Equine respiratory, cardio, head and neck (EVA, AHS, oedema, vasculitis, anaemia) 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
Where to place equine ECG leads?
Base apex lead, record on lead I
Left arm (+): left heart apex (yellow)
Right arm (-): mid right jugular furrow (red)
Neutral: remote from heart (black)
What is the P wave? What can it look like? Which heart sound corresponds?
Atrial depolarisation and contraction starting from SAN
Single, biphasic or bifid/notched
S4 ‘B’
What is the P-R segment?
Delay at AVN
Prevents synchronous atria/ventricular contraction
What is QRS? Which heart sound corresponds?
Ventricular depolarisation and contraction starting at AVN
Bundle of his -> purkinje network -> myocytes
S1 ‘Lub’
What is the T wave? What can it look like? Which heart sound corresponds in horses?
Ventricular repolarisation and relaxation
Can change morphology/polarity at different HRs = normal
S2 ‘Dup’
What do ectopic atrial/ventricular pacemakers (APC/VPC) look like in horses?
Ectopic atrial pacemaker: different wave of depolarisation, different shaped premature P wave followed by normal QRST, non compensatory pause
Ectopic ventricular pacemaker: not using normal conduction system, wide bizarre QRS T, no associated P wave, compensatory pause after non conducted P wave, can look similar if ectopic focus is close to conduction system
Which physiological arrhythmias are common in the horse?
1st and 2nd degree AV block
Sinus arryhthmia/bradycardia/tachycardia
With pathological arrhythmias are common in the horse?
Atrial premature complexes
Atrial fibrillation
Ventricular premature complexes
Ventricular tachycardia
2nd degree AV block in horses - what happens? What does it look like on ECG? Diagnosis?
Common physiological arrhythmia at rest (20% of fit horses)
Regularly irregular
Regular SAN depolarisation
Conduction pathway normal
AVN stops spread of depolarisation to ventricles every 3-4 beats
Regular R-R intervals, normal QRS and P wave morphology, pause approx double R-R interval
Resolves with increased sympathetic/decreased vagal tone so exercise or give atropine to test
What is seen on ECG in horses with the physiological murmurs: 1st degree AV block, sinus arrhythmia, sinus block?
1st degree AV block: prolonged P-R
Sinus arrhythmia: periodic waxing and waning of R-R interval
Sinus block: occasional pauses of 2+ R-R intervals, no P or QRS T on ECG
How does atrial fibrillation appear on ECG in horses?
Irregular R-R intervals (irregularly irregular)
Absence of P waves
‘F’ (fibrillation) waves
QRS normal morphology
Atrial fibrillation in horses - How common? Possible presentations? Causes?
Most common arrhythmia causing poor performance at high intensity exercise
Poor performance, fading during race, epistaxis (increased pressure in lungs -> leaking of blood)
Often incidental finding in sedentary horses
‘Lone AF’ - no underlying cardiac pathology (lone AF will not cause HF)
Regular APCs can lead to AF
Can occur secondary to cardiac pathology, esp MVR causing LA dilation
More of concern in small pony as less likely to be primary event than in horse with large heart
What sustains AF in horses?
Re-entry mechanism:
Large atrial mass and variable refractoriness of cells due to high vagal tone
Treatment for AF in horses?
If recent onset, may spontaneously revert to sinus rhythm in 24-48h
Cardioversion if no underlying disease
1. Pharmacological conversion: Quinidine sulphate (oral)
- via nasogastric tube
- every 2 hours until conversion or max 5 doses
- then prolong Tx interval every 6 hours or treat in conjunction with digoxin twice daily for 2 days only
- increases refractory period for atrial cells
- stop if does not convert or shows severe side effects
- should have emergency drugs during treatment (supraventricular tachycardia >100: digoxin, ventricular tachycardia: MgSo4 or lignocaine)
2. Transvenous electrical cardio version
Is a horse with AF safe to ride?
Low but still increased risk of collapse
Perform exercising ECG up to/beyond level he will be ridden
Ectopic ventricular beats - not suitable
No ectopic ventricular beats - suitable for light work
How many VPCs/APCs are significant in a horse?
Previously:
>2 isolated premature at peak exercise
>5 pairs or paroxysms post exercise
But exercising ECG data indicates premature depolarisations are more common
Causes of jugular distension in horses?
Increased central venous pressure
Or obstruction to venous return
Causes of variable jugular and peripheral pulse amplitude in horses?
Atrio-ventricualr dissociation
Or variable stroke volume caused by variable diastolic filling time
Definition of ventricular tachycardia? Cause? Treatment in horses?
4 or more VPCs in succession
Paroxysmal or sustained
Usually primary myocardial disease
Check for underlying disease/electrolyte imbalance/echocardiographic abnormalities
Can rapidly lead to CHF
Lignocaine IV, phenytoin sodium, flunixin meglumine
Virulence factors of Strep equi equi?
Cell wall M protein = major virulence factor:
- antiphagocytic (stops opsonisation)
- binds fibrinogen/immunoglobulin
- masks complement binding site
- Different versions have different virulence, some more likely to form carrier status
Streptolysin S = haemolytic
Iron uptake system
Hyaluronic acid capsule: mimics common vertebrate molecule
What management factors increase the attack rate of strangles?
Increasing group size Increased movement of horses Increased mixing of horses Communal feeders and drinkers Younger horses (apparent age related immunity)
Complications of Rhodococcus equi?
Polyarthritis (immune mediated) - or septic arthritis
Granulomatous ulcerative enterocolitis and mesenteric lymphadenitis
Corneal oedema and anterior uveitis
Rhodoccoccus equi: features of bacterium and virulence factors?
Gram positive pleomorphic rod
Aerobic soil saprophyte and normal GI flora
Survives in soil 12-36 months
Resistant to acid/alkali/disinfectants
Survives in large colon in adult horses
Virulence factors:
- Polysaccharide lipid rich capsule inhibits phagocytosis
- Intracellular pathogen due to inhibitory cell surface antigens
- Antigens encoded by VAP plasmid and only expressed at 34-41C
Biosecurity for Rhodococcus equi?
Resistant to acid/alkali/disinfectants
Survives in soil for 12-36 months
Survives in large colon in adult horses - foal coprophagia may be important
So..
Quarantine may work
Avoid crowding and remove foal manure from pasture
Reduce dust
Examine foals closely twice a week until 4mo
Currently no vaccine
Hyperimmune plasma given at 24-72h old before exposure (+/- at 21 days)
What equine viral respiratory diseases are there?
Adenovirus Influenza Equine herpes viruses 1 and 4 Rhinovirus (Equine viral arthritis - notifiable) (African Horse Sickness - notifiable)
When is Adenovirus a problem in horses?
Only a problem in SCID in Arab foals
Mils/subclinical disease/carrier state in normal animals
One possible cause of outbreaks of mild respiratory disease in yards of young racehorses
What type of virus is influenza? What makes of the subtypes?
Orthomyxovirus
Haemagglutinin (H) and neuraminidase (N) glycoprotein surface antigens
Pathogenesis of equine influenza?
Inhaled virus attaches to respiratory mucosal cells
Haemagglutinin (H) attaches to Sialic acid on host cells
Neuraminidase (N) facilitates entry to cell and inhibits mucociliary clearance
Virus spreads along whole resp tract in 1-2 days
Damage to epithelium and cilia -> secondary bacterial infections
Can take up to 32 days for mucociliary transport to return to normal
How does the equine influenza vaccination work?
Targets the H surface antigens
Common to get fever for 1-4 days
Useful in outbreaks
Competing regulations for timing of equine influenza vaccinations?
British Horseracing Authority: - 2nd vaccine 21-92 days after the 1st - 3rd vaccine 150-215 days after the 2nd - Boosters within 365 days FEI: - Same as above - To compete a horse the last booster must have been within the last 6 months and 21 days - No competing for 7 days after vaccination
Pathogenesis of EHV-1 and 4?
Inhaled and attaches and replicates in mucosal epithelial cells of nasal passage, pharynx and tonsillar tissues
URT inflammation
Allows secondary invasion of mucosa by bacteria
Transported by T lymphocytes to other tissues
Latent infection in CD8+ T lymphocytes and trigeminal neural ganglion
How does EHV 1 and 4 affect foals, older foals and yearlings/adults?
Foals: - almost always fatal in neonates - icterus, leukopenia, neutropenia, petechial haemorrhages, severe pneumonia Older foals: - most survive - severe disease similar to influenza Yearlings/adults: - recrudescence of latent infection - much less severe disease of URT inflammation
Diagnosis of EHV-1 and 4?
Virus isolation:
- nasal swab or tracheal wash
PCR:
- poss too sensitive
Serology:
- 4 fold rise in serum titre or single titre of >1:80
- be careful of vaccination and maternal antibodies
EHV 1 and 4 vaccination?
Primary injection at 5mo
Secondary injection 4-6 weeks later
Booster every 6mo
Pregnant mares at 5, 7 and 9 months
Equine Rhinovirus: type of virus? Signs? Vaccination?
Picornavirus
Mild resp disease of 3-5 days
Spreads rapidly
Fever, anorexia, serous nasal discharge, PLH
No vaccine
May be clinically confused for mild influenza or EHV
EVA prevention?
Detect infected stallions: - serology before breeding season - serology before vaccination Detect mares: - serology prior to breeding - breed if negative - isolate as notifiable if positive, until repeat serology declining
What causes an animal to cough?
Stimulation of irritant receptors by:
- inflammation
- chemicals
- physical: foreign body, turbulent air, mucus
What clinical signs suggest LRT disease?
Cough
Bilateral nasal discharge
Tachypnoea/dyspnoea
What causes tachypnoea/dyspnoea?
Hypoventilation
V/Q mismatch
Impaired gas diffusion in alveolus
- > hypercapnia, academia, hypoxaemia
- > aortic, carotid and medulla chemoreceptors
- > respiratory centre in medulla
- > increased resp rate and effort
Why are signs of respiratory disease not always apparent at rest?
Horses have a huge respiratory capacity
E.g. a fit TB uses approx 4% VO2max at rest
What to observe for a respiratory exam of a horse?
Posture (extended head and neck = severe respiratory distress)
Abdominal effort
Resp rate and depth
Resp pattern - biphasic?
Hypertrophy of external abdominal oblique = heave line
Nares and nasal passages - airflow obstruction, discharge
Ventral oedema?
Guttural pouches and LNs - enlargement, discharges
What do normal resp sounds sound like in a horse?
From turbulent air in large (>2mm) airways
Soft blowing sound
Inspiration > expiration
Faster air = louder
What resp adventitious sounds can be auscultated in the horse and why?
- Wheezes
= airway narrowing and vibration
- thickened wall: oedema, inflammation
- intraluminal obstruction - mucus, foreign body
- bronchospasm
- extra-luminal compression - Crackles
- course crackles: bubbling mucus, inspiration or expiration, radiate widely
- fine crackles: popping open of collapsed small airways, most common on early inspiration - Pleural friction rubs
- inflamed parietal and visceral pleural membranes rubbing together
- variable: fine crackles to sandpaper rubbing together
- usually inspiratory and expiratory at same point in resp cycle
What is the Bernoulli effect?
Explains wheezing
Higher velocity air -> lower pressure -> further narrowing of airway -> higher velocity air
LRT: most common end expiratory
URT: most common inspiratory
Why is a re-breathing test with a bag for thoracic auscultation useful for horses?
Increases PaCO2
Increases respiratory rate and tidal volume
So increases normal and abnormal respiratory sounds
Cough = abnormal
Clinical pathology for respiratory disease?
Blood sample: - inflammatory profile: WBC, proteins, fibrinogen, serum amyloid A - lactate: tissue hypoxia - arterial blood gases Paired serology Virus isolation from: - buffy coat - nasopharyngeal swabs PCR to identify specific viruses/bacteria Bacterial culture/identification
Advs and disadvantages of endoscopically guided tracheal aspirate?
Advs: - easy - non invasive - sample representative of whole lung Disadvs: - sample contaminated by nasopharyngeal flora and equipment - specialist equipment required
Advs and disadvantages of a transtracheal wash?
Advs:
- no pharyngeal contamination
- no specialised equipment
- useful in young foals when endoscopes are too large
Disadvs:
- horse may cough catheter into pharynx and contaminate sample
- invasive: cellulitis, subcutaneous emphysema
Advs and disadvantages of BAL?
Advs:
- sample obtained from distal airways = most commonly affected
- best correlation with pulmonary function and histopath
- cheap and accessible equipment (unless endoscopically obtained)
Disadvs:
- site may not be appropriate in animals with localised pulmonary abscesses or pneumonias
- pharyngeal contamination so culture not useful
- invasive
Normal BAL values?
Macrophages: 40-70% Lymphocytes: 30-60% Neutrophils: <5% Mast cells: <2% Eusinophils: <1%
When to use BAL or TA?
BAL better correlation with: - airway obstruction (pulmonary function testing) - exercise induced hypoxaemia - lung histopathology TA most useful for: - bacteriology - focal lung lesions - tracheal inflammation
Radiography for resp disease of horses?
High powered machine needed
Poor sensitivity for diffuse lung disease
Most useful for pulmonary abscesses and thoracic neoplasia
Which parts of the airways are more prone to collapse on inspiration and expiration?
Inspiration: chest wall and diaphragm move outwards and creates negative pressure to pull air into lungs, pressure is lower in trachea than surroundings so prone to collapse
Expiration: pressure is higher outside the lungs but lower outside the trachea so LRT more likely to collapse
How do horses generally present with heart disease?
Incidental finding - PPE, vaccination
History of poor performance
Systemically ill
Rarely presents with evidence go heart failure
Why can neoplasia and CRF cause a heart murmur?
Neoplasia -> anaemia -> murmur (reduced blood viscosity)
CRF -> hypercalcaemia -> dysrhythmia
How can severe aortic valve regurgitation affect the arterial pulse?
Bounding/hyperdynamic
How far up should a normal jugular pulse/fill go?
Max 1/3 height of jugular
Where can the arterial pulse be felt on a horse’s limb?
Palmar artery (digital pulse) - medial and lateral palmar fetlock
Median artery - medial carpus
Great metatarsal artery
What is the most important cardiac biomarker in horses?
Cardiac troponin (I or T)
- troponin I most commonly as lasts longest in circulation
- mild increases in response to endurance/sprint racing
- indicates myocardial disease
(natriuretic peptides of minimal use in horses)
Indications for echocardiography in horses?
Previously diagnosed ‘functional’ murmur which is louder on serial examinations
Grade 3+ mitral/aortic or grade 4+ tricuspid murmurs
Suspected VSD or other congenital lesion
Any continuous murmur
Signs of CHF
PUO
Poor performance investigations when musculoskeletal/resp causes have been red out
Indications for an ECG of a horse?
Monitoring during surgery etc
Poor performance
Arrhythmia auscultated
Virulence factors of Streptococcus equi var. equi?
Cell wall M protein is antiphagocytic = major virulence factor
Streptolysin is haemolytic
Hyaluronic acid capsule mimics common vertebrate molecule
What increases the attack rate of strangles?
Increasing group size Increased movement of horses Increased mixing of horses Communal feeders and drinkers Younger horses
What suggests a respiratory disease is not infectious?
Bright and alert Eating Normal temperature No WBC response on haematology No acute phase protein response No in contacts affected No primary pathogens detected No Ab response Neutrophils in trachea: no intracellular bacteria
Differential diagnosis’s to equine influenza virus?
Strangles EHV1 and 4 Equine rhinitis virus Equine adenovirus Equine arteritis virus
Epidemiology for Equine influenza virus?
Poor ventilation and high humidity enhance transmission
Young horses in big groups = highest risk
Subclinical carriers shed and infect naïve populations
Adults can be infected esp. in crowded and stressful conditions
African horse sickness: Features? Spread? Strains? Pathogenesis?
Insect borne arbovirus - Culicoides imicola
Dog, zebra, elephant reservoir hosts
8 major strains, 42 substrains
Pathogenesis:
- severe vascular endothelial damage
- respiratory/cardiovascular systems
- leakage of protein rich fluid into interstitium
- prominent oedema: lungs, thorax, pericardium, head
What are the 4 forms of African Horse Fever? Signs?
Pulmonary form: - rapidly fatal - severely febrile - pulmonary oedema: cough, profuse nasal discharge - sweating - cyanosis - recumbency - appetite good until death Cardiac form: - insidious onset with persistent fever - oedema of head and neck - congested mucous membranes - mild colic - dysphagia (pharyngeal/oesophageal paralysis) - hydropericardium - slow death (>50%) - some survive but recovery >1yr) - appetite good Mixed form: - rapid death usually - combo of respiratory and cardiac Horse sickness fever: mild flu like syndrome
What vascular disorders do horses get?
- Vasculitis
- Arterial aneurysm and rupture
- Thrombosis and thrombophlebitis
- Lymphangitis
Indications for an ECG of a horse?
Rhythm disturbance detected on auscultation or via palpation of pulse
Poor performance
Monitoring of patients with CVS compromise (e.g. systemically ill, under GA)
What are the guttural pouches? Compartments? Opening?
Air filled, mucosa lined outpourings of the auditory tubes connecting the nasopharynx to the middle ear
Each pouch is separated into a medial and lateral compartment by the stylohyoid bone (medial bigger)
Funnel shaped pharyngeal orifice with a fibrocartilage flaps connects them to the nasopharynx (opening = plica)
What structures border the guttural pouch dorsally, medially, ventrally and laterally?
Dorsal:
- base of skull and C1
- tympanic bulla and auditory meatus
Medial:
- median septum, rectus and longus capitis muscles
Ventral:
- retropharyngeal lymph nodes and nasopharynx
Lateral:
- parotid and mandibular salivary glands, pterygoid muscles
What structures are contained in the medial and lateral compartments of the guttural pouches?
Medial compartment: - internal and external carotids - cranial sympathetic nerves - cranial cervical ganglion - pharyngeal nerve plexus - cranial laryngeal nerve - neck 'strap muscles' (longus capitus muscle) - CNs IX, X (pharyngeal branch), XI and XII Lateral compartment: - external carotid - maxillary artery - superficial temporal arteries - CN VII
Possible presenting signs of guttural pouch disease?
Epistaxis Nasal discharge Nerve dysfunction: - dysphagia (pharyngeal branch of vagus, glossopharyngeal) - laryngeal paralysis - horner's syndrome (sympathetic ganglion) - facial asymmetry - swelling/dyspnoea
What guttural pouch diseases are there?
Mycosis
Empyema/chondroids
Tympany
Otitis interna/media
Stylohyoid bone: temporohyoid osteopathy, fracture of petrous temporal/basiphenoid
Rupture of longus captious ‘strap’ muscle
Neoplasia/cysts/foreign bodies
Guttural pouch mycosis: What happens? How bad is it? Clinical signs? Diagnosis? Treatment?
Primary fungal plaque forms over vessels - most commonly internal carotid
Relatively uncommon
Potentially life threatening - must rule out in epistaxis cases
Clinical signs:
- nasal discharge
- epistaxis
- +/- nerve dysfunction (dysphagia, horners, laryngeal paralysis)
Diagnosis:
- history
- clinical signs
- endoscopy: blood draining ostium, +/- DDSP or laryngeal hemiplegia, diphtheritic membrane overlying ICA/ECA (careful to not disrupt clot and cause fatal bleed)
Treatment:
- surgical occlusion of affected artery: simple ligation (back flow from circle of willis), balloon catheterisation, coil embolisation
- medical management: only if no history of bleeding, risk of disease progression, topical/systemic antifungals
Aetiology of guttural pouch empyema? Clinical signs? Diagnosis? Treatment?
Aetiology:
- URT infection - strangles
- Infusion of irritant drugs
Clinical signs:
- intermittent nasal discharge
- parotid swelling and pain
- extended head carriage
- respiratory noise at rest
- difficulty swallowing and eating
- occasionally pharyngeal and laryngeal paralysis
Diagnosis:
- radiography: increased radio density of GP on lateral views
- endoscopy: dorsal pharyngeal compression, chonroids
Treatment:
- flush pouches using catheters inserted into ostia
- endoscopic removal of chondroids
- surgical flushing and removal of material
Guttural pouch tympany: When seen? Aetiology? Presentation? Diagnosis? Treatment? Prognosis?
Foals - congenital defect in ostia? secondari to inflammation?
Unilateral or bilateral
Clinical signs:
- Marked retropharyngeal swelling
- respiratory stridor
- dysphagia
Confirmed on radiography or endoscopy
Treatment:
- medical: place foley catheter in ossetia and leave in situ attached to nostril
- surgery: fenestration between GP, remove internal plica
Usually good prognosis if unilateral, less so for bilateral
Temporohyoid osteoarthropathy: What is it? Aetiology? Clinical signs?
Progressive disease of the middle ear and bones of the temporohyoid joint Aetiology: - inter of middle ear infection of haematogenous origin? - secondary osseous proliferation - ankylosis of temporohyoid joint - pathologic fracture Early clinical signs: - head shaking - ear rubbing - behavioural change Chronic clinical signs: - facial nerve paralysis - head tilt and ataxia - nystagmus (slow towards affected side)
Rupture of the neck ‘strap muscles’: Which muscles? Aetiology? Clinical signs? Diagnosis? Treatment? Prognosis?
Muscles: - longus capitus - rectus capitus ventralis - rectus capitus lateralis Aetiology: - trauma: usually due to rearing and falling over backwards Clinical signs: - profuse bilateral epistaxis - ataxia - head tilt - pharyngeal and tracheal compression and 2nd upper airway obstruction Diagnosis: - endoscopy: roof of pharynx collapsed, normal vessels, swollen muscle bellies - radiography: fluid line within pouch Treatment: - box rest - anti-inflammatories - supportive care Prognosis: - good if neurological signs resolve - grave if signs persist
Neoplasia in the guttural pouch?
Melanoma commonly invades but rarely causes any clinical signs
Indications for a tracheotomy?
Emergency bypass of URT obstruction
Route for intubation
Rest the URT
Bypass inoperable URT obstruction
Most important ddx for epistaxis?
EIPH Guttural pouch mycosis Nasal/pharyngeal trauma Progressive ethmoid haematoma (PEH) Head trauma
Most important ddx for dysphagia?
Oesophageal obstruction (choke) Retropharyngeal abscess (strangles etc) Other retropharyngeal masses (granuloma, neoplasia etc) Pharyngeal foreign body Guttural pouch mycosis Equine grass sickness URT infection - pharyngeal nerve plexus dysfunction Polyneuritis equi
Clinical signs of nostril/nares conditions? Possible conditions?
Facial swelling Asymmetry Nasal stertor Poor performance? Conditions: - alar folds collapse - epidermal inclusion cyst (atheroma)
What divides the two nasal passages?
Left and right passages divided by nasal septum and vomer bone
Dorsal and ventral conchae (turbinates) = thin scrolls of bone which divide the nasal passages into dorsal meatus, middle meatus and ventral meatus
Clinical signs of nasal passage disease?
Nasal discharge Halitosis Abnormal respiratory noise Dyspnoea Coughing Facial distortion Head shaking
What diseases of the nasal passages are there?
Trauma (kick/blunt trauma, ethmoid trauma during nasogastric intuition Wry nose Nasal septum deviation/thickening Neoplasia - carcinoma Progressive ethmoidal haematoma Fungal
Ethmoid haematoma: What is it? Aetiology? Clinical signs? Diagnosis? Treatment?
Encapsulated non-neoplastic mass which grows into the nasal passages/paranasal sinuses from the ethmoid region
Unknown aetiology
Clinical signs:
- mild intermittent unilateral epistaxis
- occasionally abnormal respiratory noise at exercise
- +/- malodorous smell
- +/- facial swelling
Diagnosis:
- endoscopy
- +/- radiography
- CT
Treatment:
- lesions in nasal passages treated with intra-lesional formalin
- +/- laser treatment if small/post formalin
- recurrence common
Fungal rhinitis (nasal aspergillosis): When seen? Clinical signs? Diagnosis? Treatment?
Primary is uncommon in UK
Secondary fungal disease due to sinusitis is common
Clinical signs:
- Unilateral purulent/occasionally haemorrhagic nasal discharge
- Malodorous smell
- Occasionally nasal stertor
Diagnosis: endoscopy
Treatment:
- Removal of fungal plaques and necrotic bone
Topical treatment (nystatin powder/imaverol)
Wry nose: What happens? Treatment?
Congenital shortening of maxillary, nasal and vomer bones
Deviation of nasal septum and nasal obstruction
Treatment depends on severity (mild - resect nasal septum)
What paranasal sinuses are there?
7 pairs:
- Rostral maxillary
- Caudal maxillary
- Frontal
- Dorsal conchal
- Ventral conchal
- Sphenopalatine
- Ethmoid
Drainage of paranasal sinuses?
Drainage by gravity and mucocillary action
Rostral maxillary sinus and ventral conchus sinus drain into middle meatus of nasal cavity via nasomaxillary aperture
The other sinuses drain into the caudal maxillary sinus and then into middle meatus via the nasomaxillary aperture
Aperture easily obstructed by mild swelling
What diseases of the paranasal sinuses are there?
Sinusitis most common - primary or secondary Ethmoid haematomas Fractures of overlying bones Sinus cysts Neoplasia
Clinical signs of paranasal sinus disease? Diagnosis?
Predominantly unilateral discharge \+/- Facial swelling \+/- Decreased nasal airflow Diagnosis: - history and signs - percussion of sinuses - endoscopy - radiography: fluid lines - sinoscopy - CT
Sinusitis: Types? Causes? Diagnosis?
Primary:
- usually from previous respiratory tract infection
- most commonly Strep infection
Secondary:
- most commonly due to dental disease (08, 09, 10, 11)
- also facial fractures, granulomatous lesions, neoplasia
- treat primary cause and the sinusitis
Diagnosis:
- endoscopy: visualisation of purulent material coming from nasomaxillary aperture
- radiography: fluid lines on lateral views, increased radiodensity of sinuses on DV
- CT
Treatment of primary sinusitis?
Initially: - C and S to rule out strangles - antibiotics e.g. TMPS for 7-14 days - feed from ground - dust free management - turnout as much as possible - most mild, acute cases will respond Sinuses may have inspissated purulent material - frequently occurs in VCS and RMS (poor drainage and separated from CMS by maxillary septal bulla): - lavage for persistent cases - surgery: trephination or bone flap under standing sedation or GA
Facial fractures: Diagnosis? Complications?
Diagnosis: - clinical signs - radiography - +/- US - +/- CT Secondary sinusitis Treatment: - removal/stabilisation of bone fragments - flushing of sinuses if sinusitis
Paranasal sinus cyst: Which horses? Aetiology? What happens? Significant? Clinical signs? Diagnosis? Treatment?
Uncommon Mainly young horses Unknown aetiology Filled with yellow, viscous fluid As cyst grows it causes erosion and distortion of normal bony architecture Clinical signs: - facial swelling - reduced nasal airflow - nasal discharge - nasal stertor Diagnosis: - radiography: circular area of increased radiodensity in sinuses - +/- sinoscopy - CT Treatment: surgical removal
Suturitis: What is it? Aetiology? Clinical signs? Treatment?
= Suture line periostitis Periostitis of the suture lines between the nasal and frontal bones Aetiology: - trauma? - can occur after sinus surgery Clinical signs: - bilateral, firm, non painful swellings in nasofrontal region Usually regress with time
What are the 2 main functions of the pharynx? Why are horses obligate nasal breathers? Why is there potential for the pharynx to collapse? Innervation?
2 main functions:
- delivers air from nasal cavity to larynx
- provides a pathway for food to be passed from oral cavity to oesophagus
Obligate nasal breathers as larynx sits in nasopharynx above soft palate apart from during swallowing
Pharynx can collapse as no rigid support by bone/cartilage (relies on neuromuscular function for stability)
Innervation:
- mandibular branch of trigeminal
- pharyngeal branch of vagus
- hypoglossal
- cervical nerves
Larynx: Functions? Cartilages? Muscles for abduction and adduction?
Functions: - Breathing - Protects lower aiway - Phonation Cartilages: - Cricoid cartilage - Thyroid cartilage - Epiglottis - Paired arytenoid cartilages Abduction: - cricoarytenoideus dorsalis Adduction: - CAL, vocalis
Diagnosis of laryngeal and pharyngeal disease?
Endoscopy: - at rest (limited if problem only occurs at exercise) - at exercise Radiography US
Diseases of the pharynx? Clinical signs?
Diseases: - cleft palate - pharyngeal lymphoid hyperplasia - DDSP - palatal instability - pharyngeal collapse - pharyngeal mass - foreign body Clinical signs: - poor performance - respiratory noise - dysphagia - nasal discharge - coughing - respiratory distress
Dorsal displacement of the soft palate (DDSP): Types? What happens with each?
Intermittent DDSP:
- dynamic condition that occurs during intense exercise
- soft palate displaces dorsally to result in an expiratory obstruction
- following exercise returns to normal position
- no other evidence of pharyngeal dysfunction
Persistent DDSP:
- soft palate is permanently displaced
- frequently secondary to other disease (epiglottic entrapment, sub-epiglottic ulcer, sub-epiglottic cyst)
- may have dysphagia
Dorsal displacement of the soft palate (DDSP): Diagnosis?
Diagnosis:
- history and clinical exam: exercise intolerance, expiratory gurgling/vibrating noise, rider reports ‘choking down/up/swallowing its tongue’
- endoscopy: gold standard is at exercise
Proposed pathogenesis of intermittent dorsal displacement of the soft palate (IDDSP)?
Neuromuscular dysfunction:
- pharyngeal branch pf vagus nerve innervates thyrohyoideus muscle which pulls larynx forward into pharynx
- dysfunction alters laryngohyoid position (moves caudally allowing larynx to disengage from pharynx)
- may be caused by inflammation in guttural pouch or pharyngeal lymphoid hyperplasia
Could be other causes:
- lower airway disease (IAD) causing increased negative pressure
- examine for lameness
- causes as with PDDSP
Causes of PDDSP?
Generally secondary: - epiglottic entrapment - ulceration causing pain Can be neuro dysfunction: - as IDDSP - post other surgery e.g. tie back
Treatment for IDDSP?
60-70% success rate
Conservative:
- get horse fit
- keep mouth closed when ridden (tack)
- tongue tie (stop caudal movement of tongue)
- treat inflammatory conditions of pharynx/guttural pouch
throat support device?
Staphylectomy:
- partial soft palate resection
Myectomy (rarely performed now):
- removal of some of extrinsic muscles of the larynx to reduce caudal retraction of larynx
Induction of palatal fibrosis:
- thermal/laser cautery
- palatoplasty
- stiffens soft palate?
- poor evidence for efficacy
Tie forward (currently best):
- sutures placed between basihyoid bone and thyroid cartilage
- positions the larynx more rostrally and dorsally
- returns horse to previous race performance
Nasopharyngeal collapse/dysfunction: When seen?
Nasopharyngeal dysfunction:
- foals - dysphagia
Pharyngeal collapse:
- dorsal or lateral walls
- yearlings/2yo TB (+/- other disease e.g. IDDSP)
- may resolve if milf
- sport horses (exacerbated by neck flexion)
Pharyngeal lymphoid hyperplasia: Significance?
Grade 0-4
Grade >3 significant
Normal in juvenile horse
No definitive association with other disease
Cleft palate: When seen? Signs? Treatment?
Foals: milk at nostril (ddx pharyngeal dysfunction) Repair: - direct from laryngotomy if small - split mandible at symphysis - difficult and expensive
What laryngeal disorders are there?
Recurrent laryngeal neuropathy Arytenoid chondroitis Collapse of apex of corniculate process Fourth branchial arch defect Vocal cord collapse Axial deviation of aryepiglottic folds Epiglottic abnormalities: - epiglottic ulcers - epiglottic entrapment - sub-epiglottic cysts - epiglottic retroversion
Clinical signs of laryngeal disease?
Respiratory noise Poor performance Dysphagia Coughing Respiratory distress
Recurrent laryngeal neuropathy (RLN): What happens? Cause? Pathogenesis? Diagnosis?
Unilateral paralysis of left arytenoid cartilage
Likely genetic aetiology
Pathogenesis:
- Progressive loss of large myelinated nerve fibres in the left recurrent laryngeal nerve
- ->Neurogenic atrophy of intrinsic laryngeal muscles (CAD muscle)
- loss of abductor and adductor function
Diagnosis:
- mostly large breeds
- history: abnormal inspiratory noise at exercise, poor performance
- clinical exam: +/- atrophy of left CAD (makes it easier to palpate the muscular process), -ve slap test?
- endoscopy (dynamic is gold standard)
What is the Havemeyer scale?
Used for endoscopy assessment of Recurrent laryngeal neuropathy (RLN)
Assess:
- synchrony of movement
-ability to achieve full abduction
- ability to maintain full abduction
Grades I-IV (grades II and III subdivided)
Treatment for Recurrent laryngeal neuropathy (RLN)?
Depends on intended use of horse and degree of laryngeal obstruction
Ventriculectomy/ventriculocordectomy:
- ‘Hobday’ procedure
- performed via laryngotomy under GA or standing
- roaring burr used to evert both ventricles
- ventricles then excised
- +/- removal of vocal cord
- improves sounds (and function a bit), good for show pony etc
- no risk of aspiration pneumonia
Laryngoplasty:
- ‘Tie-back’
- suture placed between dorsocaudal edge of cricoid cartilage and muscular process of left arytenoid cartilage
- mimics action of CAD
- permanent abduction go left arytenoid cartilage
- best option for significant function improvement
Complications of a laryngoplasty (tie-back) for Recurrent laryngeal neuropathy (RLN)?
Failure Dysphagia Aspiration Persistent cough Infection
Causes of laryngeal paralysis? Which side(s) affected)
Recurrent laryngeal neuropathy (RLN) (left)
Peripheral neuropathy e.g. liver disease (bilateral)
Guttural pouch disease (left or right)
Organophosphate poisoning (bilateral)
Injection of irritant drugs (jugular vein missed) (left or right)
Other CNS/neck disease
Post-anaesthetic laryngeal paralysis (bilateral)
Fourth brachial arch defect (4 BAD) (right)
Fourth brachial arch defect (4 BAD): What is it? What happens as a result?
Variable development of right laryngeal cartilage +/- cricothyroid and cricoarytenoid articulation
Rostral displacement of palatopharyngeal arch
Right sided asymmetry
Variable ability to abduct arytenoid
Vocal cord collapse: Which horses? Signs? Cause?
Bilateral in juvenile horses
Respiratory noise
Associated with other disease - ADAF
Axial deviation of aryepiglottic folds (ADAF): Which horses?
Juvenile TB:
- associated with IDDSP
- VCC
Arytenoid collapse
Epiglottic entrapment: What happens? Signs?
Subepiglottic tissue entraps epiglottis \+/- IDDSP Resp noise \+/- Poor performance Not always necessary to treat immediately - esp if performing at expected level
Sub epiglottic cysts: Cause? Signs?
Congenital?
+/- IDDSP
Resp noise, dysphagia
Arytenoid chondroitis: What happens? Which horses?
Mucosal ulceration
Infection of arytenoid cartilage
Progressive
Respiratory obstruction: younger TB, older mares
What is the normal tidal volume of a horse? Minute ventilation? At exercise?
TV 5L
Minute ventilation 75L if RR 15brpm
Minute ventilation 1500L at exercise (20xrest)
Which causes of abnormal respiratory noises at exercise are inspiratory and expiratory?
Inspiratory: • RLN • DDSP (soft gurgling) • Epiglottic entrapment • Subepiglottic cyst • Epiglottic retroversion • Dynamic nasopharyngeal collapse • ADAF • Alar fold collapse/nasal paralysis • 4-BAD
Expiratory: • DDSP (loud) • Epiglottic entrapment • Epiglottic retroversion • Sub-epiglottic cyst • 4-BAD
Radiography views of the head? What are each good for?
Latero-lateral: - paranasal sinuses - guttural pouches - pharynx Lateral oblique: - periodical regions of premolars and molars Dorso-ventral: - paranasal sinuses - nasal septum - teeth - helps decide if lesions are unilateral or bilateral
Indications for radiography, US, sinoscopy, CT and MRI of the head?
Radiography:
- Facial/mandibular fractures
- Suspected paranasal sinus disease
- Suspected dental disease (periapical infection)
- Investigations of bony swellings
US:
- Soft tissue swellings of head/neck
- Assessment of larynx
- Assessment of facial fractures
- Examination of eye and periocular tissues
- Suspected temporo-mandibular joint disease
Sinoscopy:
- Investigation of suspected paranasal sinus disease
- Aspiration of material from paranasal sinuses (e.g. culture & sensitivity)
- Obtaining material for biopsy
- Treatment
CT:
- Investigating possible periapical infection
- Investigation of masses within paranasal sinuses
MRI:
- rarely indicated
- suspected brain tumour
- investigation of masses
Interpreting tracheal aspirate results? What to assess?
Differential cell counts:
- Abnormal = >20% neutrophils
- Abnormal = Presence of mast cells, eosinophils
Presence of mucus, amount, Curschmann’s spirals
Gram stain: especially for intracellular organisms
Bacterial culture/sensitivity
Normal PCV in horses?
TBs: 35-45%
Others: 26-35%
Mechanisms of anaemia?
- Blood loss
- Increased RBC destruction (haemolysis)
- Decreased RBC production
What is the spleen’s role with regard to RBCs?
Important reservoir for erythrocytes
PCV of horses can increase during exercise or excitement by as much as 0.25L/L
Also dynamic reservoir of platelets (up to 1/3 of total blood platelets are retained in the spleen)
So can’t accurately assess a horse’s PCV after excercise, when excited or when endotoxaemia present due to splenic contraction
Clinical signs of anaemia in horses?
Occur due to lack of oxygenation..
Tachypnoea, tachycardia Pallor Exercise intolerance, lethargy, weakness Collapse May hear flow murmur if: - PCV 15-18% - decreased blood viscosity - increased turbulence
Other signs relating to underlying disease process:
- fever, icterus and/or pigmentria may accompany haemolysis
- epistaxis, haematuria or melaena (rare in horse) may signal chronic blood loss
- anorexia, lethargy and weight loss with anaemia suggest underlying disease process
Clinical signs of hypovolaemic shock in horses?
Tachycardia Tachypnoea Hypothermia Pale and dry mucous membranes Long CRT Weak pulse Cold extremities Muscle weakness
When do clinical signs of shock become apparent in a horse with acute blood loss?
When 30% of blood volume lost
8% of BW is blood, so 500kg horse has 40L of blood and cad lose 13L before shows signs
What to work out if horse with anaemia? Lab assessment?
Acute or chronic?
External/internal blood loss: paracentesis and erythrophagocytosis if haemothorax/peritoneum
Evidence of clotting disorder?
Evidence of haemolyis: fever, pigmenturia, jaundice, pink plasma?
Lab assessment:
- Complete blood count (CBC) and RBC morphology
- Total plasma protein
- Plasma fibrinogen concentration
Compensatory mechanisms for anaemia in the horse?
Spleen masks the extent of blood loss for several hours post-haemorrhage by injection of a concentrated mass of stored erythrocytes into circulation
Catecholamines induce vasoconstriction and increase cardiac output
Plasma volume is expanded by withdrawal of fluid from the interstitium and increased resorption of water in the renal tubules and from the GIT via ADH
Fluid movement into the vascular system continues at a decreasing rate for up to 72h
Decline in the TPP can be measured within 4-6h of the insult
Decrease in PCV is usually not seen until 12-24h post-haemorrhage when plasma volume expansion > compensatory effect of splenic contraction
How to diagnose acute blood loss?
History of recent haemorrhage
Clinical signs
Eventual development of anaemia and hypoproteinaemia (chronic when both PCV and TPP reduced)
Care if reduced PCV and increased TPP due to haemoconcentration )anaemia may be more severe than PCV indicates)
How to determine between regenerative and non regenerative anaemia in horses?
Peripheral signs of regeneration (reticulocytosis and polychromatic) rarely occur in horses
Serial PCVs - may see very mild anisocytosis in regenerative samples
Bone marrow evaluation to confirm non regenerative myeloid disorders
How to rule in or out haemolysis in an anaemia case?
Regenerative anaemia without concomitant hypoproteinaemia
Pink plasma if intravascular and Hburia (not if extravascular)
May see neutrophilic and regenerative left shift due to intensified erythropoiesis
Total and indirect bilirubin concentrations may be elevated
Must do:
- thorough blood smear evaluation: spherocytes, heinz bodies (IMHA)
- urinalysis
- coomb’s test
- possibly coggin’s test if suspect EIA
Differentials for acute blood loss anaemia in horses?
Haemorrhage due to traumatic or surgical wounds (e.g. open castration) - most common cause of anaemia
Guttural pouch mycosis
Uterine artery rupture
Mesenteric artery rupture (S vulgaris, now rare)
Epistaxis (rare)
Tumours - haemangiosarcoma, splenic disease
Thoracic large vessels rupture in racehorses
Renal haemorrhage
Umbilical loss in foals
Rib fractures (esp foals)
Coagulopathies in horses: How common? When seen?
Rare - usually DIC consumptive coagulopathy secondary to sepsis
Secondary to liver disease
Thrombocytopenia is rare
How does the body adapt to chronic blood loss anaemia? When are clinical signs seen?
Bone marrow regenerates erythrocytes as they are lost
Anaemia only develops when the rate of erythropoiesis is exceeded by the rate of haemorrhage
Gradual tissue hypoxia allows physiological adaptation so clinical signs of anaemia masked until PCV <15%
Differentials for chronic blood loss anaemia in horses?
Usually GIT: - parasites (large strongylosis) - neoplasia - gastric/duodenal ulceration - NSAID toxicosis May be urogenital blood loss e.g. renal, urethral
Differentials for haemolytic anaemia in horses?
True IMHA rare More likely secondary haemolytic anaemia: - penicillin (drug bound RBC recognised as foreign) - injection site abscesses - lymphoma Neonatal isoerythrolysis Babesia Infectious anaemia - EIA, Ehrlichiosis Oxidant induced haemolytic anaemia
Differentials of non regenerative anaemia in horses?
Bone marrow disorders - toxic, neoplastic
Anaemia of chronic disease e.g. renal disease (uraemia reduces RBC lifespan, reduced EPO)
Iron deficiency uncommon
Folic acid deficiency on some meds (e.g. sulphonamides, trimethoprim, pyrimethamine)
Treatment of anaemia in horses?
Identify and eliminate cause
Nursing care
Ensure adequate tissue perfusion
Minimise stress
Stop any bleeding
Control shock:
- 4-5ml/kg/10 mins hypertonic saline (2L for 500kg horse)
- 40-60ml/kh rapid infusion of crystalloids
- 10ml/kg colloids (e.g. hydroxethyl starch) - don’t overdose as will prolong clotting times
Adjunctive therapy:
- iron if deficient
- vit B12 if deficient
- anabolic steroids
- corticosteroids in IMHA or drug haemolysis
- vit C or antioxidants for red maple leaf
Blood transfusion reserved for when O2 delivery to tissues is inadequate to support life
When are blood transfusions necessary?
Acute blood loss: - if >30% blood volume lost - if clinical signs of hypovolaemic shock - if PCV <15% Chronic blood loss: - if PCV <12%
How much blood to give for a transfusion?
Deficit = ((normal PCV-patient’s PCV)/normal PCV) x (blood volume % x BW)
e.g. ((35-10)/35) x (0.08x500) = 28L
Give 30-50% of deficiency = 8-10L
Which developmental abnormality may cause a right sided laryngeal paralysis?
4-BAD
Dentigerous cyst: Presentation?
Young horse
Soft swelling over temporal region with discharging tract at base of ear (or under jaw)
How does a foal with tetralogy of fallot present?
Smaller and quieter than other foals
Can’t catch up with other foals
Lies flat out after mild exercise
Systolic murmur on both sides
Supraventricular tachycardia on ECG?
Tachycardia (e.g. 180bpm)
Normal QRS
Absent P waves
Appearance of ventricular tachycardia on ECG?
Tachycardia (e.g. 80bpm)
Wide QRS
P waves lost in QRS (normal P-P rate)
