Respiratory Medicine

Jon Wray

BVSc DSAM Cert VC MRCVS

RCVS Specialist in Small Animal Medicine (Internal Medicine)

Dick White Referrals

Station Farm

London Rd

Newmarket

Suffolk

jw@dickwhitereferrals.com

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Index to notes

1. Some definitions 3 – 5

2. Some essential respiratory physiology 6 – 17

3. Diagnostics

-history 18-20

-physical examination 20-25

-laboratory analysis 25-27

-radiography 28-34

-ultrasound 34 – 35

-endoscopy 35 – 42

-cytology and microbiology 42 – 43

-lung biopsy 44 – 46

-advanced diagnostic aids 46 – 53

4. Approach to the cat with nasal discharge, sneezing or epistaxis 53 – 64

5. Approach to the dog with nasal discharge, sneezing or epistaxis 64 – 73

6. obstructive upper airway disease in the cat 73

7. Obstructive upper airway disease in the dog 74 – 78

8. Selected lower respiratory disease in the cat 78 – 82

9. Selected lower respiratory disease in the dog 82 - 96

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1. Some Definitions

Sneezing

• Protective reflex of explosive expiratory airflow to dislodge material from nasal cavities

• Sudden onset with facial irritation suggestive of foreign body

• Pathophysiology

o Reflex initiated by stimulation of subepithelial myelinated trigeminal nerve endings

o 3 phases

inspiration

compression – thyroarytenoideus contracts, adducting vocal folds in concert

with abdominal contraction increases subglottic pressure

expulsion – sudden abduction of vocal folds with maintained increased

subglottic pressure causes explosive caudo-rostral airflow

Reverse sneezing

• Protective response aimed at ‘ripping’ adherent material from pharyngeal walls

• Pathophysiology

o Instigated by stimulation of intra- and subepithelial myelinated trigeminal nerve endings

o Repetitive forced inspiration and generation of highly negative intrapleural pressure

followed by sudden laryngeal abduction to increase airflow explosively in a rostrocaudal

direction

Cough

o Sudden expiratory effort against closed then rapidly open glottis causing explosive expulsion of

air from lungs

o Effort to strip adherent material or foreign body (real or perceived) from airway lumen

o Voluntary or involuntary

o Reflex mediated by mechanical / chemical / inflammatory stimulation of ‘cough receptors’

Rapidly adapting stretch receptors – mucosa of Tracheobronchial tree

Pulmonary C-fibres – unmyelinated, peripheral airways and pulmonary circulation

Bronchial C-fibres – unmyelinated, larger airways and bronchial circulation

o Release inflammatory mediators such as substance P, tachykinins, neurokinin A, cacitonin

gene-related peptide (CGRP) – these are broken down by a number of neuropeptidases

including ACE which is why, in humans, ACE-inhibitors frequently cause unacceptable coughing

o Vagus is main afferent arm of reflex to central cough centre within the brainstem

Stridor and stertor

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• These terms are often confused and there is much contradiction in texts as to their significance.

Both are caused by vibration of air and tissue within an obstructed area of air flow

• Stridor (from Latin Stridere, to creak or screech) is a generally high pitched sound usually

caused by a fixed narrowing of the airway with little surrounding mural movement. Stridor is a

description of a sound, not an anatomical location, though commonly stridor is heard due to fixed

obstruction in the extrathoracic airways, especially the larynx (eg laryngeal paralysis) and

trachea. Stridor can however be caused by fixed nasal obstructions also

• Stertor (from Latin Stertere, to snore) is a lower pitched, vibrational snore caused also by a

narrowing of communicating airways but usually associated with more movement of extraluminal

tissue or fluid as is common with pharyngeal disease. As with stridor, stertor is a description of a

sound not an anatomical location though it is most commonly associated with nasopharyngeal

disease

Tachypnoea

• Increased rate of breathing

Hyperpnoea

• Increased excursion of chest wall (‘effort’) during breathing

Orthopnoea

• Adaptation of body / neck / head posture to allow as much unimpeded air transit as possible

• Typically orthopnoeic animals will have extended head and neck, flared nostrils, +/- open mouth,

abducted elbows and low head carriage. They will prefer to stand or crouch rather than sit or lie

Dyspnoea

• Literally ‘disordered breathing’

Hyper / hypoventilation

• These terms are generally misused in veterinary (and human!) medicine – they describe whether

airflow within the respiratory system is adequate to allow removal of CO2 produced by normal

cellular metabolism

• Hyperventilation indicates low PaCO2 (i.e. hypocapnia) hypoventilation indicates high PaCO2 (ie

hypercapnia)

• The state of an animal’s ventilation can only be determined by blood gas analysis, not by

observation of thoracic movements. Animals which are putting much effort into their breathing

with large chest wall excursions have hyperpnoea not hyperventilation (in fact many of these

animals will be hypoventilating which is why they are hyperpnoeic in the first place!). Similarly

lack of good chest movement is described as hypopnoea not hypoventilation

Hypoxia

• General reduction in oxygen delivery because of hypoxaemia, reduced cardiac output or

reduced uptake in systemic capillaries

Hypoxaemia

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• Reduced PaO2 or arterial oxygen content i.e. hypoxaemia is a finding on an arterial blood gas

analysis, hypoxia is the result of it (but hypoxia may also result from other disorders not just

relating to gas exchange)

Cyanosis:Blue discoloration of skin and mucous membranes. Cyanosis occurs when amount of

deoxygenated haemoglobin reaches 3-5g/dl. Usually animals with normal haematocrits must have SaO2

of 73-78% or PaO2 of 40-45mmHg before clinically detectable cyanosis is present. Cyanosis is always

representative of severe hypoxaemia but severe hypoxaemia may be present without detectable

cyanosis. Cyanosis may be regional or generalised and may be difficult to appreciate in animals with

anaemia, shock, carbon monoxide poisoning or methaemoglobinaemia.

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2. Some essential respiratory physiology (for reference) Like most areas of internal medicine, understanding and becoming proficient at respiratory medicine is dependent on

having a firm grasp of the Pathophysiology. This may be an unpopular and unfashionable statement – curricula and

textbooks focus more on the ‘diagnose’ and ‘treat’ parts, but without understanding the physiological processes involved

such endeavours are bound to fail some of the time. Although the course will focus more on the practicalities I would

emphasise that academic knowledge of respiratory physiology is essential in understanding disease mechanisms,

development and treatment aims.

PULMONARY MECHANICS

overview

o parietal pleura lines rib cage and encloses visceral pleura covering lungs

o pleural space contains a small amount of fluid (c 2ml in dogs) dispersed over large area

o elastic recoil pressure of rib cage (outwards) and recoil of lung parenchyma (tendency to collapse

inwards) created negative (subatmospheric) pleural pressure (Ppl)

o inspiration: i/ thoracic pressure decreases from -2.5 to -6 mmHg, reverse happens in expiration

o during inspiration contraction of inspiratory muscles (mostly contributed to by diaphragm in veterinary

species) causes outward rotation of rib cage and expansion of abdomen, pleural pressure reduces and

inspiratory airflow occurs

o during expiration relaxation of the diaphragm raises intrapleural pressure and air movement from alveoli

to bronchi and thence to upper resp tract occurs. Alveoli do not collapse as such due to surface tension

produced by surfactant from type II pneumocytes

lung volumes

o lung volume is divided into 4 functional volumes and 2 capacity divisions:

• at end of normal (tidal) breathing, volume left = functional residual capacity

o functional residual capacity = residual volume (which cannot be reduced further) +

expiratory reserve volume (volume which can be expelled through forced expiratory

effort)

• tidal volume is that volume of air displaced during normal restful breathing – note that this does

not mean that all this air takes part in gas exchange

• inspiratory reserve volume is that volume ‘extra’ which can be inspired during exerted inspiration

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air flow, resistance and compliance

o static compliance and elastic recoil

• compliance = measure of pressure required to maintain lung volume

o = unit volume / unit pressure l/cmH2o or l/kPa

o can be thought as measure of distensibility or reciprocal of ‘stiffness’

o compliance of resp system = lung compliance(CL) + chest wall compliance(CW)

therefore compliance may be reduced by factors such as parenchymal ‘stiffness’ (eg

fibrosis) a

o

nd chest wall – non-compliance (eg obesity, pleural effusion, diaphragmatic

• is

opp expanded volume

s is disrupted in chest wall defects eg flail chest

o

o Air flow

disease)

o CL and CW contribute about equally in normal individuals

o Reduced compliance results in decreased magnitude of exchanged volumes

Elastic recoil forces cause lung tissue to have tendency to collapse at end inspiration but this

osed by chest wall recoil to a neutral position with slightly

o Thi

• During inspiration air flows from non-respiratory zones (conducting and transitional zones ie

anatomical dead space)

• Airways ramify into about 23 divisions of which the first 16 or so are conducting, next 3 are

transitional and last four take place in gas exchanges

Total lung capacity

Inspiratory reserve volume (IRV)

Tidal volume (VT)

Expiratory reserve volume (ERV)

Residual volume (RV)

Inspiratory capacity (IC)

Functional residual capacity (FRC)

VC

IRV + VT + ERV = Vital Capacity (VC)

VT

IRV

IC

VC

ERV

RV

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• Total cross sectional area varies little from the first 10 divisions then increases rapidly beco

100 X increased by 17th generation and 500X by terminal divisions

ming

nt flow) and become laminar rather than turbulent

ing expiration opposite occurs: air speeds up as it traverses from slow flow / large cross

irways

o Airway resis c

• Airway

/ nasopharynx / larynx

o

owing

Raw to about 3-4X

th

ause of the very large cross sectional area, very many small

be affected to cause significant increase in airway resistance

• Air distributio

o Decre

a

/ mural / extraluminal masses

o Increased by

Small bronchiole collaterals

moses between adjacent alveoli

o Dynami

• pliance is volume change associated with pressure

• vercome airway resistance (Raw) and static compliance /

• gs Raw is the major contributor, but Raw will also be decreased at larger lung

• Air flow in larger airways is rapid and turbulent, becomes slowed as cross sectional area

increases in smaller vessels (diverge

• Dur

sectional area to low XSA a

•

tan e and distribution

resistance (Raw) = ratio of pressure to flow (cmH2O/l/s or KPa/l/s)

o Most airway resistance is seen in the nasal chambers

(contributing about 50-60% of airway resistance) and in 4th to 9th divisions of airways

Nose breathing creates 2 X Raw of mouth breathing

o Peripheral airways account for only 20% of Raw but may increase with severe narr

or accumulation of secretions to increase

o Bronchi of 4th to 9th division with diameters of 2-4mm have decreased amounts of

cartilage and increased smooth muscle

Resistance increases according to Poiseuille’s law (inversely proportional to the 4o

power of the radius) but bec

airways need t

n may be affected by:

ased

Bronchoconstriction

Airway fluid / oedem

Mucous plugs

Luminal

Stiff walls

atelectasis

Anasto

c compliance (CLdyn)

Unlike static compliance, dynamic com

differences between peak inspiration and peak expiration

Is a measure of pressure required to o

elastic recoil of lung tissue ie is dV/dP

In normal do

volumes due to retraction of airways

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• CLdyn is decreased by hyperinflation, venous engorgement, alveolar oedema, mineralisation

and fibrosis

mphysema

o Dynamics o lv

• Alveoli

o

ree of surface tension adjusts according to degree of distension via law of Laplace –

h contribution to lung elastic recoil but also prevention of alveolar collapse

• Airways

ressure equals extraluminal pressure – the

point in the ai nt

o The extraluminal pressure is resisted by

Presence of surface tension within the alveoli

Rigid cartilaginous structures of the conducting airways

o The t uted to by/ has greatest effect

uscle predominates

c

Hyperinflation of surrounding parenchyma

o Transmural pressures across intra and extrathoracic airways dictate that:

durin intrathoracic airways resist collapse, extrathoracic airways are

prone to collapse

• CLdyn is decreased by aging an e

f a eolar and airway collapse

Pulmonary surfactant (phospholipid secreted by principally by type II pneumocytes)

helps maintain surface tension within distended alveoli

o Deg

results in bot

since surface tension reduces during reduction in alveolar diameter

o Airways can collapse when intraluminal p

rway where this occurs is the end pressure poi

ex raluminal pressure is contrib

Elastic recoil of lung tissue

Space occupying lesions

Areas where cartilage is absent and smooth m

Areas where cartilage is damaged or malaci

g inspiration,

during expiration, intrathoracic airways are prone to collapse, extrathoracic

airways resist collapse

this is commonly demonstrated in tracheal collapse:

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INSPIRATION – intrathoracic airway resists collapse due to decreased intrathoracic pressure and tractive forces. Extrathoracic airway at risk of collapse due to low intraluminal pressure

EXPIRATION – intrathoracic airway prone to collapse as extraluminal pressure increases due to elastic recoil. Extrathoracic airway resists collapse

EXTRATHORACIC TRACHEAL COLLAPSE INTRATHORACIC TRACHEAL COLLAPSE

When collapsing segment is extrathoracic, When collapsing segment is intrathoracic,

GAS EXCHANGE

Alveolar ventilation and the PaCO2 equation

o alveolar ventilation is the inspiration of all gas that takes part in gas exchange. Note that it is different

from expired ventilation which is the total volume of gas breathed in and out – this includes both gas

which is exchanged and gas which takes no part in exchange

o expired ventilation volume = alveolar ventilation volume + dead space

o dead space volume is air which does not take place in gas exchange. It is due to:

• anatomical dead space ie air contained within those conducting airways whicih does not take

place in gas exchange and

• physiological dead space –refers to areas which are anatomically capable of gas exchange (ie

alveoli) but in which gas transfer is impossible eg due to lack of blood perfusion. Physiological

dead space will tend to increase in disease states though a small number of alveolar units are

normally poorly perfused (eg those in the dorsal lungfields) and contribute to the small amount of

physiological dead space in normal individuals

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o alveolar ventilation (VA) is the total amount of air breathed per minute (VE)(expired or minute ventilation)

minus the air that goes to dead space per minute (VD)

• ie VA = VE – VD where VE = resp rate X tidal volume

VD = resp rate X dead space volume

o the importance of alveolar ventilation is not only in delivering oxygen to the alveolar spaces but in

removing CO2 generated by cellular metabolism. We measure alveolar ventilation by assessing PaCO2

(i.e. arterial pressure of CO2) NOT by observing respiratory character

o relationship of PaCO2 to alveolar ventilation is:

PaCO2 = VCO2 (ml / min) X 0.863 where VCO2 is volume of CO2 produced / min

VA (L/min)

From this you can see that increase in VA will decrease PaCO2 for a given production of carbon

dioxide (ie hyperventilation and hypocapnia will exist) whereas hypoventilation (decreased VA) will

cause hypercapnia

Ventilation is assessed by measuring PaCO2. PaCO2 is a measure of adequacy of alveolar

ventilation to meet patient need of removal of CO2 produced.

Oxygenation, inspired O2 and the alveolar gas equation

o inspired air = 21% O2, 0% CO2, 78% N2, expired = 17% O2, 4% CO2, 78% N2 ie only CO2 and O2 take

part in gas exchange.

o Factors influencing oxygen delivery to red blood cells in alveolar capillaries are:

• Inspired oxygen concentration (FiO2) typically described as decimal ie 0.21 in room air, 1.0 in

intubated animal receiving pure O2 approx 0.4 in animals in O2 cage or efficient oxygen

supplementation

• Alveolar hypoventilation (eg upper respiratory tract obstruction)

• Decreased partial pressure of alveolar oxygen PAO2 which is a function of FiO2 and barometric

pressure of desaturated air (713mmHg at sea level)

• The diffusion barrier caused by alveolar (fluid and surfactant, epithelium, basement membrane

layers), interstitial space, and capillary (basement membrane and endothelium) tissues

• Matching between ventilation and vascular perfusion

• Appropriate haemoglobin O2 uptake at capillary

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o Oxygen and CO2 diffuse at a rate determined by available surface area, thickness of diffusible

membranes, solubility of the gas and difference in partial pressure by Fick’s Law:

o Vgas= A/T . D (P1 – P2) where A = area

T = thickness

D = solubility coefficient of gas

P = partial pressures of gas at either side

o The partial pressure of O2 is far higher (typical gradient is around 60mmHg for O2) than for CO2 diffusing

the other way (typically gradient is 6mmHg for CO2), but solubility of CO2 is far higher (around 20X that

of O2). This means:

• Whilst diffusion barrier changes eg thickened alveolar septae, may reduce O2 transfer they tend

not to limit CO2 diffusion (i.e. CO2 measurement in arterial blood gases is generally only affected

by alveolar ventilation)

• {in fact diffusion ‘barrier’ problems are almost never clinically significant in the resting patient and

are usually only a cause of relative hypoxaemia in patients under Exertional stress who have

diffusion barrier disease}

• That capillary blood flow and contact with ventilated alveoli has to be present for sufficient time

for O2 exchange.

o In fact whilst CO2 removal is only in practice limited by decreased alveolar ventilation,

because gas flow in the alveoli is slow and alveolar capillary blood flow is such that

capillary transfer of O2 occurs even at faster flow rates, capillary length and flow rat

seldom limit oxygenation of blood

• The amount of O2 ‘delivered’ depends on inspired oxygen partial pressure at the alveolar level

(PAO2)

o PAO2 = FiO2 (saturated air partial pressure – partial pressure of water vapour)

o Air pressure depends on altitude but for our purposes = 760mmHg (barometric pressure

at sea level) and water vapour pressure = 47mmHg

o So PAO2 at sea level on room air should be 0.21 (713) = approx 150mmHg

o However we also need to take account of the CO2 produced which will also occupy the

alveoli and PAO2 in fact doesn’t just equal O2 delivery:

PAO2 = FiO2 (713) – 1.2 (PaCO2) where 1.2 is due to respiratory quotient

[the 1.2 figure is only for FiO2 up to 0.6, above this i.e. intubated patients, a figure of

1.0 should be used instead]

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o This means that knowing a patient’s PaCO2 we can not only tell whether a patient is

hypo or hyperventilating but tell what the expected partial pressure of O2 is at the alveoli

– in most patients it is about 105mmHg in room air

• The amount of O2 delivered into alveolar capillary blood cannot exceed this and in fact is usually

less. This is because of ventilation – perfusion mismatch. Ventilation is denoted by V and

perfusion by Q

o In the normal lung there are

some areas which are perfused (high Q) but not well ventilated (low V) ie low

V/Q ‘units’ – e.g. areas of atelectasis from lying in a prone position

some areas which are ventilated (high V) but not well perfused (low Q) ie high

V/Q units – e.g. dorsal areas of lung tissue, or pathologically areas where there

is an arterial embolism

o in reality in most healthy patients there is about 3% of venous admixture (i.e. venous

blood mixing with post-alveolar oxygenated blood)

• we measure arterial partial pressure of oxygen PaO2 by arterial blood gas analysis (note the little

a denotes arterial, the big A is alveolar)

• by looking at the difference between them, i.e. PAO2 – PaO2, we can assess adequacy of oxygen

transfer:

the alveolar gas equation states:

PAO2 – PaO2 = alveolar – arterial oxygen difference and is usually <15-20mmHg

Gas transport in blood

o oxygen carried in red blood cells but a small amount (around 3%) is carried in dissolved state

• this is what is measured by PaO2 oxygen saturation is amount of haemoglobin sites which are saturated with O2 and is designated SaO2

oxygen content (CaO2) tells us how much oxygen is in the blood and is

• [Hb (g/dL) X 1.34 X SaO2] + [PaO2 X 0.003]

• i.e. amount of oxygen bound to haemoglobin (1g of Hb binds 1.34ml of O2) + amount of

dissolved oxygen

tissue delivery (DO2) is a function of oxygen content and cardiac output (which is heart rate x stroke

volume)

haemoglobin is made up of 4 haem molecules with a ferrous (Fe++) binding site on each for O2

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total number of occupied sites = oxygen saturation SaO2 which cannot exceed 100% (is usually about

97%). In venous blood SvO2 is about 75%

oxygen is released from Hb binding sites according to the sigmoidal oxygen dissociation curve:

• the consequences of this sigmoid shape may be physiologically useful

o the 1st and 4th haem moieties bind oxygen avidly (flatter portions of curve) 2nd and 3rd

bind it loosely (steeper portion)

o this facilitates oxygen unloading at tissue levels of O2 (ie PaO2 40-70mmHg)

o means that at lower PaO2 more oxygen is offloaded due to decreased binding affinity

• but should also act as a warning in that:

o significant hypoxaemia (eg PaO2 of 75mmHg) can occur before SaO2 (eg pulse oximeter

reading) drops below 90% or so

o by the time visible cyanosis is seen (in a patient with normal Hb level – it may never be

seen in anaemic patients) PaO2 may be as low as 45mmHg

The oxygen dissociation curve 100%

reduced / altered capacity for oxygen carriage by Hb

• may be seen with

o oxidative damage in which Fe++ (ferrous) Hb is oxidised to Fe+++ (ferric) haemoglobin i.e.

methaemoglobin

o carbon monoxide poisoning

has affinity for Hb 230X oxygen (i.e. only takes tiny amount to displace O2 from Hb

binding sites)

shifts oxygen dissociation curve to left

in summary

% Saturation of Hb (SaO2)

PaO2 (mmHg)

75%

RIGHT SHIFT (more O2 offloaded into tissues at relatively higher PaO2) C

yanosis 1st visible w

ith normal H

b

Severe hypoxaem

ia occurring

-Increased temp, 2,3DPG, PaCO2

-Reduced pH

LEFT SHIFT (uptake more O2 at lower PaO2 but don’t offload so much into tissues)

-Reduced temp, 2,3DPG, PaCO2

25 50 75 100

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• PaO2 is not affected by the amount of Hb available – it is a measure of oxygenation by alveolar

O2 and the state of the alveolar / capillary interface

• SaO2 is a measure of saturation of Hb with oxygen (see later section on pulse oximetry)

• CaO2 is total oxygen content which may be altered by such things as anaemia and decreased

Hb saturation

NEURONAL CONTROL

• 3 integrated systems o Central respiratory centre – controls breathing rhythm and controls tidal volume o Chemoreceptor reflexes (mainly sensitive to CO2) – detect changes in blood chemistry and

‘appraise’ respiratory centre o Neural reflexes – largely responsive to stretch and similarly ‘appraise’ respiratory centre

• Central respiratory centre

o Medulla

o 2 groups neurones

dorsal respiratory area (inspiratory group) – discharges with inspiration

ventral respiratory area (expiratory group) – driven by dorsal group

o also over-riding ‘vegetative’ centres of pons

apneustic area – facilitates inspiration

pneumotaxic area – inhibits inspiration

o inspiration also inhibited by vagus

• chemoreceptor

o ventral surface of medulla

o CO2 dissolves, forms carbonic acid then dissociated to HCO3- and H+ - stimulates ventillatory

response to hyperventilate (i.e. decrease PaCO2)

o Similar response mediated by carotid and aortic sinus chemoreceptors but is short lived

o Over-riding fail safe is hypoxic response to v low PaO2 (less than 70mmHg) although normally

the respiratory centre is much more driven by CO2 levels than O2

• Neural reflexes include cessation of inspiration at high lung stretch (Hering-Brauer), coughing, and

muscle wall spindles

AIRWAY DEFENCES, IMMUNOLOGY AND INFLAMMATION

o There are 4 principal arms to the airway defences

• Physical barriers to deposition of harmful substances

• The mucocililary escalator

• The local innate immune system

• Adaptive immunity Deposition of particles and aerosols

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• Impaction o Large particles - >5um diameter, 50% of those 1-5um o Impinge on and become stuck to surfaces of nasopharynx / nasal chambers

• Sedimentation o 0.5-3um p-articles will settle due to their mass in areas of slower air flow in smaller

conducting and respiratory bronchi

• Diffusion

o <0.1um particles diffuse in alveoli

• most particles of <0.5um are simple exhaled during tidal breathing rather than being deposited in

lung tissue

mucociliary escalator

• mucus layer

o comprises water, electrolytes and approx 4% mucoproteins

o from plasma transudation, serous and mucus production by submucosal mucous glands

and secretion by goblet, serous and Clara cells

o under parasympathetic stimulatory control; little sympathetic influence

o 10-20um thick, 2 layers

gel: 1-2um thick, tenacious, traps particles

sol: aqueous layer in which cilia beat

• ciliated epithelium

o lines all resp tract except alveoli, respiratory bronchioles, vocal cords / epiglottis,

between Rs end of turbinates and nares

o each cell 150-300 cilia

o each cilia

6-7um long, 0.15-0.2um diameter

10 doublets of ciliary microtubules (9 doublets in circle around aa central pair)

each with 2 dynein arms (‘Dyn’amic prot’ein’) which act as ratchets to allow

tubular sliding over one another

beat 10-20 X/sec

forward rapid stroke phase (25% of motion time) as rigid unit with tip of cilia

driving gel layer forward, back stroke phase (75% of motion time) flexed within

sol layer

• mucus continuously driven forward at 0.5mm/min in small bronchi, 5-20mm/min in trachea

Innate immunity

• Alveolar macrophages

o Outnumber neutrophils by 2-3:1 in normal resp tract

o Half life in vivo is about 4 days

o Phagocytic activity increased by opsonisation by secretory immunoglobulins (esp IgA),

complement (esp C3a, C4a), lymphokines

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• Bacteria may be lysed by incorporation within phagolysosomes and fusion with lysosomes

containing hydrogen peroxide, proteinases etc

• Chemical substances may be safely removed or may provoke release of inflammatory contents

of lysosomes which may promote fibrosis

• Some substances eg alcohols, urea, ozones may inhibit macrophage activity

Adaptive immunity

• Bronchus-associated lymphoid tissue (BALT)

• Humoral immunity

o Mainly upper airway

o Abundant secretory IgA from plasma cells in bronchioles

o Secretory piece from mucous cells prevents proteolysis

• Cell-mediated immunity

o Mainly within alveolar- interstitial area

o Principally T-cell help for humoral immunity and cytotoxic T-cells

SEQUELAE TO COUGHING

• Treatment of coughing without evaluation to determine underlying cause frequently results in

inappropriate treatment, over-reliance on empirical therapy, or misdiagnosis

• However, in many cases, a diagnosis of chronic bronchitis / chronic obstructive respiratory disease is

reached (i.e. a state of ongoing Tracheobronchial inflammation accompanied by coughing and mucus

accumulation which may be an end result of many common respiratory diseases) and attempts to ‘prove’

a single defining aetiology may be fruitless

• In these circumstances understanding sequelae, complications and management options may help

develop a rational therapeutic and re-evaluative approach

3. Diagnostics

Author’s note

In my experience, the single most neglected area of medical investigation is that of the value of a good

medical history and physical examination, followed close behind by production of good quality radiographs.

There is little point investing in expensive diagnostic equipment such as bronchoscopes, ultrasound

machines with doppler capabilities or utilising glamorous and expensive imaging modalities such as CT

unless you can:

-always take, and make time for (if not initially available in allotted consultation period) a thorough

clinical history

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-thoroughly examine, and think critically about what you are observing, the patient and integrate this

information with the medical history

-take radiographs which are always of diagnostic quality and which you would quite happily have

scrutinised by others and which you would be happy to pay money for if it were your pet

3.1 History taking

o History taking with respiratory diseases, as with every other medical problem, should include:

• Review of signalment (age / breed / sex) and local history

o Length of time owned

o Vaccination and antiparasitic history

o Dietary history including supplements

o Health status of in-contact animals

o Travel history

o Where exercised / home environment

o Presence of smoke / other particulate irritants in home environment

• Review of prior medical problems (especially cardiorespiratory disease), treatment and efficacy

of treatment

• Description of the presenting complaint in the owners own words – in particular should try and

establish at this stage whether the problem is

o Cough

o Sneeze

o Reverse sneeze

o Nasal discharge

o Epistaxis

o Dysphonia

o Retch

o Stridor

o Stertor

o dyspnoea

o A combination

• Further, vet-prompted questioning about the condition including responsiveness if any to

currently prescribed medications

• Review of other body systems even if not immediately known to be related to the presenting

problem

o In particular with coughing attention should focus on:

• Speed of onset (eg sudden onset at exercise in young field-dog suggestive of FB)

• Duration of signs

• Progressive / non-progressive / resolving / waxing – waning

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• Cough in other animals in household / history of recent kennelling / hospitalisation

• History of travel abroad especially South East USA (fungi), heartworm areas

• Scavenging history especially slugs and snails (intermediate hosts for Angiostrongylus vasorum)

• Whether animal appears systemically ill, has any weight loss associated

• Nature of cough

o Harsh / hacking / honking

Suggests upper airway problem, tracheal collapse, infectious tracheobronchitis,

large airway dynamic collapse, carinal compression by enlarged left atrium,

foreign body

o Soft

Minimal upper airway inflammation

Bronchopneumonia

Diffuse parenchymal disease

Pulmonary oedema

Aspiration pneumonitis

o Productive / non-productive

Productive refers to expectoration of fluid to the pharyngeal level – dogs and

cats seldom produce visible sputum (when they do it may be mistaken from

vomiting and is usually either blood or blood –tinged pink froth) but may be seen

to swallow repeatedly by their owners

‘wet’ cough – suggests significant airway fluid accumulation

pink tinged froth accompanied by tachypnoea / dyspnoea – consider pulmonary

oedema / airway haemorrhage

haemoptosis

• main causes are airway parasites, neoplasia, coagulopathy, foreign

body

• whether accompanied by signs of respiratory distress – especially feline asthma syndrome

• timing of cough

o with excitement / exercise

upper airway disease, tracheal collapse, bronchial collapse, bronchopneumonia

o at rest

most respiratory conditions

o after a period of sleep

common with pulmonary oedema and also as clearance mechanism of

secretions which have accumulated during sleep

o with eating / drinking

consider dysphagia (pharyngeal or oesophageal) and laryngeal paralysis

o with pulling on lead

consider BOAS, tracheal collapse, infectious tracheobronchitis

  20

in particular with sneezing / nasal discharge should focus on:

• onset sudden or gradual (useful with FB which usually present with sudden onset)

• association with contact with other sneezing animals / cattery – cats with infectious URT disease

• unilateral or bilateral discharge – FB usually causes unilateral discharge. Neoplasia and fungal

rhinitis usually unilateral initially then bilaterally

• association with dysphagia

• history of depigmentation of nasal planum

• whether painful

• whether accompanied by ocular discharge

• whether accompanied by facial deformity

• whether accompanied by any head tilt or other peripheral vestibular signs, aural discomfort

(polyps)

• whether epistaxis seen (most common with neoplasia in cats, neoplasia and fungal rhinitis in

dogs)

3.2 Physical examination

o General observation Before ‘hands on’ examination

• Look for

o Nasal discharge (uni-or bilateral, nature)

o Ocular discharge

o Facial asymmetry / deformity

o Altered head posture

o Mucus membrane colour

o General body condition

o Mentation (level of consciousness, content of consciousness)

o Nasal depigmentation or crusting

o Oedema particularly regional eg head and forelimbs

o Alteration of head / neck body posture which may be associated with ‘air hunger’

position or orthopnoea

o Respiratory rate, effort (an timing of that effort), synchrony of chest wall and abdominal

excursions, inspiratory:expiratory ratio

o Pouching / billowing at thoracic inlet

o Presence / absence of coughing, nature, timing if present

• Listen for

o Stertor

o Stridor

  21

o Pleural rub

o Murmur (may be audible if grade 6/6 in a quiet room!)

o Wheeze

o Cough

o Reverse sneeze

o Observe type of breathing pattern

• Normal:

o Cats and dogs usually breath with a rate of 10-30 breaths / minute (when dogs are

panting this is usually 60-140/min) with an inspiratory :expiratory ratio of approx 1:1.3

o usually have a slight expiratory pause (i.e. pause after expiratory phase) but unlike

humans do not usually have an inspiratory pause

o The rib cage will usually expand slightly laterally and be drawn slightly cranially during

inspiration with slight inward movement of the abdomen

o Expiration is a passive process and in the normal animal requires no effort

• Slow respiratory rate, large chest excursion, large inspiratory effort with increased

inspiratory:expiratory ratio = inspiratory dyspnoea

o Usually due to airway narrowing cranial to thoracic inlet

• Rapid, shallow breathing with 1:1 inspiratory to expiratory ratio and small chest wall excursions =

restrictive breathing or pleural breathing

o Usually due to pulmonary fibrosis, rib fracture/pain, pleural effusion, Pneumothorax

• Rapid, exaggerated breathing with short inspiratory phase and long, exaggerated expiratory

phase often with abdominal effort = expiratory dyspnoea

o Usually a sign of small airway disease and air trapping

• Inward collapse of caudal chest wall and abdominal bulging during inspiration = paradoxical

respiration

  22

o Usually a sign of prolonged respiratory effort, increased force of contraction of the

diaphragm and caudal displacement of central tendon of diaphragm

o is a sign of prolonged dyspnoea and often of impending muscular fatigue and ventilatory

failure

• do not forget that altered respiratory rate and effort may also be caused by extra-respiratory

factors:

o acid-base disturbances

eg slow, shallow breathing in response to metabolic alkalosis (hypoventilation to

counter)

eg tachypnoea / hyperpnoea in metabolic acidosis (hyperventilation to counter)

o pain

o thermoregulatory responses

o neurological disease

o Hands on examination

• Perform general physical examination

• Examine

o Nasal system

Planum – discharge, depigmentation, ulceration, pain, symmetry

Frontal bones / maxilla – asymmetry, pain, swelling, deformity, ocular discharge,

exophthalmos

Dentition

Hard and soft palate

o Oral cavity / pharynx

Cannot examine pharynx in conscious animal

Examine oral cavity for mucous mb colour, hydration, ulceration, integrity of hard

and soft palate, depigmentation, obvious masses, sublingual area, dentition

Any aggressive animal examined under GA

Palpate temporomandibular area, retropharyngeal soft tissue, mandibular

salivary gland (frequently confused with submandibular lymph nodes), parotid

salivary gland (palpable in some dogs)

o Larynx and trachea

Palpate, feel for symmetry, palpate trachea down to thoracic inlet, note any

dorsoventral flattening (may palpate sharp lateral ridges of cartilage), not areas

of collapse, malacia, sensitivity

Note: tracheal sensitivity is not pathognomonic for tracheobronchitis!!

o Neck and thoracic inlet

Palpate neck and thoracic inlet, observe for jugular venous distension, jugular

pulsation – rate, type, height of neck reached.

Palpate for oesophageal distension, oedema etc

  23

o Auscultation

Think as you auscultate:

• Where am I auscultating? in relation to

the airways

the lung lobes

the mediastinal contents and heart

the structures of the chest wall

• What am I auscultating?

o bronchovesicular sounds

• normal

• louder than expected

• quieter / absent

o adventitious lung sounds

• crackles (rales)

• wheezes (rhonchi)

o heart sounds

• S1 and S2

• ?S3 and S4?

• Murmur (location in cardiac cycle, point of maximal intensity,

dynamic, duration, rate responsiveness, grade out of VI)

• When am I auscultating it?

• Integrate this with information from observation and percussion

o Bronchovesicular sounds (normal airway sounds)

Generated by turbulent not laminar flow – therefore come from trachea and large bronchi

Are easiest to auscultate over these main airways

When they are auscultated over the lungfields, especially basilar lung lobes, they are pseudosounds

transmitted in direction of airflow

i.e. will be louder on inspiration than expiration (when sound transmission in ad-orally)

will be reduced / absent due to attenuation if there is pleural space disease either penumothorax or

pleural effusion

will be increased if there is increased turgor / oedema of conducting airways eg in pulm oedema,

bronchopneumonia (can’t distinguish)

o adventitious sounds

come from small airways

wheezes / rhonchi

• usually loudest during expiration

  24

• usually caused by bronchoconstriction during expiration eg in airway bronchospasm (more

common in cats than dogs)

crackles / rales

• due to small airways having collapsed

• will only happen if equal pressure point has shifted from non-collapsible airways to smaller,

collapsible airways

• crackles made by small airway popping open during inspiration

o heart sounds

listen on both sides of the chest for adequate length of time and make sure that the basilar area of

both sides is adequately examined

a full description of cardiac auscultation can be found elsewhere

o Percussion

Percussion is an acquired skill which improves with practice. It is useful to percuss in a grid-like

pattern on both sides of the chest

The resonant pattern produced by percussion depends on:

• The thickness of the skin and chest wall

• The thickness of local musculature eg triceps

• Density of the contents of the pleural space

• Density of underlying lung and mediastinal tissue

Resonance may be

• Normal dull – eg behind shoulder, overlying heart and liver

• Abnormally dull – eg accompanied by decreased bronchovesicular sounds in pleural

effusion, accompanied by increased bronchovesicular sounds in pulmonary oedema

• Normally more resonant – eg over well aerated portions of lung in dorsal mid-thorax

• Abnormally more resonant – eg ‘left abomasal ping’ sound of tense Pneumothorax

Can also percuss frontal sinuses

o Differentiating cardiac from non-cardiac causes of cough

In a cat coughing is highly unlikely to be due to cardiac disease

Much more likely to be respiratory disease:

• If cyanosis present – cyanosis is almost always a sign of respiratory not cardiac disease, the

main exception being right-to-left shunting congenital cardiac diseases which are rare

• If bradycardia or marked sinus arrhythmia is present

• If paradoxical respiration is present

• If cardiac auscultation abnormalities are absent

• In breeds which have a low incidence of heart disease (eg sporting / gun-dog types)

• In breeds which are brachycephalic and small (i.e. not boxers!)

  25

• In dogs which do not exert themselves enough for cardiac disease to become clinically

apparent unless advanced congestive heart failure is present (e.g. the Peke which is carried

everywhere!)

Much more likely to be cardiac disease

• If a heart murmur is present of loud grade

• If a sinus tachycardia is present

• If pulse quality abnormality is present

• If the dog is a Dobermann Pinscher or Irish Wolfhound or old CKCS!

Of course there are exceptions and confounding features with both and differentiation is not always

straight forward – a chest radiograph if of diagnostic quality is invaluable in differentiating. When

taking chest radiographs always beware the desire to ‘find something abnormal’ just because a

radiograph is taken. This is particular true when it come s to diagnosing cardiomegaly especially in

spaniel-type dogs who often have rather globoid hearts. In an average practice the majority of chest

radiographs taken will show normal hearts – if your diagnosing cardiomegaly a lot, you are probably

over-interpreting!

There is emerging evidence that some cardiac biomarkers such as NT-pro-BNP may have some

utility in differentiating cardiac from respiratory causes of coughing – I would urge a little caution

however. It is not referred to as the cardiorespiratory system for nothing – the two anatomical

regions play host to many concurrent pathological events (consider pulmonary hypertension in many

dogs with upper respiratory tract disease, cardiac and respiratory disease in angiostrongyliasis etc)

and considering the two in isolation is not always sensible!

3.3 Laboratory analysis

o Frequently not especially helpful in the investigation of respiratory diseases o Haematological changes

Polycythaemia – may be seen as chronic adaption to hypoxaemia (i.e. appropriate response by

increased erythropoeitin production) due to severe chronic respiratory disease or cardiac right to left

shunting

Anaemia – rarely caused by respiratory disease but

• Anaemia accompanied by diffuse lung infiltrates and known bleeding tendency may indicate

massive local blood loss

• Interpretation of respiratory embarrassment in anaemic animals needs to take into account

their decreased oxygen carriage and inability to observe cyanosis in them

Neutrophilia

• Must be absolute to be of diagnostic value (i.e. ignore statements of neutrophil % - these are

not diagnostically helpful and are a waste of time)

• Indicates inflammation (which may include, but is not diagnostic of, infection), stress

response or exogenous corticosteroids

  26

• If accompanied by a left shift is most likely indicative of inflammation (again infection is a

possibility but is not inferred by the presence of a left shift)

• It is entirely possible for significant inflammation (including infection) to be present without

peripheral neutrophilia

Eosinophilia

• Is an inconsistent finding in eosinophilic bronchopneumonopathy (about 60% cases have

eosinophilia) and respiratory parasitism (approximately 50% of cases have eosinophilia)

• Commonest causes of eosinophilia in dogs and cats are o Being a Rottweiler or German Shepherd o Inflammatory epithelial diseases o External parasitism o Internal parasitism o Hypoadrenocorticism

Platelet abnormalities

• Decreased platelet count may indicate o Lab error (especially clumping), acute blood loss, consumptive thrombocytopenia

(eg DIC) o Severe decrease may indicate immune-mediated thrombocytopenia (may be

primary or secondary) o If associated with alveolar-interstitial infiltrates consider ITP and intraparenchymal

haemorrhage or angiostrongyliasis (associated with both secondary DIC and ITP)

• Increased platelet count o Usually associated with inflammation or recent haemorrhage (rebound after initial

thrombocytopenia)

Coagulation panel abnormalities

• PT increase, APTT normal o Suggests extrinsic pathway abnormality especially factor VII deficiency (rare) or

antagonism (common – usually vit K antagonist rodenticide)

• PT increase, APTT increase o Suggests abnormalities of both extrinsic and intrinsic pathways

Vit K antagonist rodenticides

Angiostrongyliasis

DIC – inflammation, infection, neoplasia, parasitism

• Positive D-dimer o Indicates presence of x-linked fibrin which has been broken down i.e. presence of

clot o Seen in DIC or thrombosis/ thromboembolism

o Cardiac biomarkers

  27

• Much research still currently ongoing but at present beware / look critically at claims of high

sensitivity for these tests

• Detection of atrial ‘stretch’

o ANP and BNP

o Both appear to be relatively insensitive markers of cardiac disease until signs of

congestive heart failure seen

o BNP appears to be more useful and may have some utility in distinguishing

respiratory signs due to cardiac disease from those due to primary respiratory

disease

• Detection of myocardial damage

o Cardiac troponin I may have utility in detecting cardiac damage and predicting

severity but does not at present appear to be able to reliably distinguish between

cardiac and respiratory causes of dyspnoea

o Biochemistry

• Little direct help with investigation of respiratory disorders

• Serum protein levels should be assessed in presence of pleural effusion

• Severe azotaemia and pancreatitis may be associated with pleural effusion

o Fluid analysis

Pleural fluid should be analysed for

• Cytology (beware reactive mesothelial cells being over interpreted as evidence of neoplasia

– be sceptical about diagnosis of mesothelioma off a fluid sample!)

• Cell count

• If appears chylous assess triglyceride content: serum content (should be much higher),

cytology, cholesterol

• Assess protein content, SG and cellularity to DDx pure transudate, modified transudate,

exudates

• Culture (aerobic and anaerobic) – submit fluid not swab (should do this with all fluids)

o Faecal analysis

Should be used to attempt documentation of lungworm larvae

• Note that most of these are intermittently shed so false negative diagnoses are frequent

• Identification of larval type may be difficult without considerable experience

  28

3.4 Radiography

Complete description of radiographic technique and interpretation is beyond the scope of these notes and readers are

referred to diagnostic imaging textbooks

Nasal radiographs

o Usually indicated for diagnostic investigation of sneezing, nasal discharge and epistaxis

o Orthogonal views should be taken

o Very careful positioning is essential – interpretation of nasal images requires comparison of symmetry o If your images are not perfectly symmetrical they will not be diagnostic and trying to interpret them will lead

to misdiagnosis – do them again! o Other than poor positioning, the single most common fault I see on radiographs taken from referral cases is the DV

or VD ‘skullogram’ taken for investigation of nasal disease in which the detail of the nasal chambers is obscured by

superimposition of mandible, ET tube and tongue – such radiographs are generally a complete waste of time

o The most useful views are o An intra-oral occlusal view or an oblique ventro-dorsal palate-orientated view

With either it is essential that the structures of the maxilla and nasal chambers are orientated

symmetrically without superimposition of mandible, ET tube and tongue. Only by ensuring this will

you gain diagnostic quality nasal radiographs

A rostro-caudal skylined frontal sinus view

• This is frequently neglected and is absolutely essential in case of suspected nasal

tumour or fungal rhinitis (ie just about all cases of sneezing, nasal discharge and

epistaxis)

• Again good positioning is key and if diagnostic quality images are not obtained they

should be repeated

Lateral and oblique lateral views of the maxilla and nasal chambers – these are less useful for

investigation of nasal disease since contralateral nasal structures will be superimposed. However,

they are invaluable for assessing the nasopharynx and pharynx (when performed with the patient

briefly extubated), for assessing pharyngeal gas lucency, the relative thickness and length of the

soft palate (provided excellent positioning is achieved) and for lateral views of the bullae o Nasal radiographs should be routinely accompanied by thoracic radiographs especially

o Where nasal neoplasia or fungal rhinitis is suspected – though both are more normally confined to the

nasal region, metastasis and systemic aspergillosis respectively should be thoroughly staged for before

embarking on local treatment

o Examine sinonasal radiographs for

o patency of the nasal gas lucency o radiodense foreign bodies

o areas of turbinate or bony lysis o areas of increased soft tissue / fluid accumulation

o alterations in symmetry

Bulla radiographs

o CT and MRI are superior for examining bulla structures but are limited by expense and availability and the place of

radiography in investigation is still maintained

  29

o Accurate and self-critical positioning is essential

o Take rostro-caudal open-mouth views with positioning to avoid superimposition of the hard maxilla, mandible,

tongue and ET tube (see radiographic texts for technique description) and obtain DV and lateral / oblique views

Pharyngeal radiographs

o Patient must be anaesthetised and briefly extubated for diagnostic views of nasopharynx and oroopharynx

o Lateral and DV /VD views should be taken. Lateral views of this area are highly uncompromising to even small

deviations from perfect positioning!

Cervical views

o Again general anaesthesia, perfec6t patient positioning and taking orthogonal views is the key

Thoracic radiographs

o Thoracic radiographs should show in detail

All of thoracic cage

Thoracic inlet

Diaphragm

Heart and great vessels

Lungs and associated airway and vascular structures

Technique

o Pay attention to

Technique

Collimation

Positioning (correct centering, prevention of rotation)

Personnel training and safety

Keep log book

Label radiographs appropriately

Quality control

o Routinely

Right lateral recumbency and DV thorax for heart and great vessels

Right lateral recumbency and VD thorax for lungfields

Both R and L lateral recumbencies and a DV/VD probably best

Interpretation

o Must be fully conversant with

Breed variations / effects of conformation

Radiographic differences between DV and VD, RLR and LLR views in terms of

  30

• Lung appearance

• Cardiac and great vessel appearance

• Position of interlobar fissures

• Diaphragmatic ‘humps’

Assessment for cardiac chamber enlargement

Assessment of vascular changes

Assessment for main lung ‘patterns’

• Alveolar

• Interstitial

o Diffuse – hazy / nodular

o Focal – hazy / nodular

• Bronchial pattern

• Vascular patterns

• Mixed patterns

The phenomenon of silhouetting

Pleural space diseases

Artefacts and normal variation eg

• Overlying nipples / skin folds

• Pulmonary oesteomata Vs neoplasia

• Fat

o Common pitfalls

Trying to make a diagnosis from non-diagnostic quality radiographs

Overinterpretation of:

• Interstitial pattern due to expiratory film

• Unilateral lobar consolidation due to recumbency atelectasis

• Globoid cardiac silhouette, especially in spaniel-type conformation breeds and in LLR

radiographs

• Cardiomegaly / chamber enlargement in badly rotated films

• Pulmonary osteomata diagnosed as metastases

Under-interpretation of / missing

• Lesions overlying heart / diaphragm

• Rib / bony thoracic cage lesions

• Megaoesophagus

• Lesions which are not clear due to being in dependent (poorly aerated) lung and so not

having good contrast

  31

Over-reliance on

• ‘eye-balling’ radiograph and not examining systematically

• measurements without appreciating other factors that they are affected by

o eg Buchanan vertebral heart score

normal dogs reported as having normal values of 9.7 +/- 0.5 vertebrae

(measured from cranial edge of T4) or upper limit of 10.5 vertebrae

but

• Boxers are usually more than this

• Schnauzers and Min Dachshunds usually <9.5

• Will vary with phase of cardiac and respiratory cycle

• Significant differences between left and right recumbency

• Will be affected by positioning

o Suggested technique / pointers

If possible try to spend time reading films with a radiologist – is the best way of training

Keep a technique log

Maximise your chances of reading radiograph well

• Examine in darkened room with good viewer, shield from extraneous light source, cover light

around edges of film

Beware obvious lesions – they will make you stop looking for anything else!

Read films in a systematic manner – many variations, probably type of system used less important

than finding one you like and sticking to it. I tend to adopt the approach of

• a) assess positioning / collimation / exposure

• b) examine extrathoracic structures

o vertebral column, spinous processes

o scapulae, humerus, thoracic inlet

o sternebrae

o diaphragm/lung interface and visible abdomen (these structures will be suboptimaly

exposed)

• c) examine for pleural space disease

• d) examine mediastinal structures

• e) examine heart and great vessels

• f) examine airways and pulmonary tissue

remember that solid structures in lung field that is aerated (i.e is upper most) will have better contrast

with surrounding air than those in dependent lung

tracheal stripe sign usually indicates oesophageal air

silhouette sign – objects which are the same radiographic density but are in contact with each other

will ‘merge’ whereas those of same density with different density structure in between will appear

separate

examine small nodular structures for angularity – osteomata are usually angular if you look hard

enough whereas mets are circular

  32

o Lung patterns

Alveolar pattern

• Defining characteristics

o Air bronchograms / localised increase in lung opacity

o Alveoli and adjacent structures filled with fluid / consolidated

• Differential diagnoses

o Localised

Lobar consolidation

Atelectasis (especially after period in lateral recumbency)

Pulmonary oedema

Haemorrhage

Bronchopneumonia

Infarct

Dirofilariasis / Angiostrongyliasis

o Generalised

Severe oedema

Severe haemorrhage

Near drowning

Smoke inhalation

Severe bronchopneumonia

Bronchial pattern

• Defining characteristics

o Doughnuts, tramlines

• Differential diagnoses

o Peribronchial cuffing due to oedema, bronchopneumonia, infiltrative neoplasia,

disease in transition

o Chronic bronchitis

o Eosinophilic bronchopneumonopathy, asthma

o Bronchial calcification

Interstitial pattern

• Defining characteristics

o Nodular or hazy (unstructured)

o Localised or diffuse

o Obliteration / obscuring of normal vascular pattern by increased radio-opacity

• Differential diagnoses

  33

o Nodular interstitial (solid)

Solid tumour

o Primary lung

o Metastatic lung

o Thoracic wall

Lymphoma

Lymph node

Granuloma

o Mycotic

o Parasitic (especially angiostrongyliasis)

o Mycobacterial

o Eosinophilic (esosinophilc bronchopneumonopathy)

o Lymphomatoid granulomatosis

o Foreign body

Abscess

Haematoma / haematocyst

Fluid-filled bronchus

o Nodular interstitial (cavitary)

Cystic tumour

o Primary

o Metastatic

Granuloma

Abscess

Bulla

Cyst

Bronchiectasis

o Hazy interstitial

Artefact – expiration, underexposure

Lymphoma

Haemorrhagee

Oedema

Bronchopneumonia

Paraquat toxicity (usually dorsal distribution, severely dyspnoeic)

Pulmonary embolism

Pneumonitis

Old dog lung

Vascular pattern

• Defining characteristics

o Changes in normal vascular pattern

  34

Decreased vascularit i.e. hyperlucency

Changes in vessel diameter, shape and direction

• Differential diagnoses

o Enlargement of pulmonary lobar artery > vein

Pulmonary hypertension

Heart worm disease

o Enlargement of pulmonary lobar veins > arteries

Pulmonary venous congestion

o Hyperlucency

Generalised

o Hypovolaemia

o Hyoperinflation

o Overexposure

o Emphysema

Focal

o Pulmonary thormboembolism

3.6 Ultrasonography

A complete description of cervical and thoracic ultrasound is beyond the scope of these notes

The utility of cervical ultrasound in cats and dogs is usually limited to assessment of laryngeal movement

in cases of suspected laryngeal paralysis though this technique is highly skilled

Extracardiac structures which may be examined by ultrasound include

o Cranial mediastinal mass lesions

o Pleural effusions

o Mediastinal vascular structures is surrounded by collapsed lung tissue or fluid

o Mass lesions which are adjacent to the thoracic wall (will tend to move with respiratory

movements if in lung, with cardiac movements if attached to heart)

o Heart base lesions

Cardiac ultrasound

o Like radiographic interpretation should be performed systematically:

o 2D examination

right parasternal long axis LVOT view

right parasternal long axis 4-chamber view

right parasternal short axis views at levels of

• papillary muscle tips

• mitral valve orifice

• aortic valve

  35

• main pulmonary artery and branches

• ‘tipped’ PA view

left cranial parasternal views

left caudal parasternal 4 chamber and 5 chamber views

subcostal examination (aortic velocities)

o M-mode examination of

right parasternal short axis views at levels of

• papillary muscle tips

• mitral valve orifice

• aortic valve

assessment of M-mode indices of LV, FS%, EPSS and poss systolic time intervals

o functional / dynamic assessment

Doppler (CF, PW, CW) assessment of mitral, aortic, pulmonic and tricuspid valves

3.7 Respiratory tract endoscopy

equipment needed

For rhinoscopy / Pharyngoscopy

o Tips

A complete examination should include

• Examination of both nasal chambers, starting with one that is least affected /

normal

• Examination of the nasopharynx by a retroflexed flexible endoscope

In order to have a diagnostic view of the nasal structures

• You must use the right equipment – examination with an otoscope is unlikely to

yield any useful diagnostic information

• You must be able to constantly flush accumulated debris and blood away – the

best way of doing this is via an endoscope sheath with constant saline irrigation

or in cats where the size is too small for this by using a soft catheter placed

along side the scope with saline irrigation. With either a cuffed ET tube /

pharyngeal throat packs must be used to prevent aspiration. Intermittent

flushing with a syringe of sterile saline is an inferior alternative

• You must know your nasal anatomy!

o anterograde rhinoscopy can be accomplished by using a good quality rigid arthroscope with

outer diameter 2-3mm. Rigid scopes allow better visual acuity of nasal structures than a flexible

scope though there is limited ability to direct and ‘steer’ the scope compared with a flexible

endoscope. Use with a sheath with biopsy / flush channel results in greater versatility

  36

o anterograde and retrograde rhinoscopy / Pharyngoscopy can be performed using a 2.5-3.7mm

outer diameter flexible endoscope. 180o flexion of the tip is a pre-requisite for adequate

examination of the nasopharynx and choanae. Biopsies can be taken with an appropriate biopsy

instrument

o I tend to use a combination of both rigid and felxible rhinoscopy for naso/pharyngeal examination

For tracheobronchoscopy

o Adequate examination cannot be performed with rigid instruments except in very small patients

o In small to medium sized dogs flexible endoscope (paediatric bronchoscope ideal) – working

length 500-600mm, diameter 2.8-3.6mm, working channel 1.2mm. Can be passed through the

end port of an elbow (Cobb) connecter and down the lumen of the ET tube

o Larger dogs, gastroscope with outer diameter 7.8-10.5mm ideal for tracheoscopy, biopsy

channel usually 1.9-2.4mm, extubation.

Larger scope is warranted to achieve better visualisation and to provide greater length to reach

further bronchial divisions. In these dogs oxygen is insufflated during the procedure via a urinary

catheter inserted along side the bronchoscope and attached to the anaesthetic circuit. Very

close anaesthetic monitoring and oximetry is required and the procedure may frequently have to

be interrupted for re-intubation

o Use of video attachments to fibre-optic scopes or use of videobronchoscopy adds considerably

to expense but provides superior visual detail

For both

o A good quality light source

o A good flushing, insufflation and suction source and connections

o A means of properly cleaning and sterilising scopes between every procedure and storing them

properly – biosurveillance by intermittently swabbing scopes should be regularly performed

o A means of collecting fluid samples either

• Sterile BAL catheters

• Specimen trap to apply to suction channel (cleaning / sterilisation procedure must be

exacting if this method used)

o Elbow connector

o Pulse oximeter

o Variety of endoscopic instruments

Biopsy forceps to fit in working channel of endoscope

For foreign body retrieval

• Rat-toothed retrieval forceps

• Snares

o Simple loop

  37

o Basket snare

• Trefoil grapser

Guarded swab for cytology / culture

Sterile saline (without bactericidal / static preservative) for BAL

o Monitoring equipment

General tips

Endoscopic equipment is expensive and needs to be maintained properly. This means

o Storing it properly (i.e. hanging up not in a case – this will cause fatigue of steering wires)

o Cleaning and sterilising it properly every time it is used to prevent

Iatrogenic introduction of pathogenic organisms

Culturing of contaminant organisms on BAL samples

o Training staff properly on handling, storage and cleaning

o Regular servicing

Bronchoscopy is a hazardous procedure especially in patients with severely compromised respiratory

function (eg dogs with IPF)

o Carefully weigh up pros vs cons

o Discuss risks with owners

o Warn owner that in coughing animals some exacerbation of coughing will be seen briefly after

such procedures and that nasal discharge in sneezing animals will get temporarily worse

o Have adequate monitoring / resuscitative equipment

o Have anaesthesia monitored by a suitably qualified and experienced person

o Monitor patients very closely during recovery

o It is good practice to systematically examine the pharynx for presence of accumulated /

dislodged mucopus and cellular debris which could occlude the patients airway on recovery – I

would recommend getting into the habit of doing this in all patients and using suction and stick-

swabs (these are really useful!) to remove such debris prior to revovery

Bronchoscopy requires a systematic approach and recording of findings. The bronchial tree is complex

and disorientation common. A systematic approach will avoid confusion / repetition / areas being missed.

Your reference point is always the dorsal tracheal ligament which should be visualised periodically to

orientate up from down (the scope will rotate during exploration of the tree)

If you are not doing these things every time then you should not be doing bronchoscopy!!!

Technique

Rhinoscopy / pharyngoscopy

o General tips

Examine both sides every time; examine least affected side first

  38

Adequate rhinoscopic exam cannot be performed with an otoscope

Use adequate packing of throat if performing saline flushing to remove obscuring debris

and blood

Examine all areas before taking biopsies as these will inevitably cause haemorrhage

In animals with bilateral Epistaxis perform coagulation panel first

Always take adequate biopsies

Swabs are of limited value – you will nearly always merely grow commensal organisms

(know what commensals you would usually expect – many of these are organisms

traditionally associated with infections elsewhere!)

Realise the limitations of rhinoscopy – there are quite a few areas of the nasoturbinate

structures which cannot be seen no matter how good your equipment – warn owners of

this!

o Technique

Examine

• via dorsal meatus (will not be able to advance scope far due to luminal

compression by dorsal and ventral nasal conchae)

o ventral aspect of dorsal nasal conchae

o dorsal aspect of ventral nasal conchae

• via common meatus (direct scope ventromedially and push up nasal planum to

allow passage past alar fold)

o ventral nasal trubinates

o ethmoidal turbinates

o may examine passage to nasopharynx, choanae with suitable flexible

endoscope

• via retroflexed view of nasopharynx per os

o nasopharngeal lumen

o ventral surface of vomer

o dorsal surface of soft palate

o choanae

o pharyngeal lymphoid tissue

o may see entrance to eustacian tube

assess for

• turbinate destruction

• local mucosal hyperaemia

• patency of airspaces

• presence of FB, local secretions, neoplasia, fungal plaques

can collect samples by forceful flushing (must have airway protection and throat pack,

adequate swab-cleaning afterwards)

• in my experience main value is in nasal lymphoma (feline) and in dislodging

some FB

  39

• should not be performed with aspergillosis

biopsy after you have looked at everything – expect haemorrhage!

Swabs may be taken but take great care not to overinterpret

Post biopsy haemorrhage may be controlled with packing, topical phenylephrine or

adrenaline (external pressure is an exercise in self-delusion!)

NB unless you want to spend large amount sof money on endoscope repairs, when

taking biopsies through a flexible endoscope always place the biopsy forceps through

the biopsy channel of the scope first with the scope straight, move to the end, then flex

the tip in a J-shape – never try and push forceps forward or remove through a flexed

scope tip

Laryngoscopy

o When assessing for laryngeal paralysis

Make sure patient is under light plane of anaesthesia – should be able to swallow or you

will get false positive diagnoses

Interpret laryngeal movement with chest wall excursion

• Normally vocal folds and arytenoids cartilages are abducted (i.e. pulled laterally)

during inspiration – in laryngeal paralysis they will usually fail to abduct

unilaterally or bilaterally

• BUT in some cases of laryngeal paralysis, during inspiration paradoxical medial

movement will occur during inspiration followed by return to more lateral position

during expiration – if you are not matching what you see with phase of

respiration you will miss these cases

Tracheobronchosopy

o General tips

Look everywhere first – the presence of the scope will cause immediate mucosal

congestion and inflammation which will worsen the longer you are in

Use a memory aid (eg anatomical diagram to orientate yourself unless you do these

every day)

Record your findings

Bronchoscopy can be disorientating as the scope will rotate so you won’t know which

way is up and which down – periodically return to the carina and look at the dorsal

tracheal ligament to tell which way is up

Always collect BAL samples

Bronchospasm is a real risk in cats and the ability to administer an oxygen-enriched

environment and emergency supportive care should be available when performing

tracheobronchoscopy in cats

• Don’t do this procedure at the end of a day

• Make sure patients are very well supervised during recovery

  40

• There is some evidence that pre-treatment with bronchodilators such as

terbutaline may lessen the incidence of this though personally I believe that the

bigger risk comes from poor technique and from severity of underlying pathology

Be aware of the potential risks of this procedure before doing it eg bronchospasm as

above, but also how you would manage development of airway haemorrhage,

spontaneous low tension or tension pneumothorax

o Techniques

Trachea

• Assess luminal size, whether any dynamic or fixed stenosis is present

• Circular profile

• Presence of FB, excessive secretions, mass lesions, parasites, nodules

Bronchi

• Assess for patency and circular profile

• Assess for hyperaemia

• Assess for oedema (usually causes ‘blunting’ of inter-bronchial septae)

• Assess for extraluminal compression

• Assess for dynamic collapse / malacia

• Assess for FB, mass or local fluid accumulation

Collect BAL sample

• Select region of interest based on radiographs or if generalised pattern then

select easily accessible representative bronchi

• Pass BAL catheter down into smallest representative airway or if using fluid trap

attachement wedge scope tip in smallest airway possible.

• Infuse aliquots of 2-5 (cats) or 5-10ml (dogs) sterile saline into region of

interest, assistant briskly coupages chest on appropriate side

• Apply firm negative pressure and agitate collection catheter back and forth

slightly

• Assess for quality

o Should be foamy due to surfactant

o Fluid amount often << than that infused

o Presence of ‘floaters’ a good sign!

• Submit for cytology, culture and examine a centrifuged and rapid-stained

sample yourself

Airway brushings – may be useful for culture samples if using guarded sterile brushes

Non-endoscopic fluid collection techniques

o Blind lung BAL

  41

o Can be performed in anaesthetised canine and feline patients by passing sterile catheter

through sterile ET tube into dependent lung with patient in lateral recumbency

o Technique and sampling are as for endoscopic BAL otherwise

o Main disadvantage is that is slightly more traumatic and samples cannot be taken from a specific

region of the respiratory tract – this is less of an issue with generalised lung involvement in a

disease process.

o Samples are generally inferior to BAL

o Tracheal washing

o Not many circumstances in which it is useful since tracheal washes tend to be contaminated by

upper respiratory tract commensal organisms and debris

o Main indications are in tracheitis, obtaining culture ssampels in animals where anaesthesia may

risk exacerbation of their airway disease (eg dogs with acute aspiration pneumonitis

o Patient is gently restrained +/- sedation in sterna recumbency with neck gently extended. Ventral

laryngeal region and ventral cervical region is clipped and surgically prepared

o Insertion site is through cricothyroid ligament or just distal to larynx between two tracheal rings –

site is carefully infiltrated with local anaesthesia prior to doing wash

o Either a through the needle central venous catheter or a wide boor over the needle catheter or

special tracheal wash needle is inserted, bevel down, into the tracheal lumen. A small catheter

that has been premeasured to the thoracic inlet is then inserted into the tracheal lumen and 3-

20ml aliquots depending on patient size, of sterile saline is flushed and reaspirated. Patient

coughing during the procedure is helpful.

o Through ET tube tracheal wash

o Performed essentially as above but with anaesthetised and intubated patient

o Contaminated samples are very common and this technique often results in poorly diagnostic

samples

3.8 Respiratory tract cytology and microbiology

cytology

o Nasal

• Normal

o Non keratinised squamous epithelial cells

o Ciliated columnar cells

o Mucus

o Blood with mild trauma

o Bacteria especially Simonsiella (large ‘stack of coins’)

• Abnormal

  42

o Inflammation

Acute – neutrophils

Chronic-active – neutrophils and macrophages

Chronic – mainly macrophages

o Lymphocytic – plasmacytic rhinitis

o Bacteria – usually only significant if monomorphic population, large numbers of

intracellular organisms

o Funghi especially Aspergillus spp often oppurtunist

o Yeasts eg Cryptococcus – v rare in UK, usually seen in cats and most commonly

associated with nasal deformity

o Tracheal

• Normal

o Ciliated columnar epithelial cells

o Goblet cells

o Macrophages

o Mucus – may see Curschmann’s spirals – small spirals of mucus from small airways

o May see mast cells

• Abnormal

o Inflammatory as above

o Eosinophilic (DDx parasitism, eosinophilic bronchopneumonopathy, asthma)

o Oropharyngeal squames (contaminant)

o Simonsiella (contaminant)

o Parasite larvae

o Erythrophagocytosis – indicates prior rather than iatrogenic airway haemorrhage

o Broncho-alveolar lavage

• Great deal of variation between individuals

• Usually only semiquantitative as dilution factors variable

• Best assessed by cytocentrifugation but can have a ‘rough and ready’ look by slow speed

centrifuging for 5 mins, discarding supernatant, re-suspending pellet and making smear stained

with Romanowsky-type stain

• Predominant cell type in health is the alveolar macrophage – if these are not seen then sample

is not adequate

• Excessive oral squames or Simonsiella spp suggests excessive upper airway contamination

• Normal values (dog)

o Total nucleated cell count – 100-300/ul

o Macrophages 60-80%

o Neutrophils <10%

  43

o Eosinophils <10%

o Lymphocytes <10%

o Epithelial cells <5% (more usually indicates upper airway contamination)

• Normal values (cat)

o Total nucleated cell count – 185-340/ul

o Macrophages 60-97%

o Neutrophils <10-24%

o Eosinophils – highly variable. In some reports up to 40% eosinophils have been

obtained from normal cats!

o Lymphocytes <5%

o Epithelial cells <5% (more usually indicates upper airway contamination)

o In general BAL results in cats are difficult to interpret and the oft-used veterinary dogma

of ‘if its a cat and there’s lots of eosinophils in its airways it must have asthma’ should be

critically challenged!

• Abnormalities

o Inflammation

Neutrophilic

• Determine whether degenerate (suggests septic process) or not

• Be aware that in many infections neutrophils do not look degenerate

(i.e. is an insensitive finding) and bacteria are infrequently seen (i.e.

similar picture to synovial fluid analysis!)

Eosinophilic

o Parasite larvae

o Erythrophagocytosis

Microbiology

o Nasal cavity and pharynx

Normal commensals include:

• Gram positive aerobic or facultative

o Staphylococci (coag –ve and +ve), Streptococci (alpha-, beta-, and non-

haemolytic), Corynebacterium, Bacillus

• Gram negative aerobic or facultative

o Neisseria, Escherichia coli, Enterobacter, Pasteurella multocida, Moraxella, Proteus,

Pseudomonas aeruginosa, Alcaligenes, Bordetella bronchiseptica, Klebsiella

pneumoniae

• Obligate anaerobes

o Clostridium spp

  44

o Trachea and bronchi

Normal commensals include

• Acinetobacter, Corynebacteria, Enterobacter, Klebsiella pneumoniae, Moraxella, Pasteurella

multocida, Staphylococci, Streptococci, Pseudomonas aeruginosa

Abnormal findings

• Most bacteria implicated in bacterial bronchopneumonia are commensals with the

exceptions of Bordetella bronchiseptica and Mycoplasma (which is difficult to isolate)

• Quantitative cultures are rarely performed but where they are > 1 x 103 CFU/ml is

considered diagnostic of bacterial bronchopneumonia

• Moderate growth reported of a single bacterial isolate should be considered suspicious of

bacterial l bronchopneumonia especially if accompanied by fever, leukocytosis, degenerative

neutrophilia on BAL cytology or large numbers of intracellular bacteria

• Profuse growth is always significant

• View reporting of scanty growth with suspicion that this is due to contamination

• Most commonly implicated bacterial infections are

o E coli, Klebsiella, Bordetella, Pseudomonas, Pasteurella, Staphylococci,

Streptococci

3.9 Lung biopsy

o Types available

Fine needles aspirate biopsy

• Transthoracic

• Per-endoscopic / transbronchial

Per-endoscopic grab biopsy

Transthoracic tru-cut biopsy

Surgical lung biopsies

• Thoracoscopy

• Thoracotomy

o Indications

Fine needle aspiration

• Where a structure is solid and abuts the thoracic wall (trasthoracic) or bronchial tree (trans-

bronchial, especially bronchial lymph nodes)

Grab biopsy per-endoscope

• Endobronchial lesions, mural lesions,

  45

Transthoracic tru-cut biopsy

• Large solid mass abuts thoracic wall

Surgical lung biopsies

• Mass lesions surrounded by air

• Where excision with intent to treat and diagnose is feasible

• With progressive interstitial lung disease in the absence of diagnosis despite less invasive

diagnostic tests (eg bronchoscopy / BAL)

o Contraindications

Haemostatic defects

Uncontrolled Pneumothorax

Pulmonary hypertension

Pulmonary cyst / abscess / bulla

Absence of a perfectly still patient

Neoplasia with possibility of seeding suspected

o Complications / limitations

With all fine needle aspirates diagnostic yield and accuracy is much reduced compared with

excisional / incisional biopsies (this is true anywhere!)

Pneumothorax and haemorrhage are potential complications of all these procedures and they should

not be carried out unless you are prepared to monitor them carefully after the procedure and are

equipped to provide the necessary tube drainage and intensive care if things go awry

o Biopsy samples should be submitted for:

Routine histopathology

Culture if infectious aetiology is a differential diagnosis

Z-N staining for acid fast bacteria if a granulomatous disease is present

Special staining eg reticulin for fibrosis

3.10 Advanced aids in diagnosing respiratory conditions

Blood gases

o Much of the physiology behind blood gas analysis is outlined in the introductory section

o Arterial blood gases can help answer the following questions

  46

Is the patient ventilating sufficiently for the amount of CO2 that it is producing through normal cellular

metabolism? i.e. is the patient hypoventilating (becoming hypercaapnic) or hyperventilating

(becoming hypocapnic)?

• i.e. tells us about alveolar ventilation

Is the patient hypoxaemic? (note that this says hypoxaemic not hypoxic – this would also be affected

by haemoglobin amount available). Is the level of oxygen transfer from the alveoli to the pulmonary

capillaries appropriate to the inspired oxygen content i.e. how effective is gas transfer?

• i.e. tells us about oxygenation

what is the patients acid-base status?

• Technique

o Need heparinised syringe / pre-coated syringe

o Need practice to get arterial samples

o With practice arterial blood gas samples can be easily taken with minimal distress to patients

Can use

• Femoral artery – more painful, more risk of haematoma, bigger target

• Dorsal pedal artery – less painful (?), less risk of major haematoma, smaller

target, more risk of arterospasm

Personally I use the dorsal pedal artery and seldom find it necessary to use femoral

artery

Tips

• Clip and prepare skin minimally – the more you handle the area, the more likely

arterioconstriction will make your job harder

• 1ml syringe 25G needle

• palpate (gently), with several finger tips in a row, the course of the dorsal pedal

artery on the dorsomedial surface of the ‘instep’ distal to the hock. Rest fingers

on the pulse lightly

• try and mentally visualise where the artery is. You will usually not see it except

in some sight hounds where you may see the artery pulating

• enter the artery at a 45o angle with the bevel facing upwards; don’t apply suction

initially (sometimes the syringe will just fill under pressure)

• if you have to apply suction do so very gently

• have an assistant apply firm pressure to puncture site for at least 5 minutes by

the clock.

o Stopper sample, express air / bubbles and keep chilled until analysis – should be good for up to

6 hrs

o At room temp white cells in the sample consume O2 and produce CO2, red blood cells produce

lactic acid

  47

o Blood gas analysers are notoriously temperamental and need regular servicing and

maintenance

• Arterial blood gas analysis is invaluable in the investigation of respiratory disease. Unfortunately blood

gas analysers are very expensive to justify in the clinic setting though the I-Stat analyser distributed by

the Woodley equipment Co. is a good, reliable, clinic friendly alternative and (along with a good

microscope, Romanowsky-type stain, urine dipsticks, glucometer and centrifuge) represent a sounder

investment for the management of emergency clinical patients than many bench-top haematology and

biochemistry analysers!

• Complete guides to interpretation of arterial blood gases are beyond the scope of these notes and acid-

base disturbances even more so. However the following should help give an introduction to arterial blood

gas analysis

o Normal values

Arterial Venous

• pH 7.39 7.36

• PaCO2 36.8 +/- 2.7 mmHg 42 +/- 4.4

• PaO2 102.1 +/- 6.8 mmHg 55 +/- 6

• HCO3- 21.4 +/- 1.6 mEq/l 23.2 +/- 2

• BE -1.8 -> +1.8 mEq/l same

o PaCO2 <36.8 mmHg suggests hypocapnia and therefore hyperventilation, >36.8 mmHg suggests

hypercapnia and therefore hypoventilation

Causes of hypoventilation include

• Respiratory muscle fatigue

• Neuromuscular disease

• CNS depression eg due to neurological disease, anaesthetic / sedative agents

• Airway obstruction

• Thoracic wall / pleural space disease

• Inappropriate anaesthesia / ventilator control

• Compensation for metabolic alkalosis

o Arterial O2 (PaO2)

Measurement of O2 dissolved in plasma (is independent of Hb and anaemia)

PaO2 <80mmHg is hypoxaemia

Hypoxaemia is caused by:

• Low inspired alveolar oxygen concentration

o This is a factor of oxygen concentration (FiO2) and barometric pressure

of dry air (&13mmHg at sea level)

• Hypoventilation

• Ventilation-perfusion (V/Q) mismatch

  48

o Areas of good ventilation but poor perfusion (high V/Q, alveolar dead

space)

Eg dorsal lungs

Eg areas of vascular compromise eg pulmonary

thromboembolism

o Areas of poor ventilation but good perfusion (low V/Q)

E.g airway collapse, lung consolidation

o Areas of complete atelectasis (anatomic shunt, V/Q=0)

• Diffusion impairment

• Cardiac or lung shunt causing venous admixture

The degree of impairment of gas exchange can be calculated using the alveolar gas

equation to calculate alveolar – arterial oxygen difference (see earlier)

PAO2 = FiO2 (713) – 1.2 (PaCO2) where 1.2 is due to respiratory quotient

[the 1.2 figure is only for FiO2 up to 0.6, above this i.e. intubated patients, a figure of

1.0 should be used instead]

• Alveolar – arterial oxygen difference = PAO2 – PaO2 which should be less than

15-20mmHg

• An increase A-a difference may be caused by

o Pulmonary right to left shunt

o Cardiac right to left shunt

o Ventilation – perfusion mismatch

o Diffusion barrier

• Of these diffusion barrier and high V/Q mismatches will respond v well to

oxygen supplementation whilst the others will not, it can therefore be very useful

to assess the response of A-a difference to O2

Thus a sensible approach to hypoxaemia would be:

  49

Hypoxaemia PaO2 <80mmHg

What is PaCO2?

o If all this seems a bit laborious a shortcut is to look at

• PaO2/FiO2 ratio (P/F ratio)

o where FiO2 is inspired O2 conc expressed as a decimal (i.e. 0.21 room air, 0.4

with supplemental oxygen, 1.0 in intubated patient on 100% oxygen)

o P/F >500mmHg is normal

o P/F 300-500mmHg is mild oxygenating insufficiency

o P/F < 2-300mmHg is severe oxygenating insufficiency

Pulse oximetry

o pulse oximetry measure oxygenated haemoglobin (i.e.l haemoglobin saturation SaO2) in perfused tissue

o probes originally designed for humans are valid in animals. Normal range = 96-98%

o a pulse oximeter measures Hb saturation with O2 by measuring reflected light wavelengths during

pulsations of (assumed) arterial blood and from inter-pulsatile background blood (venous).

o Note that pulse oximetry measures Hb saturation not PaO2

increased normal

What is A-a difference?Alveolar hypoventilation

increased normal-Respiratory muscle fatigue

-Neuromuscular disease What is response like to 100% O2 (i.e. FiO2 = 1.0)?

Decreased PIO2

-CNS depression eg due to neurological disease, anaesthetic / sedative agents

-decreased inspired O2 concentration

good poor-decerased b t i

-Airway obstruction

-Diffusion impairment -cardiac shunt

-high V/Q disease -pulmonary shunt

  50

o Disadvantages of pulse oximetry which need to be borne in mind are:

It is insensitive to hypoxaemia

• Because of shape of oxygen dissociation curve, significant hypoxaemia (i.e. decrease in

PaO2 will exist before SaO2 decreases significantly

It will not detect hypoventilation

• It is possible to significantly increased PaCO2 in absence of SaO2 changes

It will not distinguish carboxyhaemoglobin from oxyhaemoglobin

It will not distinguish low SaO2 due to low PaO2 from methaemoglobinaemia

It is not very precise

It will not be reliable in the setting of hypoperfusion, vasoconstriction or hypothermia

It may be decreased by skin pigment (but not jaundice)

Capnography

o Measures end-tidal CO2 (PetCO2)

o Usually use infrared capnograph placed in series with ET tube in anaesthetised / intubated patients

o Works on principal that CO2 removal is not diffusion limited therefore in health end tidal CO2 (which

contains air expired from alveoli) approximates PaCO2

If there is severe ventilation – perfusion imbalance then etCO2 will be lower than PaCO2 but the

difference between them should vary little

Therefore before monitoring a patients PetCO2 you need to calibrate with PaCO2 first and

multiple each subsequent reading by this adjustment

o Can be used for

Patient monitoring during anaesthesia and during ventilation

Monitoring for acute onset of alveolar dead space eg due to pulmonary embolism

Monitoring success of CPR technique – as etCO2 has been shown to correlate well with cardiac

output during cardiac arrest

Scintigraphy

o Principal uses

• Assess function of mucociliary escalator especially in analysis of primary or secondary ciliary

dyskinesia

o Drop of 99Tc-MAA (Technetium-99 Macroaggregated Albumin) placed in distal trachea

and monitored for progress up trachea

o In dyskinesia, no movement will be seen

• Ventilation – perfusion scans

o Ventilation scan

Assesses which airways are adequately ventilated i.e. detects airway

obstruction

  51

Uses aerosolised 99Tc- DTPA (diamine-triamino-pentaacetic acid) or 81Krypton

(very short half life)

o Perfusion scan

Assesses which areas are perfused

Use 99Tc-MAA delivered intravenously

o Can then compare images to detect pulmonary thromboembolism

Pulmonary function testing

o These have more application in research setting than general practice

o Tidal breathing volume loop analysis with pneumotachograph

• Can monitor changes in airflow and volume versus time

• Mainly affected by upper respiratory tract disease, but can also be used to assess lower

respiratory tract diseases

o Airway resistance measurement

• Intraluminal catheter measurement of upper respiratory tract pressure

o Barometric whole body plethysmography (BWBP)

• Measures differences in volume displacement between air movement at mouth and nose from

body surface excursions – difference gives an idea of static and dynamic characteristics of lung

including

o Lung volume

o Resistance to airflow

o Breathing frequency

• Initially validated in cats this is now available in dogs also

• Can assess

o Airway obstruction

o Airway reactivity and response to therapy in bronchoconstrictive airway diseases

Exhaled breath markers

o Works on principal that exhaled breath contains aerosolised metabolites from lung s/ airway mucosa and

that these will reflect levels in extracellular epithelial fluid lining the peripheral airways

o Collection is practical in most dogs and cats

o Substances examined may include

• Hydrogen peroxide – marker of inflammation

• Leukotrienes

• Urea

• Ammonia

  52

• pH

• Nitric oxide

Work in this field is in its infancy but offers exciting new avenues to explore non-invasive diagnostic

techniques and ability to monitor objectively response to therapeutics

MRI / CT

Author’s note:

-both MRI and CT are powerful imaging modalities but their efficacy is only as good as the person acquiring

and interpreting these images. Before considering using either, you should determine

-is MRI or CT actually indicated or is there a better and cheaper alternative?

In most cases with respiratory disease the answer to this last question is usually ‘yes’ with

the exception of sinonasal disease and some interstitial lung diseases. Neither should be

performed without good chest radiographs first

-is the person performing and interpreting the images a radiologist trained in these modalities?

If they are not, are they charging less for their services? Are they sending the images to a

radiologist for interpretation? What are they going to do if the radiologist suggests other

views / techniques be taken? In the author’s opinion, having experienced several imaging

‘set-ups’ there is absolutely no substitute for having the imaging performed by a veterinary

radiologist who can adjust technique and sequences to suit the patient and to optimise

chances of a diagnosis. Protocol-based imaging studies are OK but they are no substitute

for the contemperanous expertise of a diagnostic imager.

-what is the level of monitoring / anaesthesia like in the facility being used?

Respiratory patients are often physiologically fragile and, especially in the presence of

magnets level of monitoring available may not be ideal

o MRI

• Nasal and upper respiratory tract disease

o Gives excellent detail of nasal chambers, paranasal sinuses and soft tissues of the

pharynx and larynx, tympanic bullae

o Is our imaging technique of choice where neoplasia or fungal rhinitis is suspected

It is essential to stage the extent of nasal tumours if radiotherapy is being

considered but should be performed at the institution where radiation planning is

to be carried out

  53

o Is our imaging technique of choice where radiolucent foreign bodies or retropharyngeal

neoplasia / abscess is a possibility

o Is very useful for bulla disease

• Applications in investigation of lower respiratory disease are limited

o Major barrier is significant amount of artefact generated from cardiac motion

May be reduced by cardiac gating (acquiring images at particular point on ECG)

but this is fiddly to do

o Large thoracic wall masses and cranial mediastinal masses may be adequately imaged

and assessments of vascularity made

o MR angiography can be performed and has been successfully used in our clinic to

diagnose pulmonary thromboembolism

o CT

• Allows excellent nasal turbinate detail but MRI may be superior

• Allows much better imaging of the lung parenchyma especially the interstitial compartment

• Can be useful for interstitial lung disease and bronchiectasis

• Modern CT scanners have very short acquisition time

• Assessment of airway diameters can be made

• Because magnets are not present monitoring can be more easily accomplished

4 Approach to the cat with sneezing, nasal discharge or epistaxis

o Key points

o 2 major studies of incidence of various nasal diseases in cats have been published Henderson et al JFMS 2004, 6, 245-257 reviewed 77 cases at Bristol Vet School with an

incidence of

• Neoplasia 30 cases (of which 21 were lymphoma, 4 adenocarcinoma, 2 carcinoma,

1 SCC, 1 fibrosarcoma, 1 sarcoma)

• Chronic non-specific rhinitis 27 cases

• Foreign body 8 cases

• Nasopharyngeal stenosis 5 cases

• Actinomyces 2 cases

• Nasal polyps 2 cases

• Stenotic nares 2 cases

• Rhinitis after trauma 1 case Demko and Cohn JAVMA 2007, 230, 1032-1037 reviewed 75 cases with chronic nasal

discharge at University of Missouri

• Specific aetiological diagnosis was found in only 27 (36%) of cases

  54

o Neoplasia 15 cases (of which 8 were carcinoma, 4 were lymphoma and 1

each of sarcoma and basal cell tumour) o Lymphoplasmacytic rhinitis 4 cases o Crytococcosis 3 cases o Foreign body 2 cases o Pharyngeal polyp 1 case o Tooth root abscess 1 case o Megaeosophagus and dysphagia 1 case

From both of these you can see that at referral centres, very often a specific ‘disease’ is not

found – this reflects the frequency of non-spcific rhinitis usually as a sequel to viral upper

respiratory tract infections and turbinate distortion in cats creating the familiar syndrome of

‘chronic snufflers’

o Chronic non-specific rhinitis is a frustrating entity and owners need to be carefully counselled about The likely initiating cause of viral rhinitis with local turbinate destruction / distortion and the

irreversible nature of this process, though this is essentially a diagnosis of exclusion and full

investigation should always be contemplated That cure is not a realistic proposition in some cases That treatment is symptomatic and supportive – no one has an effective treatment for these

cats that results in resolution of signs; amelioration is more realistic. Treating with healthy scepticism treatment claims that purport clinical cure Maintaining a balanced view that this is not a life threatening condition. It is frustrating for sure

but is non-progressive.

o Diagnostic techniques such as MRI and CT (if of good quality!) are revealing that some cats with

chronic upper respiratory disease may have focal / encapsulated infections or paranasal sinus disease

which is not readily apparent with other diagnostic methods such as radiography and rhinoscopy. Many

of these patients are more appropriately treated by surgical techniques. I would emphasise that these

cases are uncommon compared with the large majority of non-specific rhinitis cases and these imaging

techniques are very expensive and not appropriate in all cases. o A recent study suggests that an aetiological diagnosis is much less likely in younger cats than older

cats and in cats in which imaging studies and biopsy are not performed. The same study suggested

that an aetiological diagnosis may be elusive in the majority of cats <1yr of age 4.1 Diagnostic approach

o History

o Sudden or gradual onset?

o Unilateral or bilateral?

o Nature of discharge – serous, mucoid, purulent, epistaxis?

o Contact with other sneezing cats, recent vaccination, recent cattery visit?

o Habitual grass / plant eater?

o Hunter?

  55

o Accompanied by systemic signs of disease especially tachypnoea / dyspnoea? o Associated ocular discharge or nasal deformity? o Any dysphagia?

o Physical exam

o Determination of unilateral versus bilateral involvement o Determination of air-flow patency o Palpation for nasal symmetry and pain o Examination of dentition, hard palate o Examination for lingual / oral ulceration o Ocular examination o Good general physical examination

o Diagnostic investigation

o FeLV / FIV status o Assessment of status for feline herpesvirus (FHV), feline calicivirus (FCV) and Chlamydophila felis –

see below o Radiography o Rhinoscopy – both retrograde to examine nasopharynx and anterograde AND biopsy o Cryptococcus neoformans serology (CLAT) if appropriate o ?nasal flush biopsy o ?bacterial culture of nasal swabs (interpreted cynically!) o ?advances diagnostic imaging eg CT / MRI

SPECIFIC ENTITIES 4.2 Viral / chlamydial / bacterial upper respiratory tract disease

o Feline calicivirus

Non-enveloped single stranded RNA virus Survives for up to a week in environment, longer in damp conditions – disinfected by bleach Considerable number of genetically distinct isolates and variability leading to

• Considerable variation in pathogenicity

• Variability in level of immunity proffered by vaccination Infected by nasal / oral / conjunctival route

• Viral multiplication in oral and respiratory tissues but some strains have tropism for lung

macrophages or synovial tissue

• Following acute infection clinical signs resolve in around 7-10 days in most cases ,

though sequelae (see chronic snufflers) can b permanent

• Most infected cats continue to shed virus in oropharyngeal secretions for at least 30 days

thence declining so that by 75days around 50% cats are still shedding. Some cats will

continue to shed for life as asymptomatic carriers, though the majority of cats

spontaneously eliminate infection eventually. Shedder scan be difficult to detect – high

level shedders usually easily detected on oropharyngeal swabs but some other cats shed

less / more intermittently and are difficult to detect. It is estimated that

  56

o 40% colony cats

o 20% show cats and

o 5-10% of household cats may be persistent asymptomatic shedders

Clinical signs

• Incubation for 2-5 days then depression and pyrexia

• Lingual ulceration and occasionally nasal ulceration is most common

• Sneezing, nasal discharge and ocular discharge are less prominent / severe usually than

in FHV infection

• Occasionally dermal lesions elsewhere (ulcerative)

• Rarely

o Transient limping syndrome – tends to be shifting lameness with pyrexia,

recovery in 1-2 days. Has also been seen after vaccination

o Viral pneumonia and dyspnoea caused by very virulent strains

o A severe haemorrhagic form of disease seen in the US causing facial and paw

oedema, pyrexia, icterus, pancreatitis, pneumonia and pericarditis with a

mortality rate of 50%

• Some potential link with feline gingivitis-stomatitis complex- 80% of cases in some

studies shed calicivirus cf 20% of controls

• Isolated also from urinary tract occasionally but cause and effect relationship with FLUTD

not established

Diagnosis

• Identified usually from oropharyngeal / conjunctival swabs by virus isolation in feline cell

culture

• ELISA and PCR also available

Treatment

• Therapy is largely supportive and attention to good nutrition and hydration, clearance of

secretions, judicious use of topical decongestants and if necessary use of antibiotics to

ameliorate secondary bacterial infections

• Some degree of immunity occurs after natural infection but is probably not lifelong

• The use of antiviral agents has proved problematic due to

o Safety issues with some antiviral agents

o Lack of in vitro activity versus calicivirus

o Lack of documented efficacy in vivo

o The antiviral agent recombinant feline interferon ω is licensed for use in this

species but clinical evidence of efficacy is, to put it generously, underwhelming.

There are no controlled studies currently published that document efficacy

merely ‘testimonial’ case series which show improvement in clinical signs after

treatment (in a condition which regularly undergoes spontaneous improvement

within a few days anyway!)

Prevention

• Modified live, inactivated adjuvinated and genetically engineered vaccines are available

• Maternally derived antibody lasts for 10-14 weeks

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• After vaccination protective viral neutralisation has been shown to last 10-12 months with

moderate levels of virus neutralising antibody persisting for 4 years. Protection is usually

present from 2-3 weeks after vaccination

• Vaccines induce reasonable protection against disease but not against infection or

development of carrier state

• Care should be taken not to deposit vaccine on fur which may be ingested by licking.

Transient infections including transient limping syndrome may be seen after vaccination

though studies have shown that in most cases this is due to co-infection with field strains

rather than the vaccine strain

• Disease prevention by FCV vaccines is reduced by the heterogeneity of isolates and

variation is pathogenicity. Furthermore animals can be infected with field strains of FCV

and act as carriers / shedders of these and a reservoir for infection in other cats

• F9 and 255 FCV isolates are used in most vaccines due to their generally broad cross-

reactivity

o Feline herpesvirus

o FHV-1 is a double stranded DNA virus

o Fragile in external environment, survives <18hrs and is unstable in aerosol

o Very little strain variation (cf FCV)

o Infections

o Spread by nasal, oral, conjunctival exposure. Can be spread by sneezing but

aerosolisation does not seem to be major route

o Multiplies in soft palate, tonsils, conjunctiva, turbinates, trachea and sheds from 24hrs to

about 3 weeks after infection

o Multifocal exudative epithelial necrosis is principal lesion

o Virtually all recovered cats become persistently latently infected carriers and transient

shedders at times of stress / with corticosteroids (with lag of about a week)

o Clinical signs

o Usually more severe upper respiratory tract and conjunctival disease than FCV (in which

oral lesions predominate)

o Depression, inappetence, fever, oculonasal discharge

o Occasional coughing/dyspnoea, rarely oral lesions

o Ulcerative keratitis

o Signs resolve over 2-3 weeks

o Diagnosis

o Identified usually from oropharyngeal / conjunctival swabs by virus isolation in feline cell

culture

o ELISA and PCR also available

o Treatment

o Supportive therapy as for calicivirus

o With herpetic keratitis, topical antiviral agents eg idoxuridine and trifluorothymidine may

be helpful but consult ophthalmic texts

o Systemic antiviral agents are not of proven efficacy

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o L-Lysine

• Antagonises availability of arginine which is essential for viral replication

• When given at 400-1000mg total dose per day has been shown to decrease

severity of conjunctivitis clinical scores when given prior to infection and to

decrease quantity of viral shedding

• However a recent study (Maggs et al JFMS 2007, 9, 97-108) failed to show an

improvement in clinical severity in cats fed a diet supplemented with lysine

• Cats are exquisitely sensitive to arginine deficiency (causes hyperammonaemia

and neurological signs) and there are concerns that lysine overuse may provoke

this

• L-lysine certainly shows n vitro activity against herpesvirus replication but it

remains to be seen

o Is it effective in clinical disease?

o Is it safe and if so at what dose? Anecdotally many cats in the US have

been treated for years with L-lysine. Cynically though, as with many

treatments for chronic viral upper respiratory tract disease one has to

wonder whether the use of such unproven, potentially hazardous

therapy is motivated by clinical evidence or merely desperation in

dealing with a very frustrating clinical adversary!

o Prevention

o After naturally occurring infections, cats are usually resistant to further infection for six

months or so but naturally occurring immunity is not long-lasting

o Modified live, inactivated adjuvinated and genetically engineered vaccines are available

o Vaccination offers protection against disease but not against infection / development of

carrier state

o In contrast to FCV, there is only one serotype of FHV-1 and vaccination is likely to offer

cross-immunity against most field-strains

o Chlamydophila felis

o Gram –ve intracellular bacteria-like parasites

o Multiply within cytoplasmic vacuoles

o Have an extracellular migrating / infecting elementary body and intracellular replicating (reticulate

body) forms

o Infection

5-11% healthy cats and 45% farm cats seropositive to chlamydophila

Isolation form up to 30% of househjold cats with conjunctivitis

Usually <1yr age, unusual >5yrs age

Infected during parturition form genital mucosa of female or from close contact / aerosol

contact

Organism survives for <24hrs in environment

o Clinical signs

Usually causes conjunctivitis rather than just sneezing – serous ocular discharge,

chemosis, swelling of TEL

May be unilateral but will usually become bilateral within 7d

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Some cats have acute infection and stop shedding with resolution of clinical signs but

other cats may shed for <8 months

Persistence in extraocular sites such as GI tract and genital tract may act as reservoir for

infection of other cats / reinfection

Many cats appear to become reinfected – immunity after infection appears weak

o Diagnosis

Culture of organism

• Most definitive

• Take swabs (swab vigourously) from conjunctiva and submit in fresh

viral;/chlamydial transport medium

Serology

• Immunofluorecent antibody testing

• Limited utility as just proves exposure but high titres usually seen in affected

cats

PCR

• Available from some UK laboratories eg universities of Bristol and Glasgow

o Treatment

Systemic:

• Potentiated amoxicillin 12.5-25mg/kg p/o BID

• Doxycycline 10mg/kg p/o SID – BID (NB risk of oesophagitis – give with food or

syringe water)

• Tetracycline 22mg/kg p/o TID

• Azithromycin 10-15mg/kg p/o SID

Topical

• Chlortetracycline eye ointment TID

• Fucidic acid eye ointment SID – BID

Studies suggest

• That systemic therapy is much more effective and that topical therapy should

only really be used in conjunction with systemic therapy

• That systemic treatment for 3-4 weeks should be undertaken to prevent relapse

o Prevention

Modified live freeze-dried vaccine is available

Vaccination in face of seropositivity does not lead to increased shedding

o Bordetella bronchiseptica

o Aerobic, gram negative cocco / bacillus

o Rare cause of respiratory disese in cats

o Seroprevalence is 11% overall but is very rare in household cats. Seroprevalence is higher in

breeding cats (9%) and research colonies (13%)

o Appears to be a higher risk in multicat environments and where seropositive dogs are present in

environment

o Carrier state may exist

o Infection occurs via oro/nasopharyngeal mucosa sand bacterial replication

o Ciliostasis caused by bacterial attachment and toxins

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o Upper respiratory signs more common in cats than tracheobronchial involvement

o Appears to be primary pathogen but is more likely to be implicated in mixed infections

o Occasionally fatal severe infection seen in young kittens (<8 weeks age)

o Diagnosis is by bacterial growth and isolation from swabs / fluid but can be difficult

o Treatment in the cat has not been investigated but agents used in dogs may be appropriate

Vaccines are available but the low incidence of disease in the domestic cat population makes its

widespread use difficult to recommend at present

o Management of infectious upper respiratory tract diseases in catteries / breeding colonies

o Catteries

o Vaccinate all cats before entering facility and with adequate time for immunity to develop (see

individual vaccine inserts)

o Separate cats from different households

o Have solid non-porous fronts to cages that can be washed easily

o Food, water and litter trays should be accessible to personnel without entering enclosures

o Personnel should wash hands with disinfectant or wear disposable gloves for each pet handling

o Overshoes / shoe baths should be used

o Keep sets of food bowls / litter trays for each pen and disinfect one set whilst another is being

used

o Thoroughly dry and disinfect pens between residents, preferably with a 2d interval between

o Cats showing URT signs should be isolated and fed / cleaned last

o Humidity and ventilation should be well controlled

o Breeding colonies

o Vaccinate all animals regularly against FCV, FHV and FeLV

o Boost queens before mating or during pregnancy (use inactivated vaccine) to increase MDI of

kittens

o Do not use queens with history of respiratory disease in kittens

o Minimise stress at time of weaning and exposure of other cats to queens which shed round time of

parturition

o Move queens to isolated kittening area 3 weeks before parturition

o Wean kittens early (4-5 weeks) if queen likely to be carrier

o Vaccinate all kittens from 6-9 weeks and keep isolated until 12 weeks

4.3 Nasal foreign bodies

o Nasal foreign bodies in cats are usually plant material or bones from prey animals but I have removed

stones, toy parts and food before. Cats are generally more discerning than dogs but some individuals seem

less so!

o The majority are chewed on gagged then retched retrograde into the nasopharynx and caudal nasal

chambers rather than penetrating anterograde – it is therefore absolutely essential that if retrieval is

attempted the ability to examine and remove retrograde if needed exists

o Sudden onset uni- or bilateral nasal discharge and sneezing, often accompanied by gagging and retching is

the hallmark of nasal foreign bodies. Most owners know their cat to be habitual plant chewer and will report

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this – don’t dismiss it! A history of disease that appears to respond to antibiotics then relapse soon after

cessation should also raise suspicions.

o Discharge may be copious and because of the nasopharyngeal location of many FBs, accumulation in the

nasopharynx causing gagging and reverse sneezing is common

o Halitosis may be noted if vegetable matter with a high water content rots in this area

o Radiography may demonstrate focal increases in soft tissue / fluid opacity due to local inflammation or

accumulation of mucopus

o Examination of the nares and nasopharynx under GA should always precede further procedures: often a

tell-tail grass blade tip can be seen in the nasopharynx or with gentle rostral traction of the soft palate with a

spey hook

o Endoscopy is invaluable to examine for foreign bodies but when FBs occur in the rostral nasal cavity

visualisation may be obscured by discharge and a mechanism for repeated or constant irrigation makes the

job easier – a throat pack should always be used if irrigation or forced nasal flushing is to be used.

o Some foreign bodies may be dislodged by forced nasal flushing using 10ml aliquots of sterile saline under

pressure with the nares firmly occluded round the syringe tip anterograde and collection of flushed contents

from the nasopharynx. This technique works well in the hands of some individuals but I confess to being a

fan of endocopic retrieval and possibly persevere with this less than others!

o Provided one excercises care gentle speculative grasping with smooth tipped crocodile forceps,

premeasured to the medial canthus of the eye and systematically used to explore and grasp dorsally and

ventrally can be surprisingly effective. This should only be performed if further attempts to directly visualise

(eg by endoscopy) the area are not to be made

o Occasionally surgical retrieval may be needed

4.4 Nasal neoplasia

o Nasal tumours in cats account for between 20 and 39% of chronic feline nasal disease and appears to be

the most common cause when only cases for which a firm aetiological diagnosis is made are considered o Most cats with nasal neoplasia appear to be older cats (median age 9-10years) o 3 studies specifically examine the proportional frequency of different feline nasal and paranasla tumour

types, two with regards to all causes of nasal discharge and one based on a review of 123 nasal and

paranasal tumours at the University of Utrecht: Henderson et al JFMS 2004, 6, 245-257

• 30 tumours out of 77 cases

• 70% lymphoma

• 23% carcinoma (adenocrcinoma, carcinoma, SCC)

• 7% sarcoma Demko and Cohn JAVMA 2007, 230, 7, 1032-1037

• 15 tumours out of 75 cases

• 53% carcinoma

• 27% lymphoma

• Rest made up of sarcoma and basal cell tumour Mukaratirwa et al JFMS 2001, 3, 235-245

• 123 tumours • Presentation

o 39% (48/123) nasal discharge,

o 21% (26/123) dyspnoea

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o 20% (24/123) facial swelling

o 15% (19/123) with epistaxis

• Type

o 43% (53/123) of the tumours were of epithelial origin

adenocarcinomas (18/53)

squamous cell carcinomas (17/53) were the most common epithelial

tumours.

o 28% lymphoma (35/123) was the most common tumour

71% (25/35) B-cell tumour

29% (10/35) T-cell tumour

6 lymphomas were proved to be epitheliotropic T-cell lymphomas

o Clinical signs

nasal discharge 39-90%

dyspnoea 21-30%

Facial distortion 20%

URT noise 63%

Weight loss 27%

Ocular discharge 33%

Sneezing 27%

Lymphadenopathy 10%

Lethargy 10%

Important clinical signs are that cats with nasal neoplasia are more likely to be older, present with

epistaxis (though some will present with only serous or mucopurulent discharge) and with signs of

URT obstruction / noise

o Diagnosis

Diagnostic imaging and biopsy essential to diagnose

The combination of increased sift tissue / fluid opacity with evidence of turbinate lysis on

radiographic view is a classical finding

MRI and CT are very useful in documenting extent of lesion, and essential for diagnosis of (less

common) paranasal sinus tumours

Principal differential diagnoses are nasopharyngeal polyps (see below – don’t cause turbinate

destruction) and crytococcosis

Most cats are not FeLV positive

Metastatic disease occurs in the minority of cases (true numbers are difficult to ascertain) and

when occurs is usually to retropharyngeal lymph nodes and thence to lungs

o Treatment

92% of nasal and paranasal tumours are malignant

Lymphoma

• Can be treated with chemotherapy (C/O/P or C/H/O/P – based protocols predominantly

reported)

o Few studies documenting efficacy

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o In Henderson 2004 median survival time (MST) for cats treated with multiagent

chemotherapy (predominantly C/O/P) was 98 days (but massive range of 10d to

>1264d!) versus 28 days (range 10-130) for those that weren’t treated or

received prednisolone

• External beam radiotherapy also an option

o Lymphoma is generally highly radiosensitive but few studies document

Non-lymphoproliferative neoplasia

• External beam radiotherapy is treatment of choice but most studies contain few cases

• Reported median survival times with both hypo- and hyperfractionated regimes are in the

order of 11.5-19months, with 1 and 2-year survival rates of 44-63% and 16% respectively

• Most cats are euthanased due to tumour recurrence

4.5 Fungal Rhinitis

o Fungal rhinitis in UK cats is uncommon o Aspergillus, Penicillium and Cryptococcus have been associated with nasal disease in cats and opportunist

organisms of the phaeohyphomycosis group and Cryptococcus may cause nasal subcutaneous masses.

We have also recently documented a mucor spp infection in a cat. o Diagnosis is by serology. Diagnosis of cryptococcosis can be made cytologically and with the capsular latex

agglutination test (CLAT) which may also be used to monitor response to treatment o A variety of antifungal agents has been used to treat fungal rhinitis in cats but the most extensively reported

disease is cryptococcosis Fluconazole is successful in the majority of cats though itraconazole is favoured by some authors.

Ketoconazole, combinations of flucytosine and fluconazole and infusion / depot preparation of

amphotericin B have all been reported. The reader is referred to specific pharmaceutical

formularies for appropriate and safe use of these drugs as many are associated with high risk of

adverse effects. The optimum approach to nasal aspergillosis in cats is not well documented

4.6 Nasopharyngeal Polyps

o Non-neoplastic inflammatory growths o Extend from tympanic cavity or Eustachian tube into nasopharynx (aural polyps extend through tympanic

membrane into horizontal ear canal) o Aetiology unknown but does not seem to be associated with viral respiratory tract disease o Clinical signs

Weight loss, sneezing, stertor Dysphagia Gagging, retching Dyspnoea

Middle ear / inner ear involvement may lead to horner’s syndrome, facial nerve palsy, head tilt,

ataxia, nystagmus

o Usually younger cats (mean 13m – 3 years), no sex or breed predeliction

o Investigation

Good auroscopic examination of ears

Examination of nasopharynx under GA and palpation with finger

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• Useful to examine with retroflexed flexible endoscope or dental mirror and spey hook

Radiography of nasopharynx and tympanic bullae (false negative diagnosis for tympanic bulla

disease may be seen in up to 25% cases)

CT / MRI are useful but often not necessary

o Treatment

Removal by traction

• Simple, requires minimal equipment

• Done under GA with close attention paid to anaesthetic management of unstable airway

• Removed by simple traction

• Recurrence rate is high – 36-41%

• ?decreased recurrence when prednisolone given afterwards

Removal by ventral bulla osteotomy

• Results in exposure of origin of stalk of polyp, either tympanic bulla or Eustachian tube

• Lower recurrence rate (<8%)

• See surgical texts for technique / complications

5 Approach to the dog with sneezing, nasal discharge or epistaxis 5.1 General approach

o Epistaxis

o Epistaxis in dogs is usually caused by an aggressive / destructive local process (of which neoplasia

and aspergillosis are by far the most common) or systemic bleeding disorder

o It is rare for repeated epistaxis to be caused by a benign process such as a foreign body and repeated

episodes of epistaxis always mandate investigation

o History

o Chronic sneezing / nasal discharge – character, unilateral or bilateral

o Facial distortion

o Nasal / facial tenderness

o Speed of onset and progression

o Signs of concurrent ocular disease

o Bleeding from other sites, bruising, petechiation

o History of tumour or swelling in other locations, histological diagnosis of previously excised

lumps

o History of bleeding after other procedures

o History of mentation changes, visual disturbance, seizures

o Physical examination

o Facial symmetry

o Facial / nasal tenderness

o Oral examination of dentition, hard palate etc

o Presence of discharge / epistaxis – uni- or bilateral and nature

o Nasal depigmentation especially ventral to nares

o Crusting / dermatological changes

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o Exophthalmos, altered symmetry of eyes

o Ocular discharge

o Presence of petechiation, bruising, evidence of haemorrhage from other sites

o Presence of mass lesions elsewhere

o Differential diagnosis

o Local disease process

• Fungal rhinitis

• Neoplasia

• (trauma)

• (nasal foreign body)

• (severe inflammatory rhinitis)

• (very severe dental disease)

o Systemic disease process

• Bleeding disorders

o Disorders of primary haemostasis

Thrombocytopenia (most commonly primary or secondary

immune-mediated)

Thrombocytopathia (uncommon)

Von Willebrand’s disease

• Occasionally presents with epistaxis

o Disorders of secondary haemostasis (coagulopathy)

Acquired coagulopathies more common than congenital

Most common canine acquired coagulopathies in UK are

• Vitamin K antagonist rodenticide poisoning

• Angiostrongylus vasorum infection (this is the most

common coagulopathy I get advice calls about via our

haematology laboratory)

• Disseminated intravascular coagulation

o Not always an acute disorder, may easily be

chronic

o Usually secondary to inflammation or neoplasia

o Hyperviscosity syndrome

May cause altered platelet adherence

Most commonly as a result of

• Polycythaemia

• Hyperglobulinaemia due to multiple myeloma,

leishmaniasis or ehrlichiosis

o Hypertension

Systemic hypertension may occasionally cause epistaxis but we

have usually seen this in conjunction with local disease eg

neoplasia or aspergillosis

o Investigation

o Coagulation panel including platelet count, PT, APTT and VWF:Ag

o Assessment of systemic blood pressure

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o Diagnostic imaging

• Radiography is generally cost effective and is adequate for many cases, though

more advanced imaging techniques have some advantages

• Good quality intra-oral nasal occlusal films give most information but must be

accompanied by

o Films of frontal sinuses (best = rostrocaudal skyline)

o Thoracic radiographs)

• CT and more especially MRI give superior detail, allow better imaging of the frontal

sinuses, will help (in case of MRI) distinguish fluid from soft tissue.

o Essential for planning of aggressive surgery or radiotherapy

o Very useful in staging extent of sinonasal aspergillosis

o Essential for sinus tumours

o Rhinoscopy

• Is dependent on operator skill and equipment

o Must evaluate anterograde and also retrograde view of nasopharynx

o Need to continuously irrigate with fluid (protect airway, use pharynx packs

etc)

• Always explore systematically

• Always biopsy

o Serology testing for Aspergillosis – offers useful corroborative evidence but should not be

relied on for sole diagnosis as both false positive and false negative diagnoses reported (see

below)

o Histopathology of nasal biopsies

o Culture – bacterial and fungal

• Bacterial cultures fraught with interpretive difficulty (see section above)

o In some circumstances direct trephination and surgical exploration of frontal sinuses /

endoscopy of frontal sinuses may be warranted

o Nasal discharge

o Principal differential diagnoses are

o Non-specific chronic rhinitis (a.k.a. lymphoplasmacytic rhinitis, so called ‘allergic rhinitis’

though this is best avoided)

o Nasal foreign body

o Neoplasia

o Aspergillosis

o Nasal polyps

o Dental disease

o Rarely parasites such as Pneumonyssoides caninum (appears rare in UK), Linguatala serrata

(doesn’t occur in UK), Capillaria aerophila

o Rarely ciliary dyskinesia (see below)

o Two important differential diagnoses are:

o Accumulation of crusted secretions as a result of disorders of parasympathetic function of

facial nerve (Cn VII)

o Discharge due to dermatological disease of the nasal mucocutaneous junction (eg pemphigus

group, discoid lupus etc)

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o Investigation is similar though assessment of coagulation status and hypertension less critical

5.2 Nasal neoplasia o Usually orginate from nasal cavity and may extend to sinuses; occasionally originate in sinuses

o Accounts for around 1/3rd of nasal disease in dogs

o Majority malignant

o Epithelial tumours most likely

o most common are adenocarcinoma, then undifferentiated carcinoma and squamous cell carcinoma,

rarely transitional cell carcinoma

o a minority are mesenchymal tumours, mainly osteosarcoma and chondrosarcoma. Haemangiosarcoma and

undifferentiated sarcoma rare

o rarely round cell tumours – lymphoma, mast cell tumours, melanoma

o dolichocephalic and mesaticephalic breeds more at risk than brachycephalic

o usually older dogs, median age 10 years (tendency for dogs with sarcomas to present at younger age than dogs

with carcinoma)

o metastasis uncommon and usually a late finding

o clinical signs usually present for 2-4 m before diagnosis

o sneezing

o nasal discharge: serous to mucopurulent becoming sanguinous

o stertor

o may develop facial swelling and pain, exophthalmos, neurological signs including seizures

o investigation

o diagnostic imaging

radiography

• take intraoral oclusal nasal cavity views and rostrocaudal frontal sinus views

(excellent positioning for symmetry is essential)

• classical appearance is of turbinate destruction accompanied by increase in soft

tissue / fluid opacity

• radiography should include thoracic radiographs

CT / MRI is more accurate for staging extent of disease for treatment planning but may only

be useful if treatment is being considered. Most reports in the literature concern CT but we

find that MRI gives much better detail

o Rhinoscopy and biopsy

Rhinoscopy is the best way to obtain guided biopsy specimens but blind biopsies based on

radiographic landmarks can often be successful

Appearance of tumour does not correlate with histological diagnosis

Occasional dogs will sneeze-out tumour chunks spontaneously!

o Other staging

Thoracic radiographs

Palpation and aspiration of local lymph nodes

MRI / CT to stage extent and intracranial extension

o Treatment

o NB Discuss treatment with owners at an early stage. If clients are considering radiotherapy as an

option unless you have extensive experience of the practicalities of this, which few vets do, it is best to

consider referral to an oncology specialist early. These treatment options are a big commitment and

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best discussed with the owner by a specialist, even if the owner simply wishes for consultation.

Similarly, though access to advanced imaging like MRI is more widely available, at centre where both

MRI / CT and radiotherapy are performed it is best for this to be assessed by one individual rather than

supplying images from another source which may not be suitable for radiation therapy planning.

o No treatment / palliation

Overall median survival time with no attempts at primary treatment is 95 days

• Dogs with epistaxis have a median survival time of 88 days

• Dogs without epistaxis have a median survival time of 224 days

Palliation with NSAID analgesics is reported

There is some limited evidence that NSAIDs that preferentially inhibit cyclo-oxygenase 2 (eg

piroxicam, meloxicam) may retard tumour growth

o Surgery

Surgery alone is unlikely to be successful and is not generally recommended for nasal

tumours

Mean survival time with surgery alone for dogs with nasal tumours is 4 months (range 1m –

11m)

Surgical debulking can be considered prior to radiotherapy (cytoreduction) but it is not

apparent that this results in substantially improved results over radiotherapy alone so is

generally not performed

Surgical therapy is associated with high patient morbidity

o Chemotherapy

Chemotherapy alone has not been shown to be highly effective for canine nasal tumours with

the exception of lymphoma

Platinum containing drugs (cisplatin and carboplatin) and anthracyclines such as doxorubicin

have been evaluated in a limited number of cases

Cisplatin therapy resulted in median survival time of 20weeks with an overall response rate

(complete or partial remission) in 27% of dogs

Combined cisplatin, doxorubicin and piroxicam therapy has been evaluated in a limited

number of dogs

Cisplatin has been employed as a radio-sensitising agent prior to radiotherapy

It is strongly advised that an oncologist be consulted if considering using any of these agents

o Radiotherapy

The most successful treatments for nasal tumours in dogs have involved radiotherapy

In the UK, to date most treatment employed has been hypofractionated (treatments usually

given once weekly) rather than hyperfractionated regimes (usually given on a Monday –

Wednesday-Friday basis)

Radiotherapy generally does not cure disease

Large owner commitment is needed

With the hypofractionated regime used in the UK (megavoltage radiation, 4 doses of 9 Gy at 7

days intervals)

• Clinical signs improved in 95% dogs

• Median survival time after last dose 212 days

• 45% dogs alive after 1 year, 15% after 2 years

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Other reports using hyperfractionated regimes report slightly longer median survival times of

around 12-16months, with one and two year survival rates of about 50-60% and 20-40%

respectively

• These regimes may become available in the UK as the latest generation of

radiotherapy units begins to be commissioned at a small number of centres but cost

and owner ability to commit to such a time-consuming therapeutic regimen are likely

to be limiting factors

5.3 Sinonasal aspergillosis Key point

o Sinonasal aspergillosis is an aggressive disease. The efficacy of the first treatment given usually dictates ultimate

prognosis. In my opinion, successful treatment depends on

o Determining extent of disease from the outset (not when treatment has been tried and failed) and tailoring

treatment approach accordingly

o If disease is not confined to the nasal cavity not confining treatment to non-invasive fungicidal flushing

o Not taking treatment on if there is an option of referral to someone with experience of managing this

condition

o Not pursuing too long with non-invasive therapy if it is clear that you are not getting anywhere. I have seen

many cases where therapy has been persistently given that was doomed to fail because the extent of the

disease had not been properly evaluated in the first place and appropriate treatment selected. These cases

have suffered from the resulting time-lapse before more aggressive therapy and their disease has

consequently become harder to manage.

o Successful therapy is often costly and needs owner committment

o Epidemiology

o Young to middle aged predominantly

o Mesaticephalic and dolichocephalic breeds

o Usually Aspergillus fumigatus, ubiquitous soil-borne saprophyte

Also A.niger, A.flavus, A.nidulans

Penicillium spp

o Clinical signs

o Sneezing and nasal discharge, mucoid to mucopurulent becoming Epistaxis

o Usually unilateral to begin then bilateral

o Stertor and stridor

o Nasal crusting and depigmentation is a classical feature – depigmentation commonly occurs ventral to

nares in areas of contact with discharge (should remember though other depigmentary disease associated

with nasal crusting and discharge such as discoid lupus erythematosus)

o Often nasal tenderness

o May have facial deformity, exophthalmos

o With deep orbital involvement often get periorbital swelling, exophthalmos, discharge, pain

o May get systemic involvement rarely (usually in immunocompromised GSDs) though this is most commonly

seen without nasal discharge predominating and A.flavipes, A.terreus and A.deflectus are more commonly

implicated

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o Diagnosis

o Usually made on a combination of imaging, serology and rhinoscopy with histopathology

o Beware placing too much emphasis on fungal culture. Aspergillus is a ubiquitous organism and common

contaminant – treatment decisions should not be based on fungal culture alone

o I would be happy with a diagnosis of aspergillosis based on any of the following:

Direct and unequivocal visualisation of fungal plaques / aspergilloma on rhinoscopy (in order for

this you must have an excellent rhinoscopic view and some experience of normal inspissated

nasal secretions viewed via a rhinoscope)

Histopathology of nasal epithelial biopsies demonstrating fungal hyphae in large numbers

Evidence of turbinate lysis on radiography or MRI without associated soft tissue opacity in

combination with corroborating evidence from at least 2 of

• Positive serology

• Direct rhinoscopic visualisation consistent with aspergillosis

• Fungal culture

o I would not be happy to

Diagnose aspergillosis based on serology alone

Diagnose aspergillosis based on fungal culture alone

Diagnose aspergillosis on response to treatment

Rule out aspergillosis on the basis of negative serology

o Diagnostic imaging

Radiography

• Remember to include imaging of the frontal sinuses

• Documentation of bony involvement mandates aggressive treatment

• Intraoral oclusal nasal films most useful

• Classical radiographic findings are

o Unilateral or bilateral turbinate destruction

o Increased radiolucency

o Focal ‘pepperpot’ radiolucencies

o Frontal sinus osteomyelitis

• Sensitivity of radiography is considered about 84%

• Sensitivity of CT is considered about 92%

• Sensitivity of MRI is not reported but is likely to be equal or better than CT

CT / MRI

• CT gives extremely good bony detail but is less accomplished than MRI at distinguishing

extent of soft tissue and fluid

• Is only as good as the person diagnosing the images – should be a radiologist

• Turbinate destruction without increase in soft tissue is hallmark finding as in radiography

• Is essential for surgical planning with extensive (eg orbital) disease

o Serology

Agar gel double diffusion method

• Sensitivity reported as 67%

  71

• Specificity reported as up to 98% but one study reported 15% false positive diagnosis in

dogs with nasal neoplasia

Counter immunoelectrophoresis (CIE)

• Reported as being reliable but no robust studies have been performed to verify this

ELISA

• Sensitivity of 69% has been reported

• Specificity has not been robustly examined but is thought to be high

o Culture

Aspergillus can be cultured from 30-40% of normal dogs

o Treatment

Medical management alone

• Ketoconazole 5mg/kg p/o q12hr – resulted in short-term cure in 47% cases

• Fluconazole 60% response rate reported

• Itraconazole 60-70% response rate reported

Topical treatments / combined treatments

• Enilconazole 10%

o 10mg/kg BID through tubes implanted in nasal chambers or frontal sinuses –

90% cure rate when given for 7-14 days

o Non-invasive prolonged soaking of 10% enilconazole is not recommended –

seems to result in lower success rate ?due to damage to epithelium and

subsequent superinfection

• Enilconazole 1-2%

o 60ml per side infused over 1 hour via non-invasive method

o cure rate of 89% for 1% enilconazole (47% cured after 1 treatment, 31% after

two treatments, 10% cured after 3 treatments)

o cure rate of 100% for 2% enilconazole (86% after one treatment, 14% after two

treatments)

• Clotrimazole 1%

o Topical 1hr soak of 60ml / side clotrimazole results in cure in 65% of dogs with

one infusion and 87% of dogs after one or more treatments

• Combined infusion of 25ml/side of 1% clotrimazole solution and instillation of 10-20g/side

of 1% clotrimazole cream

o Cure rate of 86%

• Combined rhinotomy, turbinectomy, 2% enilconazole infusion and 5mg/kg p/o BID

itraconazole for 30 days

o Variable results and difficult to interpret - not recommended

• Topical povidone-iodine soaked dressings

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o May be used in combination with aggressive debulking surgery in recurrent

cases – not recommended if you are not a very good ENT surgeon

• My approach to treating these cases is dependent on diagnosing extent of disease:

o Perform excellent clinical staging of disease

If disease confined to nasal chambers i.e. no evidence on imaging (usually MRI) of frontal

sinus involvement

• Topical clotrimazole 1% 1hr soak 60ml/side on 2 occasions 4 weeks apart

• If marked improvement is not seen by the time of the second treatment or if

recurrence is seen I do not continue with this but assume that frontal sinus

involvement is present and modify treatment

Any evidence of frontal sinus involvement or failure to respond to non-invasive soaking

quickly

• Trephination of frontal sinuses, infusion of 1% clotrimazole solution followed by

installation of 1% clotrimazole cream depot

Failure to respond to above

• Hospitalisation, placement of foley catheters in frontal sinuses and BID flushing for

14 days with 10% enilconazole

Evidence of disease outwith the nasal / pranasal sinuses

• Combined aggressive topical therapy with surgical debridement and systemic

itraconazole 5mg/kg p/o BID for 6-12 weeks.

5.4 Non-specific inflammatory rhinitis

o Goes by many names including

o Lymphoplasmacytic rhinitis

o Allergic rhinitis

o Inflammatory rhinitis

o Steroid-responsive rhinitis

o I would argue that non-specific rhinitis is a more ‘honest’ description of the condition than the others because

o The presence of lymphoplasmacytic inflammation merely represents a response of epithelium with a limited

pathological repertoire to a wide variety of potential insults

o It is not proven to be an allergic aetiology

o Pathogenesis

o Histologically characterised by lymphoplasmacytic infiltration of nasal mucosa (but also eosinophils and

neutrophils)

o Mucous accumulation, hyperaemia, vasodilation

o Impaired local ciliary activity

o Local congestion and bacterial overgrowth

o Aetiology unknown. May be multifactorial including

Immune-mediated

Allergic

Environmental irritants

o Epidemiology and clinical signs

o Usually young adults and middle aged

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o Especially dolichocephalic breeds including whippet and dachshund

o Usually serous to mucopurulent (depending on degree of secondary bacterial infection) nasal discharge

associated with sneezing, stertor and facial rubbing often

o Animals may cough due to post-nasal drip

o Are usually very well

o Diagnosis

o By exclusion of neoplasia and aspergillosis, exploration for dental disease and foreign bodies, biopsy of

affected epithelium

o Should include

Nasal imaging

Rhinoscopy and retrograde flexible rhinoscopy

Aspergillus serology

Nasal biopsy

o Little evidence for skin ‘allergen testing’ or for ‘allergy profile’ blood tests

o Management

o Glucocorticoids

Systemic

• Prednisolone 1-2mg/kg p/o in divided doses BID for 1-2 weeks then taper to effect or to

0.5mg/kg p/o EOD

Topical

• Can use metered dose inhaler and fluticasone or beclomethasone

• Objective assessment of response is difficult and most work examining efficacy is merely

descriptive

o Judicious antibiotic therapy for secondary infections

o Client counselling

This is a frustrating condition but no more debilitating than having a chronically blocked nose;

owners may sometimes need counselling as to the largely mild nature of this condition but the

palliative nature of therapy

6 Obstructive upper airway disease in cats

o Most upper airway obstruction in cats is caused by nasal disease and nasopharyngeal polyps and is described

above o Primary laryngeal and tracheal diseases of cats are not well described

o Laryngeal paralysis has been reported in a low number of cats. Treatment with surgery for bilateral laryngeal

paralysis has resulted in improvement in a small number of cats reported.

7 Obstructive upper airway disease in dogs

7.1 Brachycephalic upper airway syndrome

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• components

o stenotic nares

o excessive nasopharyngeal soft tissue

o excessively long / thick soft palate

o evertion of laryngeal saccules

o tracheal hypoplasia

• presenting signs

o upper respiratory stertor (usually nasopharynx) or stridor (usually larynx / trachea) accompanied by

cough / gag / retch/ cyanosis / exercise intolerance /exercise-induced collapse

o often snore

o brachycephalic breed

• diagnosis

o somewhat subjective!

o Stenotic nares

Usually obvious on physical examination

o Nasopharyngeal soft tissue / elongated soft palate

Combination of radiography and visual inspection – flexible rhinoscopy is essential to

adequately evaluate the nasopharynx for concurrent disease such as mass lesions

Extubate lateral (need to be perfectly positioned) pharyngeal radiographs are helpful in

showing

• Extent of laryngeal air lucency

• Length of soft palate compared with epiglottis and skull

• Thickness of soft palate

o Everted laryngeal saccules – laryngoscopy

o Tracheal hypoplasia – lateral thoracic radiographs

• Treatment

o Surgical resection of redundant tissue

7.2 Laryngeal disorders

• Laryngeal paralysis

o Congenital in Bouvier de Flandres, Siberian huskie, Dalmatian, EBT, Rottweiler, setter, Labrador –

central and peripheral degenerative neuropathy

o Acquired – idiopathic, hypothyroidism, trauma, local surgery, FB, neoplasia, electrocautery, as part of

polyneuropathy / polymyopathy

Usually older medium to large breed dogs – Labrador, St Bernard, Afghan

o failure of innervations of dorsal cricoarytenoideus mm – failure of abduction of the arytenoids cartilages

unilaterally or bilaterally

o larynx usually contributes 6% of airflow resistance – markedly increases with LP

o consequences

increased airflow resistance

laryngeal oedema

hyperpnoea / dyspnoea / cyanosis

hypoxaemia

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hyperthermia

non-cardiogenic pulmonary oedema if sudden

o clinical signs

loss of bark

inspiratory stridor

gag, cough, signs of aspiration

exercise intolerance

often exacerbated / brought on in hot weather

tachypnoea / hyperpnoea / dyspnoea

o Diagnosis

Must visualise larynx under light plane of anaesthesia

• Dog must be able to swallow – check with gag reflex (too ‘deep’ and you will get

false positive diagnosis)

• Must observe chest wall movements – in some dogs the massive negative

intrapleural pressure generated ‘sucks’ arytenoids medially then they ‘blow’ outwards

during expiration (i.e. paradoxical movement compared with normal) – if you are not

observing chest wall movement to look for this you will get false negative diagnoses

Failure of abduction of one or both arytenoids

Neurological examination, thoracic and laryngeal radiographs, T4/TSH

Investigation must be undertaken carefully as these patients are often extremely fragile

o Treatment – surgical arytenoids lateralisation

Success rate / complication risk very experience – dependent

• Laryngitis

o Clinical signs

Dry hacking cough, inappetence, depression, change of bark, stridor

Discomfort on swallowing

o Aetiology

Repetitive barking, infection (usually Bordetella, Parainfluenza, Mycoplasma), trauma,

granulomatoud disease,, foreign body, neoplasia

o Diagnosis

Direct visualisation

Biopsy to rule out neoplasia

Culture of tracheal material

Histopathology usually inflammatory

o Treatment – symptomatic / empirical

Antibiotics if infection suspected

Glucocorticoids if granulomatous inflammation

• Laryngeal tumours

o Majority are malignant

o Benign include chondroma, myxochondroma, leiomyoma, lipoma, fibropapilloma, rhabdomyoma

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o Malignant include melanoma, plasmacytoma, mast cell tumour, squamous cell carcinoma, lymphoma,

chondrosarcoma, adenocarcinoma, rhabdomyosarcoma

o Most dogs will show gradual onset inspiratory stridor and laryngeal discomfort, sometimes gag / cough

/ retch

o Investigation should include – local and thoracic radiography, biopsy of the mass and local lymph

nodes

o Treatment approaches vary according to tumour type – these are uncommon tumours and should be

discussed with a medical or surgical oncologist prior to embarking on therapy

7.3 Tracheal disorders

o Tracheal collapse

• Middle aged toy and miniature breeds (but will sometimes present young)

• Typical signs are goose honking cough, severe and paroxysmal, worse with exercise and excitement, gag /

retch, stridor

• Have changes in structure of tracheal rings – decreased chondrocytes, decreased glycosaminoglycans,

loss of hyaline cartilage with replacement by fibrocartillage

• Diagnosed by o radiography (remember that extrathoracic segment collapses on inspiration / intrathoracic on

expiration!) avoiding overinterpretation of overlying oesophagus, fat or longus colli muscles sensitivity 60-84% laterals and skyline thoracic inlet

o fluoroscopy o tracheosscopy

gold standard

• grades I-IV depending on severity

• treatment o medical

must always be tried first weight loss is the single most effective treatment antitussives bronchodilators short, anti-inflammatory courses of corticosteroids

o surgical external ring prostheses

o endoscopic / fluoroscopic expandable balloon stenting (still in relative infancy)

Tracheal neoplasia

• Most commonly lymphoma, squamous cell carcinoma, osteosarcoma, chondrosarcoma, mast cell tumour,

adenocarcinoma

• Approach as for laryngeal tumours

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Tracheal hypoplasia

• Normal size o Ratio of tracheal width to thoracic inlet on lateral radiograph = 0.16 (smaller in Bulldog)

• Exertional dysnoea, recurrent RTI

• Treatment is merely supportive but many dogs will improve as they grow

Infectious tracheobronchitis

• Bordetella bronchiseptica, canine parainfluenza, CAV2, reovirus, herpesvirus, Mycoplasma

• Acute onset, harsh coughing, may be febrile, inappetant, retching, change of bark

• Recent history of contact with infected dog / kennel / hospital

• Do not necessarily need antimicrobial therapy in all circumstance

• Treatment

o Antibiotics – suitable choices would include doxycycline, trimethoprim sulphonamide or

potentiated amoxicillin (less desirable). Fluoroquinolones probably not warranted

o Glucocortoccoids

o Antitussive agents

7.4 Airway foreign bodies

• majority are vegetable in nature and lodge in first divisional (mainstem) bronchus

• typical history is of sudden onset coughing / gagging / distress in young sporting breed (typically a springer

spaniel) occurring whilst out on walk, but some dogs will only present with a soft cough and halitosis

• most will develop fairly foetid breath after a while

• most commonly grass seeds, but toy, stuffing, bones, small balls, food fragments and stick fragments also seen

• commonly reported to lodge in right mainstem bronchus (straighter)

• strategies for removal (grass seeds)

o never underestimate the potential severity / sequelae of inhaled grass seeds – the majority of them can

be easily retrieved but I have seen many dogs have to undergo lengthy surgery, develop

pneumothoraces and to have transthoracic grass seed migration with associated pyothorax all

because of single grass seeds – warn owners of this from the start!

o These patients are fragile and if they have a grass seed and much pus completely blocking one

mainstem bronchus they have a huge area of physiological dead space – have someone who is a

proficient anaesthetist assisting

o if you don’t have good bronchoscopic equipment do not even attempt to get these out – send them to

someone who can!

o The ideal time to remove grass seeds is when they have got slightly mushy about 1-3 weeks after

inhalation – earlier seeds have rigid barbs which may penetrate bronchial epithelium – if they won’t

come out without excessive trauma consider leaving them and re-scoping a week or two later

o If the grass seed is not visible / has fragmented and there is complete lobar consolidation – surgery is

the better option +/- lobectomy

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o Beware grass seeds where the sharp tip has penetrated the bronchial wall – these may form a seal

which, on removal of the grass seed forms a tension pneumothorax. Always be primed to insert a

chest drain when removing grass seeds that have lodged in this way.

o Endoscopic biopsy forceps are terrible for removing seeds – you need a proper rat-tooth grasper,

snare, basket or trefoil grasper

o Always examine every other airway division (and cross them off on a list) to document that no other

seeds are present. Look distal to the first seed you remove also.

8 Selected lower respiratory tract disease in cats Lower airway disease in cats is dominated by the chronic bronchitis / asthma group and these notes reflect this bias.

8.1 Chronic bronchial disease in cats

o Overlapping syndromes of ‘feline asthma’ and chronic bronchitis

o Asthma = airway hyperreactivity and reversible bronchoconstriction

o Chronic bronchitis = airway inflammation and mucus accumulation and trapping leading to irreversible airway

damage (COPD)

o Clinical signs may be identical

o Aetiology / pathogenesis

o Decreased airflow caused by either airway hyperresponsiveness to inhaled particulate matter (asthma) or

accumulation of mucus

o Smooth muscle constriction and hypertrophy causes airway narrowing

o With chronicity hyperinflation and air trapping leads to bronchiectasis and signs of COPD especially in right

middle lobe

o Accumulation of eosinophils may result in their release of highly charged cationic proteins which cause

epithelial damage and sloughing

o Imtercellular adhesion molecules such as ICAM-1 may be important targets for eosinophil attachment and

attraction

o Serotonin may contribute to airway hypersensitivity

o The role of exogenous allergens, viral, bacterial, mycoplasmal and fungal irritants is unknown though many

models of feline asthma involve airway sensitisation with allergens

o Epidemiology / clinical signs

o Coughing most common sign

o Also

Wheezing, dyspnoea, tachypnoea - all caused by lower airway obstruction

May get retching

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Signs will often be paroxysmal, intermittent, waxing and waning

o Breed predispositionin Siamese and oriental shorthair

o Most are young to middle aged but any age can be affected

o Physical examination

o Observation of breathing pattern useful

Expiratory push is hallmark of lower respiratory obstruction but may not invariably be present

May have wheezes / crackles on lung auiscultation

May be able to induce cough

May have hyperresonant lungs on percussion

o Investigation

o Routine laboratory assessment

Unhelpful usually

Up to 20% have peripheral eosinophilia (but is not specific for this disease entity)

May have hyperglobulinaemia

FeLV / FIV testing

o Faecal analysis

To rule out Aelurostrongylus and Oslerus

o Radiography

Diffuse bronchial pattern

Hyperinflation / diaphragmatic flattening

May have patchy alveolar infiltrates

May have old rib fractures

Bronchiectasis

May have aerophagia

Helps rule out neoplasia and other focal lung disease but is not pathognomonic and does not

distinguish between chronic bronchitis and asthma

o Bronchoscopy and bronchoalveolar lavage (BAL)

Limited by patient size / scope size

Rule out structural. Obstructive / dynamic collapse of proximal airways

Collect BAL samples

• Cytology (see above section)

o Very difficult to interpret – although commonly people get into the habit of

‘diagnosing’ asthma based on finding eosinophilic predominance, studies have

shown that some individual healthy cats may have proportions up to 85%

though less than 30% is more normal.

o Neutrophilic inflammation more common in chronic bronchial disease

• Bacteriology

o Usually negative

o May occasionally identify mycoplasmas (usually not seen in normal cat BAL)

o Pulmonary function testing

  80

Probably most applicable method is whole body barometric plethysmography

Can demonstrate airway resistance and exaggerated response to low dose of irritants

Can also document efficacy of treatment

Is a research tool rather than being of use in an individual animal.

o Treatment

o Normal control of airway diameter

Baseline airway smooth muscle tone

• Parsympathetic (Ach)

Smooth muscle relaxation

• Sympathetic (alpha02 adrenergic)

Also NANC (non adrenergic non-cholinergic)

o Airway sensitivity also mediated by

Inflammatory mediators causing bronchoconstriction (hitamine via H1 receptor, serotonin,

prostaglandins, leukotrienes)

Inflammatory mediators causing vasodilation (histamine via H2 receptor)

Presence of mucus and inflammatory debris in airways

o Glucocorticoids

Mainstay of treatment

• Reduce inflammation

• Sensitise and increase number of alpha-2 receptors

• Reduce formation of leukotrienes and prostaglandins

May be given systemically

• Oral prednisolone 1-2mg/kg p/o BID then tapered to effect

• Methylprednisolone sodium succinate 50-100mg / cat i/v, i/m in acute / emergency

setting

• Betamethasone sodium phosphate 0.8mg/kg i/v, i/m in acute / emergency setting

• Dexamethasoen sodium phosphate 1mg/kg i/v, i/, in acute / emergency setting

Or by inhalant therapy

• Fluticasone 1-2 doses of 200-250ug via spacer device (Aerokat) / day

o Expensive

o May take 1-2 weeks to see effect

o Very little documented efficacy but reduces airway inflammation in a model of

feline allergic airway disease

o It is a misnomer that these aren’t absorbed systemically – reduction in ACTH

stimulation can be seen

o Bronchodilators

Systemic

• Terbutaline (alpha 2 agonist)

o 0.01mg/kg i/v, i/m in acute / emergency setting

o 0.625 – 1.25mg/cat p/o BID for chronic use

• Theophylline (sustained release)

o 20-25mg/kg p/o SID

• Adrenaline

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o Acute bronchodilator used in emergencysetting only – mixed adrenergic effects

o 0.1ml of a 1:1000 dilution i/v, i/m or via ET tube

By inhalant therapy

• Salbutamol has been most widely used

• Documentation of efficacy is lacking

• Is some evidence that chronic use may actually increase airway inflammation – therefore

currently recommended just to use in the acute setting

• Use of 2 doses every 30 minutes for up to 4 hours during acute settings

o Miscellaneous agents

All considered speculative at present

• Zafirleukast (leukotriene antagonist) 10mg/cat p/o BID

• Cyproheptidine (serotonin antagonist) 1-2mg/cat p/o SID to BID

8.2 Airway parasites of cats

o Aelurostrongylus abstrusus

o Metastrongylooid nematode

o Prevalence in UK may be as high as 9.6% but many infestations asymptomatic

o Life cycle

Adults in terminal bronchioles and alveolar ducts causing bronchiolitis, alveolar infiltration and

muscular hypertrophy of pulmonary arteries

Females 9-10mm, male 4-6mm

Eggs produced by female develop to L1 in the lung and are coughed up, swallowed and

passed in faeces

Requires intermediate molluscan host to develop into infective L3 larva

o Clinical signs

Usually asymptomatic

Cough, weheeze, dyspnoea, poor dooers

Require 50-400 larvae to develop marked bronchial disease (may be found in a single snail)

Clinical signs usually self-limiting within several months but pulmonary arterial thickening may

persist longer

o Diagnosis

Radiography

• Bronchial pattern

• Patchy alveolar infiltrates

• Usually most severe 5-21 weeks post-infection

Larval identification

• Identifying L1 larvae on airway cytology from BAL or faeces by Baermann technique

• Larvae are 0.4mm long with notched tail and j-shape

• May be shed only intermittently so false negative diagnosis easy to make

o Treatment

Fenbendazole 50mg/kg p/o SID for 10 days (note extended treatment compared with many

other parasites is needed)

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o Capillaria aerophila

o Trichuroid nematode

o Adults found in trachea and large bronchi (more likely to see adults on endoscopy than other parasites)

– look like white coiled masses

o Adult female 20-38mm, mal, 12-25mm

o Eggs coughed up and swallowed and passed in faeces – may be directly infectious to another host or

via paratenic hosts such as earthworms

o Usually asymptomatic, occasionally coughing, dyspnoea

o Diagnosis – similar radiographic pattern to Aeleurostrongylus. Identifiction of double-operculated egg in

faecal sample (DDx trichuris)

o Treated with fenbendazole 50mg/kg p/o for 10 days

9 Lower respiratory tract disease in dogs

9.1 Functional disorders of the communicating airways

Chronic Bronchitis

• presentation o all breeds affected but esp WHWT, Cocker spaniels, usually middle aged or older o no sex predisposition, obese animals more prone o cough, gag, retch cough, usually progresses, usually worse with excitement / exercise, tachypnoea, ex

intolerance but are usually systemically well o cough usually harsh / dry, usually tracheal sensitivity o increased adventitious lung sound including crackles and wheezes

• diagnosis o is by exclusion o haematology and biochemistry rarely helpful o radiography typically shows a bronchial pattern and may show blobs of mucus in airways o bronchoscopy – typically shows airway hyperaemia, oedema and increased intraluminal mucus,

mottled / irregular surface o BAL cytology – usually neutrophilic in nature but no evidence of sepsis o Blood gas analysis

Changes are rarely pathognomonic but may be helpful in monitoring progression of disease o Should get negative culture

• Treatment o Client communication (i.e. this is not a curable disease and eventual progression is assured, but

progression is often very slow) o Corticosteroids

Oral prednisolone0.5-1mg/kg/day

Then taper after 3-7 days to 0.25-0.5mg/kg/day

Always in conjunction with weight loss program if obese

o Inhaled corticosteroids

Could consider but be aware of sever limitations of this sort of therapy (see above)

o Bronchodilators especially theophylline

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o Treat secondary airway infections as they occur

o Hopeful measures to reduce airway mucus accumulation

Bromhexine

Saline nebulisation and coupage 3-4 X daily

o Prevent obesity

Ciliary dyskinesia

• cilia o 200 on each cell of ciliated epithelium o 9 pairs of outer doublets (each subunit B, subunit A, outer dynein arm, inner dynein arms, nexin link)

and central core of one pair of doublets o hydrolysis of ATP for energy

• can have a variety of structural abnormalities eg lack of dynein arms, displacement of outer doublets, absence

of inner core, shorter outer arms

• may be primary ciliary dyskinesia (i.e. a congenital dfect of cilary doublet structure) or secondary to a variety of

inflammatory airway disorders ie. Acquired ciliary dysfunction

• primary ciliary dyskinesia

o associated with other defects

hydrocephalus, renal fibrosis, renal tubular dilatation, abnormal spermatozoa, abnormal

vertebrae and ribs

Kartagener’s syndrome (ciliary dyskinesia, bronchiectasis and situs inversus totalis)

Usually do not have any neutrophil dysfunction

o Normal dogs have up to 7% cilia abnormal – more than this is needed to Dx ciliary dyskinesia

o Newfoundland, OES, Dobermaan, Dachshund, Bull Mastiff, Springer Spaniel, Pointer, Chow chow,

Rottweiler

o Chronic recurrent upper and lower respiratory tract disease

o Diagnosis

Radiography – to Dx situs inversus, bronchiectasis

Cytology and culture of BAL

Sperm evaluation in male dogs

99TcMAA scintigraphy to determine lack of ciliary movement (see above) – acquire image

every 5 mins – if no movement after 30 mins then dyskinesia

• does not distinguish between primary and secondary ciliary dyskinesia

definitive Dx (difficult) biopsy and electron microscopy of cilia – usually not done on a

commercial basis

ciliagenesis and beat frequency – experimentally can culture cilia – if have primary defect

then all cultured cells will have the defect – of acquired will be normal after culture

o treatment – supportive

• nebulisation, coupage, physio

• airway hydration

• Tx of secondary infections

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9.2 Structural disorders of the communicating airways

Bronchiectasis

o Loss of elastic and muscular portion of the bronchial wall leading to distortion and dilation

o Tubular or saccular

o Caused by vicious cycle of inflammation, release of local inflammatory mediators (mainly from neutrophils)

causing local destruction of supportive connective tissue

o Seen especially in conjunction with ciliary dyskinesia

o May be congenital

Usually due to ciliary dyskinesia

May be due to connective tissue defects

o Acquired

Usually secondary to eosinophilic bronchopneumonopathy, chronic bronchitis, pneumonia

Usually permanent once occurs (occasionally can be reversible in early stages)

o Leads to disruption of mucociliary escalator, pooling of mucous, inflammation, release of neutrophil

lysosomal enzymes with associated local connective tissue destruction

o Usually diagnosed by radiography but can also be appreciated endoscopically

o Treatment is supportive

Hydration

Treatment of secondary bacterial infections

Nebulisation / coupage

Bronchomalacia

o End stage of chronic bronchial disease

o Segmental dynamic aairway collapse, usually during expiration

o Only diagnosed by bronchoscopy or fluoroscopy

o Treatment is merely supportive - ?future role of endobronchial stenting?

9.3 Infectious diseases of the pulmonary parenchyma

o Bacterial bronchopneumonia

• Mostly caused by resident Microflora – especially Staphylococci, Streptococci, Eneterococci, E.coli,

Klebsiella, Pseudomonas, Bordetella, Pasteurella, Bacteroides, Clostridium

• Compromise / evasion of innate immune-defense and mucociliary clearance mechanism

• Inflammation mainly at broncho-alveolar junction

• Diagnosed by combination of clinical suspicion (usually systemically unwell / febrile, clinical signs referable

to the respiratory tract), radiography, bronchoscopy and BAL

• Bacterial isolation can be difficult

o Will frequently isolate these organisms in low numbers from the respiratory tract anyway

o Index of suspicion raised by a profuse, pure growth associated with degenerate neutrophilia

o Intraneutrophilic / macrophage organisms is diagnostic but is an infrequnetgly encountered

cytological picture

  85

• Treatment

o Antibiosis

Empirical therapy

• Implicated organisms are mostly aerobes, about 50% gram positive , 50% gram

negatives, but anaerobic infections also sometimes encountered

• Effective drug therapy should be bactericidal and should attain good

concentration compared with plasma levels, within bronchial secretions i.e.

should be lipophilic

• Beta-lactams are not always good choices – they attain a very low bronchial

secretory concentration compared with plasma. Cephalosporins are better but

not great

• Highest penetration is afforded by metronidazole, fluoroquinolones (but these

have no anaerobic activity and are probably best reserved for problem infections

in which culture and sensitivity data are known), doxycycline and trimethoprim /

sulphonamide combinations

Based on culture / sensitivity

Continue for at least 4-6 week then re-assess

o Adjunctive therapy

Bronchodilators

Nebulisation / coupage

o Viral bronchopneumonia

• CDV, CAV2, parainfluenza, reovirus, herpesvirus, equine influenza recently implicated in some kennelled

hounds

• Majority probably asymptomatic / subclinical and only really cause problems wwhen secondary bacterial

infections arise

• More commonly cause large airway disease and Tracheitis

o Protozoal bronchopneumonia

• Toxoplasmosis, neosporosis appear to be extremely rare causes of protozoal bronchopneumonia in dogs

• Usually seen as part of generalised disease in very young or immunocompromised animals

• Pneumocystis carinii

o Saprophytic organism -opportunist infection

o Rare cause of bronchopneumonia in dogs

o Usually seen in Dachshunds with common variable immunodeficiency

o Most less than a year of age, have rapidly progressive cough, dyspnoea, cyanosis

o Can be diagnosed by organism detection and immunohistochemical staining

o Therapy can be attempted but is usually unrewarding – most dogs succumb to disease

o Fungal bronchopneumonia

Most commonly seen in dogs from SE United States (Histoplasmosis, Blaastomycosis) or dry arid areas of the south

/ southwestern US (Coccidiomycosis)

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Usually diffuse / nodular interstitial pneumonia associated with marked hilar lymphadenopathy

Associated with systemic signs in majority of cases

Aspergillosis

• Occurs as opportunistic disseminated fungal infection in immunocompromised host

• Usually GSDs

• More commonly A. terreus and A deflectus than A. fumigatus and very rare occurrence in the UK

9.4 Inflammatory diseases of the pulmonary parenchyma

Aspiration pneumonitis

o I’ve put aspiration pneumonitis here and emphasised pneumonitis not pneumonia to highlight that this condition is

primarily an inflammatory airway disease, though it is commonly assumed to be infectious in origin

o The initiating factor is chemical alveolar injury due to aspirated material from the gastrointestinal tract and physical

irritation due to food particulate matter

o Secondary infection is very common and antibiosis plays an important part in management but it is important to

remember that dogs with aspiration pneumonitis will rarely, in my experience, make miraculous recoveries with

antibiotics alone

o Common initiating factors include

• General anaesthesia

• Megaoesophagus

• Laryngeal paralysis

• Airway / pharyngeal surgery and procedures

• CNS depression

• Iatrogenic

o Barium swallows (always avoid these in patients with potential megaoesophagus – the majority

can be diagnosed with plain radiography)

o Nutritional support

• Recurrent vomiting / delayed gastric emptying

• Myasthenia gravis

Severity if clinical signs depends on amount of material aspirated, its particulate content, its pH and its enzymatic

content and bacterial ‘load’

Phase 1- immediate chemical lung injury

• Haemorrhage, bronchial epithelial degeneration, wall oedema, destruction of type I pneumocytes,

increased capillary permeability and alveolar flooding

• Atelectasis, collapse and plugging of small airways

Phase 2 – inflammatory response

• Begins 4-6 hrs after aspiration

Phase 3 – secondary bacterial infection

o Diagnosis usually made on basis of predisposing factor identified, clinical signs (acute respiratory compromise, soft

productive cough) signs of alveolar lung infiltrate usually cranioventral lung lobes on lateral thoracic radiograph

o Tracheal wash / BAL if patient anaesthetised to gain material for culture and sensitivity

o Treatment

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• Prevention

• Oxygen therapy

• Bronchodilators

• Intravenous fluid therapy

• Very frequent nebulisation and coupage, regular turning, measures to prevent further atelectasis

• Monitoring of arterial blood gases

• Antibiosis – intravenous route, attention to dose and frequency

o Good empirical choices are trimethoprim / sulphonamides, cephalosporins, and in hospital

acquired infections fluoroquinolones / metronidazole or second generation cephalosporins

o Give for minimum of 3-4 weeks

o Monitor radiographically for improvement q 3-4 days

Eosinophilc bronchopneumonopathy (pulmonary infiltration with eosinophils)

Diverse group of airway sensitivity disorders – probably not one disease but a group Does not necessarily imply an allergic aetiology Seen most commonly in young dogs of mid-sized breeds – predisposition in Huskies seen Typical signs are intractable initially dry becoming productive cough +/- signs of exercise intolerance and sometimes

mild weight loss / tachypnoea

Occasional animals will present with fulminant pulmonary signs and dyspnoea

Thoracic radiography may be highly variable

• May appear normal

• Mild bronchointerstitial infiltrate

• May see marked granulomatous interstitial nodules, sometimes to extent that neoplasia may be suspected

• May have bronchiectasis

Peripheral eosinophilia is not a dependable finding

Bronchoscopy usually demonstrates airway inflammation and some degree of airway mucus / pus accumulation.

Pus may be extremely inspissated and is often misdiagnosed based on appearance as bacterial bronchopneumonia

or foreign body

BAL is usually diagnostic – massive eosinophilic predominance

• Princcipal DDx is airway parasitism

Treatment

• Prognosis is generally good – condition is exquisitely sensitive to corticosteroids but warn owners that

around 50% of cases relapse and need long term therapy

• My general approach is

o To always worm these dogs with fenbendazole at lungworm dose

o To introduce oral prednisolone at 1mg/kg/day initially until clinical signs go into remission then to

rapidly taper over 1-2 weeks to 0.5mg/kg p/o EOD for a further 1-2 months before stopping

o If clinical signs relapse then I tend to repeat this but with the addition of inhaled fluticasone which

is continued twice daily beyond reduction in the prednisolone

o If relapse occurs with this then I continue with prednisolone at 0.5mg/kg EOD to every

third day

o If signs are kept in remission then attempts to reduce fluticasone frequency are regularly

performed

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• In some fulminant cases, hospitalisation, oxygen support, bronchodilators and aggressive thoracic

physiotherapy are helpful

• If pus is extremely tenacious, hydration of the patient by intravenous fluid therapy is very useful

9.5 Cardiorespiratory parasitism

Angiostrongylus vasorum

• Metastrongyloid parasite ubiquitous in UK but especially prevalent in certain ‘hotspots’ which include South Wales

(especially Swansea), Cornwall, Bristol, Southampton, Surrey, the Northwest Midlands and Ireland

• Dog and fox are definitive host, lifecycle requires intermediate host which are usually slugs and snails (and frogs?)

• Lifecycle: o L1 larvae shed in faeces of definitive host

o Penetrate foot process of intermediate host, develop from L1 to infective L3 stage in intermediate host

(takes c17 days)

o Intermediate host is eaten by definitive host

o L3 larvae penetrate wall of small intestine and migrate to liver via mesenteric lymph nodes thence to right

side of heart via post sinusoidal circulation and caudal vena cava. During this migration two further moults

occur, the parasite developing from L3 to immature L5. Both male and female worms occupy small

pulmonary arterial vessels rather than the right ventricle or RVOT except in very heavy infestations

o Adults may reach the right side of the heart from 10 days post infection but require a further 23-33 days to

become sexually mature. Adult female worms are up to 25mm in length and have a grey translucent body

with dark spiral ovigut

o After sexual reproduction females are oviviparous and will produce eggs lifelong unless adulticide therapy

is given

o L1 larvae penetrate alveolar spaces and are coughed up and cleared by mucociliary escalator, being

swallowed into GI tract and passing intact to infect intermediate hosts which are adapted to feeding on

faeces. Pre-patent period is reported between 38 and 60 days.

• Affected dogs are usually young, majority being <12-18months. Certain breeds appear over-represented especially

Staffordshire Bull Terriers and CKCS

• Pathophysiology

o Angiostrongylus infestations can cause a bewildering variety of clinical signs and I would recommend

worming any dog with compatible signs. In general respiratory signs predominate but I have seen so many

different presentations of angiostrongyliasis as to make it a common feature on most differential diagnoses

lists!

o Most effects are due to pulmonary disease caused by L1 parasite penetration of the alveoli with associated

haemorrhage, granulomatous inflammation, vasculitis/thrombosis and eventual fibrosis. Most severe

inflammation occur 30-60 days post infection

o Additionally the large amount of vasculitis, small vessel thrombosis and shear stress placed on platelets in

areas of vascular injury, frequently lead to:

Chronic DIC caused by excessive thrombosis and consumption of coagulation factors (especially

factors V and VIII)

Secondary immune-mediated thrombocytopenia

Consumptive von-Willebrands deficiency

Thromboembolic disease

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Haemolysis

Systemic inflammatory response syndrome / acute respiratory distress

• Clinical signs

o Most common is coughing and tachypnoea. Cough is usually soft but persistent and sometimes becoming

harsh. Haemoptysis is seen in heavy infestations

o Less commonly encountered signs

Bleeding diatheses, most commonly

• Acute CNS bleeds – some of these dogs will develop massive intracranial haemorrhage,

often after fairly mild trauma, due to coagulopathy – their prognosis with adulticide

therapy and with appropriate investigation and supportive care is surprisingly good and

most will regain full function

• Intrapulmonary and intrabronchial haemorrhage which may be sudden, massive and fatal

• Bleeding within craniofacial soft tissues especially

o Periorbital bleeding (often initially suspected to be cellulites, FB, retrobulbar

abscess etc)

o Scleral haemorrhage

o Sublingual haematomata

Stunted growth

Episodic collapse (suspected due to large worm burden causing sudden transient pulmonary

arterial outflow obstruction)

Spinal pain and focal spinal signs similar to IVDD or FCE – suspected that most of these are due

to haemorrhage rather than aberrant parasite migration

Ocular changes

• Granulomatous retinopathy (usually found as incidental findings)

• Haemorrhage

• Sometimes free larvae can be seen within the eye – best seen on distant direct

ophthalmoscopy as they swim infront of the tapetal reflection!

• Diagnosis

o Best made if you maintain a high index of suspicion for it! Easier in areas where parasite is endemic

o Laboratory findings

Inflammatory leukogram and peripheral eosinophila are inconsistent findings

Mild hypercaalaceemia sometimes seen (?hypercalcaemia of granulomatous disease)

Hyperglobulinaemia (usually beta-2 fraction) is often seen duee to acute phase inflammatory

response but is not pathognomonic

Coagulation abnormalities consistent with DIC or ITP may be seen

• Extended PT, APTT, thrombocytopenia, shistocytosis , positive FDP or D-Dimer

o Respiratory form

Thoracic radiographs will usually show a diffuse, patchy alveolar / interstitial infiltrate, in my

experience most marked in the caudodorsal lung fields often vasculocentric in nature

• Large infiltrates may appear almost nodular in nature but will usually not have very sharp

outlines

• Perihilar Lymphadenomegaly may be seen

• Evidence of right sided heart enlargement and pulmonary arterial tortuosity is not

commonly seen

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Bronchosopic findings are relatively non-specific – airways appear inflamed, frequently contain

excessive mucus, blood and sometimes purulent discharge, macroscopic worms are not seen.

BAL frequently demonstrates L1 larvae though are difficult to distinguish from other metastrongyle

parasites (esp Crenosoma vulpis)

Echocardiography is seldom helpful but may show sigsn consistent with pulmonary hypertension

and right ventricular pressure overload – I have yet to see echo evidence of worms within the

RVOT and pulmonary vasculature on echo. Angiostrongylus is a lot smaller than Dirofilaria adults

which may explain why we don’t see them compared with the ‘tram-lines’ of Dirofilaria

Faecal analysis

• Will frequently demonstrate L1 larvae but since these may be intermittently shed it is not

foolproof and a negative faecal should not be used to ‘rule out’ angiostrongyliasis. Most

species of lungworm are difficult to distinguish from each other and some laboratories

have poor expertise in diagnosing Angiostrongylus.

o Haemorrhagic diatheses

Extended PT and APTT (take care when collecting samples for coagulation panel – technique and

sample handling need to be exemplary if artefactual changes are to be avoided)

• Usually both are extended but sometimes see one without the other

• Most common DDx of acquired coagulopathy are anticoagulant rodenticide toxicity and

chronic DIC (especially secondary to neoplasia, inflammation or vascular disease). In any

dog initially suspected of anticoagulant rodenticide poisoning which fails to respond to

Vitamin K administration consider angiostrongyliasis as a possible diagnosis!

Platelet count often reduced mildly to moderately (in case of chronic DIC or recent haemorrhage),

or severely with ITP. After a recent bleed reactive thrombocytosis may be seen

FDP and D-Dimer may be positive due to DIC or thromboembolism

Schistocytes may be seen due to RBC fragmentation

CNS disease caused by angiostrongyliasis is usually diagnosed by a combination of

neurodiagnostic imaging (if available and financially practical), identifying coagulopathy and

demonstration of L1 larvae on BAL or faecal examination

• It is my opinion that, unless there is a mitigating financial limitation, regardless of local

availability of equipment, neurodiagnostic imaging should only be performed by a

radiologist with expertise in neuroradiological techniques to distinguish CNS

haemorrhage (which often requires specialised scanning techniques) and should be only

undertaken if extensive patient monitoring (during the scan itself which requires MRI-

compatible monitoring equipment and a veterinary anaesthetist to be present) and critical

care facilities are available.

• Therapy

o Acute / emergent cases

May require oxygen therapy, transfusion support, management of intracranial haemorrhage

o Chronic cases

No clinical trials have been performed to establish the ‘best’ course of treatment

By consensus most people regularly treating angiostrongyliasis find fenbendazole at a dose of

50mg/kg (of fenbendazole not the carrier granules / liquid!) for 5-10 days to be efficacious. Do not

rely on intermittent routine single dose worming to be effective in clearing adults or use recent

worming as a reason to rule it out. In my experience most dogs with angiostrongyliasis are

regularly wormed!

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I generally recommend worming in this fashion twice at an interval of around the pre-patent period

ie two sessions 1-2 months apart then regularly eg every 3-4 months therafter recognising that the

dog will be living in an environment where there are probably infested intermediate hosts

• Prognosis

o Generally good if picked up early and treated. Untreated angiostrongyliasis can be a fatal disease. In

severely affected cases long term sequelae of granulomatous lung disease and persistent CNS deficits can

be seen.

o Stunted dogs will often ‘catch up’ if treated when young

o Re-infestation appears uncommon if

A) regular worming continues

B) the dog ‘grows out’ of eating snails!

Crenosoma vulpis

o Also a metastrongyloid nematode with an indirect lifecycle requiring infection of an intermediate molluscan host with

infective L1 larvae, in which they develop to L3 before being ingested by the definitive host

o Unlike Angiostrongylus vasorum adult stages are not confined to pulmonary vasculature and may be found within

airways where they are sometimes seen as small white worms on Bronchoscopic examination. Prepatent period is

considerably less than in Angiostrongyliasis and has been reported as 17days

o Larvae may be demonstrated in both faeces and BAL fluid but may be difficult to distinguish from A. vasorum.

o Adult dogs appear more commonly affected than juveniles c.f. A.vasorum

o Treatment with fenbendazole appears to be effective

Oslerus osleri

o Has direct lifecycle not requiring intermediate host

o Larvae emerge from nodules and expectorated – swallowed

o Nodules at tracheal bifurcation highly suggestive (may be seen radiographically but best diagnosed on

bronchoscopy)

o Finding of larvae and ova on BAL

o Clinical signs usually seen in dogs <1yr of age

o Chronic cough, rarely systemically unwell

o Treated with fenbendazole

Capillaria aerophila

o Uncommon cause of respiratory disease – most infections are asymptomatic

9.6 Non-infectious / inflammatory diffuse disorders of the interstitial compartment

o Remember primary differential diagnoses of radiographically diffuse (aka hazy, lacy , unstructured) interstitial

patterns include

• Artefactual

o Under-exposure

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o End-expiratory exposure

• physiological

o Patient obesity

o ‘old dog lung’

• haemorrhage

• oedema (remember this needn’t be cardiogenic only)

• infiltrative neoplasia eg lymphoma

• fibrosis

• paraquat exposure

• contusion

o diseases of the interstitial compartment represent a diagnostic challenge – if a disease process is purely interstitial

then results of diagnostic testing including bronchoscopy and bronchoalveolar lavage may be normal or at least not

in keeping with the severity of the radiographic / clinical findings

o in some cases only surgical / thoracoscopic biopsy yields sufficient appropriate material for histopathological

diagnosis but these procedures are invasive, expensive and not without risk to the patient – very careful client

counselling may be required!

o Haemorrhage

Diffuse haemorrhage within the lung is radiographically indistinguishable from other diffuse increases in soft tissue /

fluid opacity

Index of suspicion is raised in patients with

• Known bleeding disorders

• Known respiratory parasitism

• Evidence of bleeding diatheses elsewhere

Parenchymal bleeding may be seen most frequently with

• Anticoagulant rodenticide toxicity

• Thrombocytopenia

• Angiostrongyliasis

• Neoplasia

Investigation should include:

• assessment of a platelet count (remembering that a manual count should be performed in case of doubt).

Clinically significant bleeding usually occurs with counts <50 X 109/l but there is nothing magic about this

number – dogs will often bleed with counts higher than this!

• Assessment of prothrombin time (PT, assesses extrinsic and common pathway), and activated partial

thromboplastin time (APTT, assesses intrinsic and common pathway). Whole blood clotting time can be

examined but many vets confuse this with activated clotting time – if you are not using specially coated

tubes, blood placed in a glass tube may take 7-8 minutes to clot normally in dogs

• Assessment for causes of acquired coagulopathy (rodenticide poisoning, liver failure, malabsorption,

parasitism, neoplasia)

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• Assess buccal mucosal bleeding time (assesses primary haemostasis i.e. platelet number, platelet function

AND Von Willebrand’s status), should be <4mins.

• Faecal analysis / trial fenbendazole therapy for angiostrongyliasis

• Possibly further assessment for DIC (combination of coag panel D-dimer / FDPs and platelet count)

Treatment should include:

• Identification and correction of underlying cause

• May include specific therapy

o Vitamin K in rodenticide toxicity, liver failure, malabsorption

o Worming

• Supportive therapy

o Whole blood transfusion, fresh plasma, FFP, cryoprecipitate

o Idiopathic Pulmonary Fibrosis / Cryptogenic Fibrosing Alveeolitis

• A.k.a. ‘Westie lung’

• Also seen in Scottish terriers and other small breed

• Median age 9 years, slow progression of dyspnoea, exercise intolerance, cyanosis and cough

• Due to progressive alveolar septal fibrosis and epithelialisation, squamous metaplasia and inflammation

• Usually increased interstitial pattern n radiography, CT can be useful and is being evaluated experimentally

• BAL usually normal or neutrophilic infiltrate

• Most dogs develop progressive hypoxaemia

• Median survival time from first onset of signs is 15 months, from diagnosis is 7 months

• Corticosteroids and bronchodilators are mainstay of therapy

• Anti-fibrotic agents are almost certainly too late to be effective in this condition

o Paraquat poisoning

• 1,1’-dimethyl-4,4’-bipyriddylium dichloride

• nitrogen herbicide

• toxic dose around 40-50mg/kg (around 1ml is toxic dose in average sized dog)

• malicious poisoning or accidental exposure to discarded paraquat

• cyclic reduction / oxidation after ingestion results in superoxide radical formation and disruption of

membranes of type I and II pneumocytes

• initial exudative pneumonia then progressive fibrosis and hypoxaemia over 2-4 days

• vomiting dyspnoea, hypoxaemia, cyanosis, respiratory distress

• diagnosis

o severe, largely dorsal distribution, interstitial opacity (‘white out’), usually sudden onset

o dyspnoea

o severe hypoxaemia

o can detect metabolites in urine (use human toxicologist)

• treatment:

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o if acute, known exposure

emesis and activated charcoal

IV fluid therapy

Diuresis to enhance renal excretion

o If presented when in respiratory failure and known paraquat

Euthanase on humane grounds – survival is not reported

o There is no specific treatment or antidote and paraquat poisoning is uniformly fatal after exposure.

Supportive therapy may be attempted: oxygen support (though it is theoretically contraindicated

due to enhanced superoxide radical production), use of acetylcysteine. Euthanasia should always

be considered in humane grounds unless very small amounts have been ingested

9.7 Nodular disorders of the interstitial compartment

o Principal differential diagnoses are

Solid tumour

• Primary lung

• Metastatic lung

• Thoracic wall

Lymphoma

Lymph node

Granuloma

• Mycotic

• Parasitic (especially angiostrongyliasis)

• Mycobacterial

• Eosinophilic (esosinophilc bronchopneumonopathy)

• Lymphomatoid granulomatosis

• Foreign body

Abscess

Haematoma / haematocyst

Fluid-filled bronchus

o Neoplasia of the lung and bronchial tree

• Metastatic tumours >>>cmn than primary tumours

• Incidence of primary tumours 2/100,000 cats, 5/100,000 dogs approx

• 25-50% are asymptomatic at presentation

• cough is most common presenting sign, but may also see-

o pneumothorax

o haemothorax

o haemoptysis

o dyspnoea

o lameness due to metastasis or hypertrophic osteopathy

• signs of systemic illness eg anorexia, wt loss are often not seen

• most are adenocarcinomas but bronchial carcinoma and squamous cell carcinoma also common

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• 50% metastasise, usually locally (local lymph nodes, other intrathoracic sites) but occasionally to bone and

CNS

• Diagnosis

o in one study radiographs failed to identify necropsy confirmed primary or secondary lung tumours

in 13% of cases

o 3 views, inflated, excellent quality radiographs

o CT may be advantageous

o May be nodular but can be diffuse alveolar / interstitial or miliary pattern

o SCC usually perihilar, adenocarcinoma usually peripheral, bronchial carcinoma usually middle of

lobe

o May attempt u/sound guided biopsy

Tru-cut: diagnostic accuracy 83%, fatality rate 12%, pneumothorax in 31% cases

FNA – diagnostic accuracy 79%, safest with lesions abutting thoracic wall

• Therapy

o surgical resection is Tx of choice

o best prognosis is tumours <5cm diameter in peripheral location with no lymph node involvement

o overall median survival time is around 12 months but factors examined include:

peripheral location (MST 16m) Vs entire lobe involvement (MST 8m)

tumour size <5cm diameter (MST 20m) Vs >5cm (MST 8m)

lymph node involvement (MST 30- 60d) Vs no node involvement (MST 12-15m)

low tumour grade (MST 16m) Vs high tumour grade (MST 6m)

no clinical signs (MST 18m) Vs clinical signs of systemic illness (MST 8m)

o Lymphomatoid granulomatosis

• Unusual nodular interstitial disease, poorly reported in dogs

• Behaves like a lymphoid neoplasm

• May respond to C/O/P based protocols

• Little useful information in veterinary literature