Equine respiratory, cardio, head and neck Flashcards
How to determine if a horse’s respiratory disease is infectious?
Compatible clinical signs - fever, dull, outbreaks, specific to agent
Detection of infectious agent - culture, PCR, virus isolation
Detection of immune response against infectious agent - antibodies (usually ELISA)
What is the main subtype of Equine Influenza in the UK? Why is there a problem compared to previous strains?
H3N8
Displayss more antigenic drift (changes surface proteins) so vaccines less able to prevent all outbreaks
Pathophysiology of Equine Influenza?
Loss of ciliated epithelium:
0
Exposes URT to secondary bacterial infection
Clinical signs of Equine Influenza?
Fever up to 41C Cough: dry and hacking -> moist Oedema and hyperaemia of URT Nasal discharge: serous -> mucopurulent Lethargy, inappetence +/- muscle soreness
Incubation and recovery periods for Equine Influenza?
Incubation period = 1-5 days (proportional to 1/virus dose)
Recovery usually complete in 1-3 weeks unless secondary respiratory infections occur
Diagnosis of Equine Influenza?
Usually in outbreaks
Lymphopaenia, neutropaenia initially
Later monocytosis, neutrophilia and hyperfibrinogenaemia
Virus isolation from nasopharyngeal swabs or tracheal wash
Serology: rising antibody titre in serum (4 fold rise) over 14 days (care: vaccination)
Nasal swab direct ELISA
Treatment of Equine Influenza?
Supportive care – hydration, NSAIDs, air hygiene
+/- Antibiotics for secondary bacterial infections
+/- Antivirals - mixed evidence, cost
Generally improve after 7-10 days
Require prolonged period of rest (1 week off for every day of fever)
If not rested then often develop chronic cough and persistent pharyngitis/tracheitis
Spread of Equine Influenza?
Rapidly spread by the respiratory route especially if close direct contact - coughing, windborne virus may spread for up to 8km, morbidity in naive horses close to 100%!
Excrete virus for up to 8 days after initial infection
Survives in the environment for up to 36 hours but is easily killed by cleaning and disinfection
Can be spread by Fomites
Management of Equine Influenza?
Difficult as rapid spread/short incubation period
Isolate cases in separate stable or yard (20-40ft)
Monitor all horses for pyrexia + isolation
Separate personnel, equipment etc
Disinfect (bleach, iodophor, phenol, soap)
Outcome of Equine Influenza?
Mortality very low in adults - secondary bacterial (pleuro)pneumonia, purpura haemorrhagica
Mortality in Foals higher esp. if low immunity - myocarditis, secondary Bacterial bronchopneumonia, Acute Respiratory Distress syndrome (ARDS)
Vaccinated horses may mild signs similar to rhinovirus or mild EHV-1&4
What do EHV-1 and EHV-4 cause?
Both: respiratory disease (main form)
EHV-1 also: abortion, neurological (Equine herpes myeloencephalopathy)
Most foals seroconvert to EHV1 and 4
Becomes latent and reactivates under times of stress - shed virus, often subclinical
Clinical presentation of EHV-1 and 4 (respiratory)? Treatment?
Clinical signs: Dull, +/- mild coughing/serous ND
Often spreads through yards
Viral = presumptive diagnosis
Haematology:
- Acute: reduced neutrophils/lymphocytes
- Then: lymphocytes ‘reverse differential’
Often several weeks duration
Symptomatic therapy – rest, NSAIDs, antibiotics
for secondary infections?, Interferon?, cautious use of inhaled steroids for chronic cough
Rhodococcus equi - age affected, what does it cause, transmission? clinical signs, diagnosis, treatment?
= 'Rattles' 1-4 month old foals Pyogranulomatous pneumonia Inhalational and oral routes (coprophagia) Acute in young foals: - Fever - Anorexia - Nasal discharge - Cough Chronic in older foals: - Cough - Dyspnoea - Weight loss - Exercise intolerance - Loud moist crackles on auscultation Forms large pulmonary abscesses Evades immune system in alveolar macrophages (also destruction of peyer's patches in gut and alveoli) Diagnosis: - Consistent clinical signs - Culture/PCR VAP from TTW (culture must correlate with clinical disease - healthy foals can be positive) - Radiography and US - Bloods: fibrinogen Non pathogenic strains exist Treatment: - Low dust, warm, feed intake, anti-inflammatories - Prolonged antibiotics (macrolide e.g. erythromycin, and rifampin)
Strangles - Proper name? features of agent? Spread? Survival in environment?
Contagious Equine Rhinopharyngitis
Bacterial respiratory disease affecting mainly the URT and head LNs
Streptococcus equi var. equi:
- Obligate parasite (not part of normal flora)
- Gram positive coccoid
- Catalase negative facultative anaerobe
- Beta haemolytic
- Lactose fermentation negative
High morbidity, low mortality
Survives well in environment, especially in discharges (up to 12mo)
Sensitive to desiccation/sunlight/heat - killed at >55C in 30 mins
Sensitive to most disinfectants
Spread via nose or mouth contact, fomites, distant spread rare
Carrier animals harbour in guttural pouches
Clinical presentation of Strangles?
Usually affects 1-3yo (but can be any age)
2 phases after incubation period:
- multiplication in lingual and palatine tonsils
- haematogenous and lymphatic spread to draining LNs
Can be carriers for a prolonged period
Can develop systemic abscesses ‘bastard strangles’ High morbidity, low mortality
Incubation and clinical course time of strangles?
Incubation period 1-14d
Clinical course usually within 3 weeks
Early clinical signs of strangles?
Depression, fever (2-3 days before shedding)
Mucoid nasal discharge
Slight cough
Anorexia
Difficulty swallowing
Swelling (slight) of intermandibular area
Later clinical signs of strangles?
Purulent nasal discharge
Head LN enlargement and abscesses
Retropharyngeal LN swelling -> dyspnoea, if ruptures -> guttural pouch empyema (LNs ventral to guttural pouch)
Chronic guttural pouch empyema if not treated -> chondroids (= solid balls of thick pus, removed by breaking up and flushing, or surgery)
Complications of strangles?
Pharyngeal compression -> tracheotomy required Cellulitis and local tissue damage Pneumonia and abscessation Immune mediated myositis/myocarditis Purpura haemorrhagica: - Vasculitis - Type III hypersensitivity (Ab-Ag complexes) - Serum/blood leakage - Treat with immunosuppressants Bastard strangles: - Transient bacteraemia - Abscesses form in muscle/kidneys/liver/lungs or may cause peritonitis Persistent carriers: - 10% of recovered horses - Can persist for >5y - Mostly in guttural pouches - Intermittently shed - Asymptomatic
Diagnosis of strangles?
Culture or PCR from:
- nasopharyngeal swabs/lavage
- guttural pouch washes/aspirates
- aspirate from abscess
- primary pathogen so positive test is always significant (oropharyngeal contamination not a problem)
Serology: ELISA for antibodies - tests for exposure only, most horses seroconvert from 2 weeks, remain seropositive >6mo after infection
In outbreaks often just use characteristic clinical signs
How to confirm a horse is free of strangles?
3 negative nasal swabs - 1/week for 3 weeks (85% sure no infection)
1 negative guttural pouch wash (88% sure no infection)
Treatment of strangles?
NSAIDs: analgesic and antipyretic to help appetite and reduce swelling
Soft, wet feed
Hot pack - helps to mature the abscess
Flush abscesses once draining
Tracheostomy is necessary in horses with respiratory distress
Antibiotics controversial - contraindicated when lymphadenopathy present as inhibits maturation of abscesses, can give penicillin for 5-7d at onset of pyrexia (e.g. when monitoring horses in outbreaks)
What to do in a yard outbreak of strangles?
Isolate affected and recovered animals as often shed bacteria for 3-6 weeks
‘Clean’ and ‘dirty’ areas (traffic light system):
- red = confirmed cases
- amber = been in contact with confirmed cases
- green = no contact with confirmed cases
Isolation procedures (clothing/equipment etc)
Stop movement on/off yard
Monitor temperature/nasal discharge of all in-contacts daily (usually pyrexia 3d before nasal discharge so identify quickly and treat)
Ideally swab all horses after outbreak to identify a possible carrier and ensure all horses are free of infection
Deep clean premises
Prevention of strangles?
Quarantine new animals coming to yard for 2-3 weeks (even if negative ELISA) - check temperature daily
Use ELISA to detect subclinical carriers
Guttural pouch PCR if positive ELISA or temperature
Vaccination
- modified live strangles vaccine (Equilis Strep E)
- first licensed in the UK in 2005, taken off due to side effects, returned 2010/11
- immunity 3 months, reduction of signs and complications versus full protection
What is Inflammatory Airway Disease (IAD)? Who does it affect?
Part of Equine Asthma
Non septic inflammation of the lower airways
Hyper-responsiveness rather than allergy
Common in young/new racehorses
2nd most common cause of poor performance after musculoskeletal
Risk factors for Inflammatory Airway Disease (IAD)?
Co-mingling - just brought into racing training and exposed to other horses and environment
Exercise:
- strenuous exercise decreases immune function
- inhalation of dust and cold, unconditioned air
Transport
EIPH
Age - younger horses most at risk
Stable environment - poor ventilation and bedding
Aetiology of Inflammatory Airway Disease (IAD)?
Infectious and non-infectious components
Viral infections - reduce immunity, decrease
mucociliary clearance and increase airway reactivity
Bacteria - not direct cause, but infections may reduce airway protective mechanisms and immunity
Environment - RAO lectures
Clinical signs of Inflammatory Airway Disease (IAD)?
Often no/very subtle clinical signs at rest
Poor performance
Cough
Nasal discharge
Diagnosis of Inflammatory Airway Disease (IAD)?
Endoscopy: mucopus in the trachea
BAL or tracheal aspirate
Neutrophils >40% (tracheal aspirate) or >10% (BAL)
> 3% eosinophils and mast cells
Reasons for why horses are good athletes?
Haemoglobin concentration Gas exchange Heart size Skeletal muscle properties Biomechanics Anaerobic capacity
Equation for VO2?
VO2 = CO x C(a-v)O2
Linear increase with exercise until max
What is VO2max?
Maximal aerobic metabolic rate
Measurable (mlO2/kg/min)
Closely related to performance ability
Supramaximal intensities - anaerobic (can gallop faster than VO2max but will get tired)
Functions of the respiratory system?
Gas exchange - primary function
Humidification, filtering and warming of air
Thermoregulation
Phonation
Olfaction
Acid‐base regulation
Blood filtering & pulmonary defence mechanisms
What is the relationship between airflow resistance and radius?
Airflow resistance proportional to radius^4
What is the minute ventilation of horses at rest and exercise?
Rest: 80L/min
Exercise: 1800L/min
What changes during exercise to allow respiratory function?
Increased TV, RR, minute ventilation, perfusion, CO, diffusion, Hb concentration (oxygen carrying capacity)
Increased diffusion at tissues - oxyhemoglobin curve shifts to right with hypercapnia, acidosis and hyperthermia
Decreased physiological dead space
Linked respiratory/stride (visceral piston)
What causes exercise induced hypoxaemia in horses?
75% due to diffusion limitation, 25% V/Q mismatch, min. shunting
Despite increased haemoglobin, increased gradient for diffusion
Horse extremely high pulmonary vascular pressures and rel. thick diffusion barrier
How does heavy exercise affect pulmonary resistance in horses?
Obligate nasal breathers
Pulmonary resistance more than doubles despite nares dilation, full laryngeal abduction and bronchodilation
What causes of decreased pulmonary gas exchange are there in horses?
Increased pulmonary resistance - URT disorders, hypersecretion/blood/inflammation of small airways
Decreased pulmonary compliance - oedema, hypertension, fibrosis, interstitial disease
Dynamic airway collapse - IAD, tracheal collapse
Respiratory muscle/chest wall disease
Decreased CO - decreased lung or tissue perfusion, V/Q inequality
Decreased Hb
Diagnosis of EIPH? Prevalence?
Currently based on post exercise endoscopy
BAL for several weeks post exercise looking for haemosiderophages
No consistent signs except epistaxis if occurs
2yo - 40%
3yo - 65%
4yo - 82%
Thought that a small amount of haemorrhage occurs almost every time a horse gallops and that this is normal
Gross pathology and histopathology of EIPH?
Blue discolouration - result of haemosiderin accumulation
Lesions start caudo-dorsally and extend cranially
Histo - peribronchial inflammation and fibrosis
What is epistaxis after exercise correlated with? What if sudden death?
Consensus not more severe form of EIPH
Pulmonary abscesses and rupture of large vessels
Atrial fibrillation producing high left atrial pressures
Sudden death associated with epistaxis may be related to cardiac dysrhythmia rather than blood in the airways
Endoscopy for EIPH? Grades?
Used to visualise the tracheal blood
Performed 30-60mins after exercise
Graded 0 (no blood) to 4
Grade 1 - flecks of blood or single short stream of blood extending less than a quarter of tracheal length
Grade 2 - one continuous stream of blood extending at least one half the length of the trachea or multiple streams covering less than one third of tracheal surface
Grade 3 - multiple streams covering more than one third of tracheal surface
Grade 4 - abundant blood in trachea, completely covering tracheal surface and pooling at thoracic inlet
What events may cause EIPH?
High pulmonary vascular pressures appear to be necessary to predispose a horse to EIPH:
- Extreme vascular pressures
- High inspiratory pressures
- Inflammation
- Locomotory shockwaves
- Regional differences in dynamic compliance
Effect of EIPH on performance?
Grade 1 and 2: associated with normal performance
Grade 3 and 4: associated with poor performance
Inflammation seen with EIPH?
Blood within airways is removed quite slowly
By 3 days airway inflammation develops and lasts weeks
Initially response is neutrophil dominated
Then a more chronic and persistent phase characterised by increased macrophage numbers and marked macrophage activation and erythrophagocytosis
Suggests horses require period of rest to remove haemorrhage and may benefit from anti‐ inflammatory therapy
Treatment for EIPH?
No single therapy found to stop EIPH
Grade 1/2 may be physiological - may not need treatment
Goal is to reduce severity and remove performance limiting effect of EIPH
Furosemide - evidence that it reduces severity and incidence , given prior to racing but is banned in UK (makes run faster)
Poor evidence for anything else
Why does grade 3/4 EIPH affect performance?
Intrapulmonary blood -> macrophage influx
Results in reversible disruption of alveolar septal architecture
Chronic macrophage activity -> alveolar septal wall thickening and fibrosis
Alveolar septal fibrosis likely to result in premanent alterations to alveolar blood-air barrier and reduces local pulmonary compliance
Common differential diagnosis of LRT disease in adult horses?
RAO and IAD = Equine Asthma Syndrome Viral and bacterial infections Fairly common: - EIPH - Pleuropneumonia - Aspiration pneumonia
What makes up Equine Asthma Syndrome?
Recurrent Airway Obstruction (RAO) and Inflammatory Airway Disease (IAD)
RAO - cause? age affected? When usually seen?
Usually older >7yo
Hypersensitivity to molds, bacteria/endotoxins, mites, plant debris, inorganic dust, noxious gases
Non specific inflammatory responses
More common with housing and hay feeding
Associated with inhalation of organic dusts from hay and bedding
Probably also genetic component
Summer pasture associated - warm/humid weather, plant/soil allergens
RAO clinical signs?
Early: often minimal signs, mild exercise intolerance
Tachypnoea, increased expiratory effort, cough, nostril flare, nasal discharge
Expiratory +/- inspiratory wheeze
Forced expiration -> biphasic expiratory effort = heaves
Heave line
Severe cases: respiratory distress, weight loss
Pathophysiology of RAO?
Dust etc causes inflammation
-> stimulates muscarinic and B2 adrenergic receptors -> peribronchiolar smooth muscle contraction
-> bronchoconstriction
Mucosal hyperplasia/inflammatory infiltrate/oedema
Goblet cells and increased mucus production
Decreased mucociliary escalator
Increased inflammatory cells
Histopathology of chronic RAO?
Smooth muscle hypertrophy and bronchoconstriction
Peribronchiolar inflammation -> fibrosis
Mucus and inflammatory exudate in lumen (mucus plugging)
Epithelial cell hyperplasia and goblet cells
Diagnosis of RAO?
Clinical signs Tracheal aspirate cytology Mucus score 0-5 good correlation BAL cytology Response to IV atropine/NBB or clenbuterol
Tracheal aspirate for RAO?
Poor correlation with lung function/BAL results
Cytology
Neutrophils >40% = inflammation
Small numbers of bacteria but very few intracellular
Lots of intracellular bacteria and degenerate neutrophils = bacterial infection
BAL for RAO?
200 cells - % and qualitative cytology
Neutrophils >25%
Mast and eosinophils >1%
Curschmann’s spiral
When to think about differential diagnoses when investigating if RAO?
If <7yo
If ‘sick’ - dull, anorexic, pyrexic, weight loss
Diagnostic tests don’t show lower airway inflammation
Lack of response to therapy
RAO environmental control?
Aim to reduce respirable particles
Time outside ideal
Best -> worst feed: pasture > complete pelleted feeds > haylage > soaked hay (at least 10mins) > dry hay
Feed from ground
Low dust bedding: cardboard, dust extracted shavings, paper, fitted rubber matting
Take horse out during/1hr after mucking out
Not deep litter
Maximise stable ventilation
Consider ‘airspace’ sharing
Bronchodilators for RAO - indications? Types with examples and problems?
Indications:
- emergency therapy in flare ups
- before other inhaled medication
- before exercise
- diagnostic
B2 agonists
- clenbuterol, salbutamol, salmeterol
- tolerance via down regulation of receptors so paradoxic bronchoconstriction may occur after long term use of bronchodilators alone
- tolerance reduced by corticosteroids
Muscarinic antagonists
- atropine: single dose only, systemic side effects
- NBB (buscopan): single dose, fewer side effects, shorter duration of action
- ipratropium bromide: minimal side effects, given before exercise, 15-30min onset, 4-6h duration
Corticosteroids for RAO?
Reduce cell accumulation and activation
Reduce vascular changes
Reduce bronchoconstriction
Systemic: pred, dex
Inhaled: beclomethasone dipropionate, fluticasone propionate, nebuliser dex
Rapid effect, residual effects up to 7d after stopping treatment
Pros and cons of inhalation therapy for RAO?
Pros: - lower total dose - rapid onset - fewer systemic side effects - shorter detection times Cons: - expensive - owner compliance - distribution of drug if dyspneic
Mucolytics forf RAO?
Dembrexine (Sputolosin)/ Bromhexine - alters mucus structure, increases respiratory clearance, very questionable efficacy!
Acetylcysteine
Saline nebulisation or overhydration
Agents that may cause pleuropneumonia in horses?
Aerobic facultative anerobes: - ß haemolytic strep. spp. - Pasteurellaecae - Actinobacillus spp. - Enterobacteriacae - Pseudomonas Anaerobes (usually in combo with facultative anaerobes): - Bacteroides - Eubacterium - Fusobacterium
What is pleuropneumonia?
Bacterial pneumonia and secondary pleural effusion
Predisposing factors for pleuropneumonia?
Long distance transport (shipping fever) - head elevation, aspiration of dust/debris
Viral respiratory disease - damage to respiratory epithelium
Exercise - EIPH + aspiration of debris
General anaesthesia/surgery
Stages of pleuropneumonia in horses?
(1. Bronchopneumonia)
2. Acute exudative stage:
- Inflammation of the lung and pleura – sterile protein rich pleural exudate
3. Fibrinopurulent stage
- Bacteria invade and multiply in the pleural fluid
- Fibrin deposits on pleural surfaces
- Lymphatic obstruction
4. Organisational Stage
Clinical signs and diagnosis of pleuropneumonia in horses?
Systemic illness - pyrexia, depression, increased HR and RR Reduced lung sounds ventrally, dull on percussion Pleurodynia Soft cough Diagnosis: - signs - ultrasonography - thoracocentesis - TTW and culture
Pleuropneumonia treatment?
Best early in stage 1! Thoracic drainage Antimicrobial therapy - Penicillin - Gentamicin - Metronidazole if complicated Monitor, supporting therapy
Equine lungworm - species? Source of infection? Diagnosis? Treatment? Prevention?
Dictyocaulus arnfieldi
Donkeys: asymptomatic reservoir of infection for horses
Uncommon now
Diagnosis by identification of worms in tracheal wash or BAL
NB eosinophils in TW or BAL DO NOT INDICATE lungworm
Treat with ivermectins
Horses grazed with donkeys should receive ivermectin
regularly
What is aspiration pneumonia commonly secondary to?
Oesophageal choke
Gastric reflux
Pharyngeal dysphagia
Iatrogenic – liquid paraffin
Multi nodular pulmonary fibrosis - aetiology? Diagnosis? Other signs? Prognosis?
Associated with Equine Herpes Virus -5 (EHV-5)
Inclusion bodies may be detected on BAL or on lung biopsy tissues
Often weight loss / pyrexia
Ddx RAO
EHV-5 can also be isolated from normal horses
Px Guarded - poor
Thoracic neoplasias in horses?
Cranial Mediastinal Lymphosarcoma Pulmonary Granular Cell Tumour Malignant melanoma Haemangiosarcoma Metastatic adenocarcinomas Metastatic carcinomas
How to listen to a horse’s heart? Which heart sounds are loudest where?
Right: pull leg forwards, put stethoscope bell right under triceps just dorsal to point of elbow, harder than left
Left: start with apex beat = mitral valve, then move dorsal/cranial and cover whole cardiac window
S2 and S4 loudest in basal area
S1 and S3 loudest in apical area
What are S3 and S4? How common to hear in horse? When?
S4: atrial contraction, ‘B’, very common, just before S1, p wave
S3: end of rapid ventricular filling, ‘D’, less common, just after S2
How to know when systole and diastole is for murmurs with higher HRs in horses?
Feel arterial pulse - will feel straight after S1
Useful if can hear S4 as S2 is single sound with diastole after, then ‘B’ ‘Lub’
What is the equation for Reynolds number (Re)?
Re = (velocity x diameter x density) / fluid viscosity
Influences turbulence
Why can anaemia cause a heart murmur?
Reduced viscosity of blood
Increases Reynolds number (turbulence)
Heart murmur grades?
Grade 1: Barely audible
Grade 2: Definite murmur quieter than S1 and S2
Grade 3: Obvious loud murmur as loud as S1 and S2
Grade 4: Very loud murmur louder than S1 and S2
Grade 5: Very loud and has a palpable thrill
Grade 6: Audible with stethoscope just off chest wall
Timing, quality and shapes of murmurs?
Timing: - Systolic/diastolic/continuous - Early/mid/late/pan/holo Quality: - Harsh/coarse/buzzing/honking/musical/blowing - High/medium/low pitched Shape: - 'Plateau'/crescendo/decrescendo/crescendo-decrescendo
How to describe a murmur?
Grade Timing Point of maximum intensity (PMI) Radiation (away from PMI) Shape of murmur Quality of murmur
What timing, shape, PMI and radiation are mitral/tricuspid valve regurgitation murmurs? When to investigate further?
Holo/pansystolic Plateau or crescendo PMI heart apex May radiate dorsal and cranial Investigate if mitral valve grade 3-6, tricuspid 4-6
What are the 2 main types of physiological/functional murmurs in horses? What is the timing, shape, PMI?
Flow murmur: - early mid-systole - up to 60% normal horses - L>R - localised over heart base (aortic/pulmonic valves) - grade 1 or 2 - may change intensity with HR/exercise - always finishes before S2 - crescendo-decrescendo Filling murmur: - early diastole, L or R - fit, young animals - squeak/whoop/click - short duration between S2 and S3 - localised over heart base or apex - may change intensity with HR
What timing, PMI and radiation are ventricular septal defect murmurs in horses? Which aged horses? Ddx?
Pansystolic Loudest on right Loud - thrill Radiates cranial/ventral Normally young horses Ddx: tricuspid insufficiency Sometimes secondary left sided pulmonary artery flow murmur
What timing, shape, PMI, radiation and quality are aortic insufficiency (AV valve regurgitation) murmurs? Which aged horses?
Holodiastolic Decrescendo PMI left heart base May radiate ventrally Buzzing/cooing Common in older horses 'teenage murmur'
What timing, shape and PMI, are PDA murmurs? Which aged horses?
Continuous
Waxes and wanes in intensity during cardiac cycle (loudest during systole)
PMI left heart base, also loud over right heart base
Normal in neonates -> 5 days
Which murmurs are heard left systolic, left diastolic and right systolic?
Left systolic: mitral valve regurgitation and aortic flow
Left diastolic: aortic valve regurgitation and ventricular filling
Right systolic: tricuspid valve regurgitation and VSD
Oedema definition?
Abnormal and excessive accumulation of fluid in the interstitium
Oedema distributions?
Local vs generalised
Dependent (ventral) - accumualtion in the lowermost parts of the body, due to gravity and increased hydrostatic pressure in capillaries, often manifestation of generalised oedema
Local - occurs where local conditions favour its development e.g. head or single limb
‘Anasarca’ - generalised subcutaneous oedema
What are the 4 mechanisms of oedema?
Increased capillary hydrostatic pressure
Decreased capillary oncotic pressure (colloid osmotic pressure, COP)
Lymphatic obstruction
Increased capillary permeability
What causes are there of increased capillary hydrostatic pressure, causing oedema?
Congestive heart failure Pulmonary hypertension from L sided HF Portal hypertension (liver disease) Intra-thoracic mass Venous thrombosis e.g. jugular thrombosis Increased intra-abdominal pressure Elevated Na+
What causes are there of decreased capillary oncotic pressure (COP), causing oedema?
Protein losing enteropathy/nephropathy Haemorrhage Proteinaceous effusions Chronic hepatopathy Malnutrition
What causes are there of lymphatic obstruction, causing oedema?
Confinement - 'stocking up' Lymphangitis Tumours Post partum Other local swelling
What causes are there of increased vascular permeability, causing oedema?
Vasculitis - immune mediated/infectious/toxic/neopalstic/traumatic/UV light
Systemic Inflammatory Response Syndrome (SIRS)/Endotoxaemia - inflammatory cascade: margination and activation of neutrophils, endothelial dysfunction
Local inflammation
Infectious Equine Viral Arteritis (EVA) - Type of virus? Transmission? Clinical signs? Diagnosis?
Arterivirus - causes panvasculitis
Respiratory or venereal transmission -> viraemia
Carrier stallions = reservoir (asymptomatic) - intermittent shedding
85-100% of mares bred to carrier stallions infected (depends on immune status)
Very variable clinical signs:
- most subclinical
- +/- pyrexia, dull, anorexia, peripheral oedema of limbs/sheath, stiff gait, oedematous mm
- generalised vasculitis in severe cases
- respiratory disease
- abortion (3-10m)
- temporary subfertility for stallions
- can be fatal in young foals
Diagnosis:
- history of contact with infected stallion
- serology
- virus isolation
- PCR
Notifiable
Infectious causes of vasculitis in horses?
Infectious Equine Viral Arteritis Equine Herpes Virus-1 Equine Infectious Anaemia Hendra Virus African Horse Sickness
Immune mediated vasculitis - Cause? Forms?
Allergic oedema/ types 1 and 2 hypersensitivity reactions
Local: urticaria, wheals
General: swollen limbs/head
Severe generalised = purpura haemorrhagica
Liberation of vast-active substances
Very variable in severity of presentation
Often affects white areas
What are the types of hypersensitivity?
Type 1: IgE - histamine
Type 3: immune complexes
Non infectious, non immune mediated causes of vasculitis?
Septic
Traumatic
Verminous e.g. Strongylus vulgaris in cranial mesenteric artery
Photosensitisation
Toxic e.g. IV glucose, chemotherapy agents toxic to endothelium
Neoplastic
What arterial aneurysm and rupture is most common?
Most commonly from aortic root in stallions
Aneurysm dissects into pericardium or cardiac chamber
Thrombosis and thrombophlebitis seen in horses?
Aorto-iliac thrombosis: - uncommon - unknown aetiology - lameness/HL pain - diagnosis by rectal +/- US Jugular catheters - polyurethane/silicon less thrombogenic - teflon more thrombogenic - presence of hyper coagulable state e.g. SIRS predisposes
What is lymphangitis (‘fat/big leg/monday morning leg’)? Presentation? Clinical signs? Ddx? Cause?
Inflammation of lymph vessels Common Usually localised (e.g. one leg) Normally pain on palpation over lymphatics Will normally bear weight on limb Swollen, +/- serum ooze, crusting Examine for primary wound Ddx septic synovitis Sometimes secondary to penetrating wound or cellulitis Often unknown aetiology
Treatment for lymphangitis?
Anti-inflammatories: NSAIDs +/- ccorticosteroids
Antibiotics: staph often involved, broad spectrum with good penetration
Topical cleaning
Local cold/support
Encourage walking
Tetanus prophylaxis
