EIPH Flashcards

1
Q

What is EIPH?

A

Exercise induced pulmonary haemhorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the clinical signs of EIPH? (5)

A
  • None!
  • Most don’t bleed significantly to the point where they get epistaxis usually! EPIH is the most common cause of epistaxis, but not every horse will bleed enough with EIPH will have epistaxis
  • poor performance
  • sudden onset exercise limitation
  • swallowing after exercise
  • Epistaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do we diagnose EIPH? (2)

A

Endoscope

Cytology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the clinical significance of EIPH?

A
  • a large proportion of horses are positive following racing in endoscopic surveys
  • there is no relationship between the presence or absence of EIPH and finishing place
  • When they bleed a lot, can result in poor performance, but not every horse with small amount of EIPH will result in poor performance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pathogenesis of EIPH? (2 theories)

A
  • UNKNOWN – controversial
  • haemorrhage is from pulmonary rather than bronchial vessels
  • typically located in the caudodorsal lung lobes
  • Capillary stress failure theory
  • High pressures in pulmonary vasculature due to CO and capillaries rupture
  • Mechanical theory
  • As horse gallops, pressure from GI onto diaphragm and caudal lung lobes, result in mechanical failure
  • Haemorrhage is always from pulmonary vessels and caudal dorsal vessels where pressures are highest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the CAPILLARY STRESS FAILURE THEORY?

A
  • Pressures generated within the pulmonary capillaries during exercise exceed their stress failure point
  • Pulmonary capillaries are an inevitable anatomical weak point due to normal equine cardiopulmonary physiology:
  • THIN WALLED
  • normal Thoroughbreds become hypoxic and hypercapnic during exercise, at peak gallop. That may be an important contribution as to why you get vasoconstriction
  • Hypoxia induced vasoconstriction, don’t perfuse the part that doesn’t have enough oxygen! Therefore by doing this, increase pressure in lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why does EIPH affect the CdD lobes?(3)

A
  • Higher blood flow
  • lower intrinsic vascular resistance – but if this is exacerbated by vasoconstriction, may have important part
  • Displacement of the diaphragm causes transient falls in alveolar pressure
  • Lower alveolar pressure leads to greater transmural pressure
  • Wall stress: Transmural pressure x radius/ wall thickness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What predisposes a horse to EIPH? (5)

A

Age

Type of horse

  • LOWER AIRWAY DISEASE
  • E.g. IAD or RAO – important risk factor
  • Need to identify the risk factors and take them away
  • UPPER AIRWAY DISEASE
  • CARDIAC DISEASE
  • Increases pulmonary artery pressure
  • Atrial fibrillation
  • Mitral valve disease
  • Only clinical sign for a cardiac abnormality might be bleeding at exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How can we diagnose EIPH? (5)

A
  • Clinical evidence of EIPH
  • only present in more severe cases
  • Bilateral epistaxis, but only present in most severe cases
  • Endoscopy
  • Can be scoped as screening process
  • Bronchoalveolar lavage
  • RBCs, haemosiderophages
  • Radiography
  • Not something used regularly
  • Scintigraphy
  • currently experimental
  • Not something used regularly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can be seen here?

A

EIPH

RBCs, haemoglobin within foamy macrophages – haemosiderinphages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can be seen here?

A

EIPH

Lots of blood and coating walls of trachea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is this?

A

Mild case of EIPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can we manage EIPH? (3)

A
  • Difficult to manage
  • Identify and address any predisposing diseases
  • Break haemorrhage-inflammation cycle
  • Modify training programme to reduce episodes
  • Dust-free environment
  • Furosemide
  • Not allowed in horse races in UK, shown to protect from developing of EPISTAXIS, not EIPH- so less likely to bleed from their nose if they have this
  • Probably works by reduced circulation volume – may reduce circulation BP and it is also it is a weak vasodilatory effect
  • ?antibiotics
  • Horses that have had a severe bleed will need treatment, blood is also culture media for bacteria also – so antibiotics to prevent pneumonia after severe bleed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What drugs can we use for EIPH and what 2 effects does it have?

What is the problem in the UK?

A
  • Diuretic effect
  • Reduce circulating volume
  • Reduce weight
  • Vasodilator effect
  • In USA, but not UK, horses can race on furosemide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a nasal strip? What do they do?

Where can and can’t we use them?

A

•Hold nostrils open and widely used in eventing world, not allowed in racing in the UK at this point – can train with them though

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the prognosis for EIPH?

A
  • GOOD TO FAIR
  • if associated with respiratory infection or other predisposing cause can be identified and treated
  • or having minimal impact on performance
  • POOR
  • for idiopathic bleeders with performance limitations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the impact of EIPH on UK racing? (3)

A
  • No restrictions on ‘bleeders’
  • Furosemide is not allowed for racing
  • Nothing to make them rest them
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the effect of EIPH on the ROW horse racing? (2)

A
  • 3 Strikes and out
  • If epistaxis, not acceptable – they are removed from racing
  • Furosemide allowed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What diseases are foals susceptible to? (3)

A
  • Infectious causes (bacterial)
  • Congenital abnormality
  • Sepsis, trauma, other
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What diseases are weanlings susceptible to?

A

•Infectious causes (bacterial) & contagious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What disease are youn adults susceptibe to?

A
  • Inflammatory airway disease
  • Infectious causes (bacterial and viral and mycoplasma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What disease are old horses susceptible to?

A

•Recurrent airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

IS URT more or less common than LRT?

What type of horse is it more common in?

A
  • Less common than lower airway disease
  • Mainly young horses (yearlings and two-year-olds)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What viral (3) and bacterial (1) disease is tehre of the URT?

A
  • VIRUSES
  • Equine influenza
  • Equine Herpes Virus 1&4
  • Equine Viral Arteritis** Notifiable Disease
  • BACTERIA
  • Streptococcus equi equi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What viral (4), bacterial (5) and mycoplasma diseases are there of the LRT?

A
  • VIRUSES
  • Equine influenza
  • Equine Herpes virus 1&4
  • Equine Rhino virus
  • Equine Viral Arteritis ND
  • BACTERIA
  • Streptococcus zooepidemicus
  • Streptococcus pneumoniae
  • Pasteurella/actinobacillus
  • Rhodococcus equi
  • Streptococcus equi equi
  • MYCOPLASMA
  • M. felis
26
Q

What horses are most at risk of bacterial infection?

  • Strep. pneumoniae
  • Strep. zooepidemicus is the most common isolated pathogen from equine lung
  • Pasteurella/Actinobacillus spp.
A

•Horses entering training yards for the first time (2 and 4 years) are at particular risk

27
Q

M. Felis causes what?

How to we identify?

How do we treat?

A

LAD

  • Culture from tracheal aspirates requires specialised laboratory and strict transport conditions
  • Sensitive to oxytetracycline
28
Q

What do the 5 different EHV cause?

A
  • EHV1 - respiratory disease, abortion, neonatal, neurological
  • EHV2 - respiratory disease in foals
  • EHV3 - penile vesicles
  • EHV4 - respiratory disease
  • EHV5 – Equine Pulmonary Nodular Fibrosis
29
Q

What is the epidemiology of EHV 1 and 4?

A
  • EHV1 and EHV4 endemic in UK and worldwide
  • Incidence: 4.4 cases/100horses/month
  • 75% of horses have latent infection acting as a reservoir for on-going infections
  • Become infected when young, then are permanenetly infected for life – stress will reactive and lead to spread throughout herd.
  • “Stress” may activate latent infection
  • transport, other illness, influenza, vaccinations
30
Q

What is the pathogenesis of EHV 1 and 4?

A
  • Inhalation / direct contact much more important than aerosol spread
  • Incubation 3-7 days – SLOW PROGRESSION in yards
  • Replicates in URT epithelium
  • Transported to other organs in T lymphocytes, can induce vasculitis (and abortion due to this)
  • Viraemic for up to 3 weeks
  • Vasculitis
  • May be accompanied by secondary bacterial infection
31
Q

What is the pathogenesis of eqine influenza?

A
  • Inhalation
  • Infects epithelial cells of upper and lower airways: larygnitis, tracheitis, bronchitis, bronchiolitis - Incidence 0.8/100horses/month
  • No viraemia phase
  • Attaches to the epithelium via Haemagglutinin spike and gains entry to the cells
  • Styas within resp tract and therefore diagnosis will require sampling of this tract
  • Loss of ciliated epithelium, compromise of the mucocillary mechanism
  • May be associated with secondary bacterial infection
  • Severity of signs depends on dose of virus
32
Q

What is equine rhinovirus? Where is it most common?

A
  • Picornavirus, types 1 and 2
  • Role as a pathogen is controversial
  • can be isolated from asympomatic horses as well as those with signs of URTI – don’t know the importance of it
  • Most common in young horses
33
Q

What is the pathogenesis of equine viral arteritis?

A
  • Transmission by respiratory and venereal routes
  • direct contact with an infected horse and its secretions
  • Reservoir of infections
  • Stallions that are chronic shedders and until they are castrated, will continue to spread disease
  • Prevalence of seroconversion
  • Thoroughbreds: 0.5 - 6% - severe signs if infected
  • Standardbreds: 80% - mild signs
34
Q

What does equine viral arteritis cause? (4)

A

NOTE: NOTIFIABLE

  • abortion and still birth
  • peripheral oedema
  • rhinitis and bronchitis/bronchiolitis
  • Respiratory signs mild
  • conjunctivitis and periorbital oedema
35
Q

Why is there variability of pathogenicity of EVA strains?

A

•Replicates in macrophages and endothelial cells and disseminates via the circulatory system

36
Q

What supportive treatment can we give for respiratory infections? (3)

A
  • Rest
  • Improve environement - dust free management – to prevent IAD following this
  • Anti-pyretics
37
Q

How do we manage an EHV 1 outbreak according to the national trainers federation and TB breeders association?

A
  • Impose isolation policy on premises
  • Serology on all in-contacts
  • Separate negative and positive horses, re-test two weeks later
  • Repeat until all horses have two negative samples
  • NB - these are totally voluntary schemes.

Vets important fomite for spread of disease

38
Q

What are the neonate respiratory diseases?

A
  • Neonatal septicaemia (bacterial pneumonia)
  • Viral pneumonia
  • Usually secondary and failure of passive transger plays an important part
  • Respiratory distress syndrome
  • Meconium aspiration
  • Aspiration pneumonia
  • Usually occurs with bottle fed foals, foals should not be bottle fed!
  • Haemothorax and pneumothorax
  • Central respiratory depression
  • Non-respiratory disease
39
Q

What are the risk factors for foal resp disease? (10)

A
40
Q

What is respiratory distress syndrome and what is it associated with (2)?

A
  • Atelectasis (failure of lungs to expand) due to
  • inadequate surfactant function
  • structurally immature lung and muscles of respiration
  • associated with prematurity and dysmaturity
  • Maturity of lungs requires formation of surfactant to break down lung surface tenion so airways can be patent
41
Q

What is the pathogenesis of meconium aspiration?

A
  • Stress in utero or during parturition leads to defecation,
  • meconium enters airways with fetal fluid,
  • aspirated when foal is born and starts breathing
  • chemical pneumonia develops – poor prognosis
  • secondary bacterial pneumonia
42
Q

What are the clinical signs of meconium aspiration? (2)

A

Respiratory distress

Nasal discharge

43
Q

How can we diagnose meconium aspiration? (2)

A
  • meconium staining
  • Faecal material down nostrils
44
Q

What can cause aspiration pneumonia in foals? (3)

A
  • Dysphagia
  • neurological - uncommon, transient, manifestation of NMS
  • Cleft palate
  • Inappropriate bottle feeding
  • very common in sick foals with inexperienced nursing staff
  • Largely due to inappropriate poor management through bottle feeding! DO NOT BOTTLE FEED A SICK FOAL
45
Q

What are the common causes of PNEUMOTHORAX & HAEMOTHORAX in foals? (2)

A
  • trauma at birth
  • rib fractures are common and affected foals are often asymptotic
46
Q

What is Perinatal Asphyxia Syndrome and when is it apparent?

A
  • Ischaemia, oedema and reperfusion injury to foal’s brain, kidneys, intestine and other organs due to lack of oxygen
  • In utero hypoxia
  • Interruption of oxygen supply during birth
  • May not be apparent until the foal is 12-24 hours old
  • Severe cases may have central respiratory depression and might stop breathing completely
47
Q

What events often lead up to Perinatal Asphyxia Syndrome?

A
  • Foals born through dystocia, get brain reperfusion after ischaemic event, results in multi organ failure
  • Born normal and within 12-24h, become a bit ill and then can become recumbent
48
Q

Why do we need to be careful with cardiac auscultation in foals? (4)

A
  • not a sensitive diagnostic tool
  • extensive parenchymal disease may be unremarkable
  • normal foal lungs have harsh bronchovesicular sounds, little skin, don’t sound like normal adult horse lungs so often difficult to differentiate pathology from these
  • crackles are present in the ventral dependent side if in lateral recumbency
49
Q

What is this?

A

BACTERIAL & ASPIRATION PNEUMONIA

Focal, bronchialveolar

ventral and hilar area

50
Q

What is this?

A

ATLECTASIS

Alveolar

Premature foal

No visible lung tissue, can only see cartilage enclosed main stem bronchioles

51
Q

What is this?

A

VIRAL PNEUMONIA

Diffuse, Interstitial

52
Q

Why do we need to be careful when assessing MM colour?

A
  • Cyanosis: < PaO2 30 - 40 mmHg
  • Will only come when arterial oxygen below 40mmHg, wont see it above this
53
Q

What signs should we be looking out for in foal MM?

A
  • Also looking for signs of sepsis: congestion/injection, petechiae
  • Results in congestive MM
  • Inappropriate MM vasodilation in a face of an animal that is hypovolaemic

Right pic - pinna of ears with petechial haemorrhage

54
Q

Rather than a diagnosis, what is it more important to do in foals? (3)

A
  • Identify sepsis
  • Determine need for respiratory support
  • Oxygen insufflation bottom pic
  • Top pic – sternal on a ventilator to improve lung function
  • Determine need for general supportive care
55
Q

What bacterial pneumonia is seen in weanlings> (4)

A
  • Strep. equi equi,
  • other Streptococcus spp.
  • Pasteurella / actinobacillus spp.
  • Rhodococcus equi
56
Q

What parasitic pneumonia is seen in weanlings?

A

•Parascaris equorum – important cause of mild nasal discharge to weanling – yearling age group, fairly normal sub mandibular LN, discharge whiter than creamy of strangles, not typically pyrexic. Also important cause of GI disease

57
Q

Where might Combined immunodeficiency syndrome be seen in weanlings and what is it?

A
  • Seen in arabs
  • No B-cells or T-cells
  • As soon as maternal antibodies go – they get every infection going and often die
58
Q

What is the pathogenesis of Rhodococcus Equi?

A
  • Inhaled pathogen
  • Ingested from soil (via faeces)
  • Foals 2-6 months of age
  • As Maternally derived Antibodies reduces
  • Intracellular survival
  • Likes to live within macrophages, so they cannot target it
  • Granuloma formation and abscess formation (bottom pic)
  • Respiratory, intestinal, sporadic, bone
  • Also non-septic synovitis
  • Farms that have this will usually get it year to year as lives in soil
59
Q

What is the problem with Parascaris Equorum?

A
  • Not a major pathogen
  • Can cause transient nasal discharge as migrating through lungs
60
Q

What do foals with COMINBINED IMMUNODEFICIENCY SYNDROME present with?

A

•Affected foals frequently present with respiratory disease at around 2 months of age