuse crackles on auscultation, dyspnoea, coughing

–Thoracic radiographs

–Generalised interstitial lung pattern

–+/- right sided cardiomegaly, +/- pulmonary hypertension

–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 CB

–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
• Bld gases – severely affected individuals can show hypoxia and show ventilation – perfusion mismatch

Question 29

Describe what is happening here

Answer 29

• Idiopathic pulmonary fibrosis. Pulmonary hypertension
• Severe interstitial/alveolar pattern
• Generalised cardiomegaly. Right sided emphasis. Abdominal distension
• Airway with IPF, wide trachea – a lot of effort to breathe, may have degree of instability. Also got interstitial pattern and a heart that’s big

Question 30

What is the treatment for idiopathic pulmonary fibrosis?

Answer 30

–Success of therapy depends largely on whether active inflammation present – depends on if its inflammatory or non-inflammatory

–Symptomatic treatment

•Avoid collars, harness only, avoid smoke inhalation

–Inhaled therapy

•Bronchodilator, corticosteroids

–Oral therapy

• Bronchodilators - especially if concurrent airway collapse
• Corticosteroids

–Additional immunosuppressive medication

• Azathioprine and cyclosporin
• No evidence of clinical efficacy

–Antibiotics as necessary

–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 – secondary complication of the fibrotic lung, if you can improve this right sided compliance and the hearts ability to get blood into to the lungs can improve

•Phosphodiesterase inhibitors

–Sidenafil, tadalafil

–pimonbendan

Question 32

What is the prognosis for IPF?

Answer 32

–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

• Some dogs reported to survive up to 4 years
• In humans the DIP form of the disease shows markedly improved prognosis over UIP
• This would suggest in dogs that the prognosis is heavily dependent on biopsy findings

Question 33

Is A. Vasorum a problem I am likely to encounter clinically UK?

Answer 33

• Historically regionally endemic in UK
• Now accepted to be widespread in South of UK and wales, with reports arising of infections in northern UK and Scotland
• Rural environments were the mainstay of distribution initially
• Becoming more widespread throughout the country due to increased fox urbanisation and more widespread travel with dogs
• Also endemic in regions of Spain, France, Hungary, Germany, Italy, widespread in Ireland

•

•Big challenge is identifying it. Something you saw down south originally, but has spread more so now as people travel with their dog – UK wide problem. Less so in the states. Big issue is that it causes a lot more than just what you’d expect, but the most common problem this gets referred is because of coagulopathies. Any animal that has a clotting problem, that you check for lung worm.

Question 34

What are the coagulopathies with regards to signs of A. vasorum infestation?

Answer 34

–Clinically - anaemia, subcutaneous haematomas, internal haemorrhages, prolonged bleeding from wounds 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?

Question 35

What are the neurological dysfunction with regards to signs of A. vasorum infestation?

Answer 35

–Paresis, depression, seizures, spinal pain, behavioural changes, ataxia and loss of vision have been described

–Associated with aberrant nematode migration or subdural haemorrhage secondary to coagulopathies

–Either because they may have bled into spinal cord or parasite migration through their parenchyma.

Question 36

Why are the signs of A. vasorum so diverse?

Answer 36

–Adult antigens

• Cause Type III hypersensitivity (immune complex deposition)
• Complement activation
• Immune infiltrate in lungs and other tissues

–Egg deposition/L1

• Pulmonary inflammation/granuloma formation
• Pulmonary arteriolar vasoconstriction
• End arteritis and fibrosis of vessels

–Eggs, larvae and adults can all cause problems

Question 37

What is this?

Answer 37

A. Vasorum

L1 in BAL

Lots of eosinophils and coiled up larvae on left

Right – coiled up view

Question 38

How can we diagnose A. vasorum?

Answer 38

• SNAP test from IDEXX
• PCR – on BAL or pharynx swabs

Question 39

What is the management for A. Vasorum?

Answer 39

–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
• 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 unlicensed used 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

•Levamisole and ivermectin also effective but unlicensed

–alternative products are equally effective and licensed with fewer potential side effects

Question 40

What is the problem with treating dogs with lungworm?

Answer 40

• Treatment and prophylaxis are different…
• Dogs with sever lungworm, when you start treating, if all worms die – can get anaphylactic shock from this and the dog can look much worse! So be careful that when you start the treatment, warn owners the dog might die with treatment!! Don’t underestimate the severity of the disease

Question 41

So how do we treat A. Vasorum?

Answer 41

–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 – keep them rested when you start treatment as if you have made them worse by increasing inflammation with dead lung worms, decreased lung capacity even more!

–if dyspnoea present

•Considerations for haematological dyscrasias

–May be ongoing despite therapy for angiostrongylus

Question 42

How can you prevent A vasorum infestation?

Answer 42

–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 – its contact with contaminated trails also! Not just eating them themselves, but avoid any contacted material

Question 43

What is a pulmonary embolism?

Answer 43

Pulmonary embolism (PE) is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream (embolism)

–Occur and they are difficult to identify

–Acute onset dyspnoea

–Few radiographic signs – because clot may have resolved by the time they present

Question 44

What is pulmonary thromboembolism often associated with?

Answer 44

–Often associated with hypercoagulable states

• Trauma/surgery
• Sepsis/DIC
• HAC/exogenous corticosteroids
• HypoT4
• IMHA
• Glomerulonephropathies

–Pulmonary hypertension

–Its supportive care whilst their clots are being dealt with by the body and reducing the chances of other clots forming

Question 45

What are some other physiologic/metabolic things that can cause LRT disease?

Answer 45

• Hyperthermia/heat stroke/fever
• Obesity
• Excitement/fear/stress/pain/shock
• Parturition/false pregnancy/eclampsia
• Anaemia/abnormal haemoglobin
• Acidosis – does it have DKA?
• CNS disease – any changes in central control of breathing?
• Endocrine dz, e.g. HAC & steroid tx, hypert4
• Neuromuscular disease where there is diaphragmatic weakness?