Horses 5 Flashcards
(89 cards)
1
Q
Equine MRI what mainly used for for musculoskeletal injuries
A
- Again cannot get whole body within
- Just distal limbs and hooves
- Laying down in some machines - GA
- Standing MRI -> can move up and down the limb but cannot have movement - sedation as need to be able to stand
- lots of soft tissue, ligaments and joints
2
Q
Choke what results from, clinical signs and causes
A
- A blockage of the oesophagus - produce large volumes of saliva
- Profuse nasal discharge with or without food particles usually with no dyspnoea
Causes - Hay/chaff after prolonged fasting – worse if no water
- Via hay net in transportation and no water
- Rapid eating
- Hay after sedation because of reduced oesophageal motility
- Dry sugar beet that has not been soaked ( and it then expands from the saliva)
3
Q
Respiratory disease clinical examination what are important respiratory characteristics to look at
A
○ Rate (normal 12 to 20/min) ○ Depth ○ Effort - normal or increased § Inspiratory vs expiratory ○ Abnormal noise § Stertor/stridor § Inspiratory vs expiratory ○ Patient posture § Elbows abducted - sign of pleural pneumonia
4
Q
What are he 4 important aspects of the upper respiratory tract examination
A
- Airflow present at each nostril
- Check sub-mandibular LN
○ Often slightly more prominent in young animals
○ Important for strangles - Sinuses
○ Facial symmetry generally good indicator
§ Also fowl breath, unilateral mucopurulent discharge
○ Percussion - dullness - Induce a cough
○ Easily elicited cough from trachea pressure suggests airway inflammation
5
Q
Thoracic auscultation what is needed, how sensitive, what listening for and what other diagnostic tool needs to be done at this point
A
- Quite room is essential
- No very sensitive in adults, more sensitive in foals
○ Absence of abnormal sounds does not indicate absence of disease - Bronchovesicular (normal) sounds often difficult to appreciate in normal horses
- Listen carefully for…
○ Region where bronchovesicular sounds are dull or absent especially in horses with tachypnoea
○ Adventitial sounds (crackles, wheezes, friction rubs) indicate pulmonary pathology
Re-breathing examination is next
6
Q
Re-breathing examination what does it do, what is the goal and what assessing
A
○ Increases inspired CO2 -> increasing the depth and rate of respiratory
○ Should be able to appreciate (normal) bronchovesicular sounds throughout entire lung-field
○ Accentuates adventitial sounds/wheezes if present
§ Listen for areas of dullness especially ventrally
○ Also access
§ Tolerance to re-breathing examination
§ Coughing - SHOULD NTO COUGH AFTER
§ Recovery - should recovery within 5 to 6 breaths
7
Q
Ultrasound evaluation of the lung what is it good at evaluating therefore diseases it can see and what is it not good at evaluating
A
- Excellent for evaluating pleura and superficial lung
○ Pleural effusion
○ Superficial abscess
○ Consolidation
○ Pneumothorax - lack of glide sign - Does not penetrate aerated parenchyma
○ Unable to image deeper lung structures unless consolidated
8
Q
Radiogrpahic evaluation of lungs in adults and foals what is needed, what is good and not good about it
A
- Adults
○ Appropriate equipment
○ Lateral views only - usually aren’t mobile
○ Comparatively poor detail especially in ventral region
○ Large amount of views to see whole lung - Foals
○ More like small animals - Parenchymal lesions
○ Contrast to ultrasound - Not as sensitive for pleural disease
9
Q
What are the 3 main things radiogrpahic evaluation is used for with respiratory disease
A
○ Evaluate sinuses and guttural pouches
○ Look for presence of fluid lines or soft tissue opacities
○ Dorsoventral view very useful to evaluate the sinuses but can be difficult to obtain
10
Q
Tracs-tracheal aspirate or wash what are the 5 steps in the technique
A
- Aseptically prepare site
- Pass stylet trans-cutaneously into trachea - palpate tracheal rings
- Introduce long catheter - cranial to the U bend within trachea
- Deposit small volume of sterile saline at carina via catheter
- Then begin to aspirate back
11
Q
Trans-tracheal aspirate or wash what is it appropriate for, therefore what disease would you do for, additionally what part of the lung is sampled and what use sample for
A
- APPROPRIATE FOR CULTURE - most important way to do - WHEN THINK IT IS INFECTIOUS DISEASE
- Pooled sample from entire lung
○ Good for focal lung disease - due to mucociliary clearance moving everything from distal lung up into trachea
SAMPLE USED FOR
1. Cytology
○ Variable neutrophils in normal horses (3 to 50%) - do get false negatives
○ May be bacteria present in normal TTW
§ Interpret in the light of evidence of inflammation
§ Intracellular more convincing of active infection
○ Fungal hyphae common in normal TTW
2. Culture and sensitivity
3. PCR can be useful for some pathogens
12
Q
Which wash preferred trans-tracheal or trans-enoscopical and why
A
Don’t do trans-endoscopically for infectious disease as going through upper respiratory tract and therefore sample will be contaminated - instead - TRANS-TRACHEA ASPIRATE
13
Q
Bronchoalveolar lavage what are the 5 steps in the echnique
A
- Moderate sedation (xylazine and butorphanol) and twitch
- Pass BAL tube (or endoscope) via nasal passage into trachea
- Wedge in bronchus and inflate cuff
- Infuse and then aspirate sterile fluid (LRS)
○ Variable volumes used (3 x 120ml) - need to infuse at least 250mls - Mix final sample
14
Q
Bronchoalveolar lavage where in the lung does it sample therefore which disease is it better for and not appropriate for
A
- Samples a random, relatively small region of the lung
○ BETTER REFLECTS ALVEOLAR INFLAMMATION
○ Appropriate for global lung disease (RAO, IAD) - not focal disease - NOT appropriate for culture (pharyngeal contamination) - NOT FOR INFECTIOUS DISEASE
15
Q
What are 3 additional tests that can be done on the lung but aren’t common
A
- Thoracocentesis
- Lung biopsy
- Pulmonary function testing - not common
○ measure pulmonary compliance in the face of histamine - those with equine asthma have an exaggerated response
16
Q
If suspect a viral respiratory infection what 4 things in diagnostic approach and what 2 things can also add
A
- Complete blood count
- Thoracic ultrasound
- Serology
- PCR analysis (viral DNA) - nasopharyngeal swab
Can also add -> thoracic radiograph, transtracheal wash
17
Q
EVH-1 and 4 when infected, how contagious, age of onset and why
A
- EHV infection is ubiquitous in horses
○ Most horses infected in first year of life
○ 80% seropositive
○ Highly contagious - Clinical disease common and occurs most frequently in weanlings, yearlings and young adults
○ Disease often seen after entry into a training stable
○ Mixing new animals, stress
18
Q
EVH-1 and 4 clinical signs and what individually associated with
A
- EHV-1 and 4 clinically indistinguishable
- Incubation period 3-7 days
- Biphasic fever (up to 41 degrees)
- Depression, inappetence
- Serous (to mucopurulent) nasal discharge
- Cough (inconsistent)
- Disease often confined to upper respiratory tract - immunosuppressive
○ May predispose to secondary bacterial pneumonia - EHV-1 is also associated with Abortion storms (later gestation) and neurological disease
- EHV-4 typically causes less severe respiratory disease
○ Very rarely causes abortion or neurological disease
19
Q
EHV-1 and 4 diagnosis and pathogenesis
A
Diagnosis confirmed by
- Rising serum titre (or very high initial titre)
- PCR identification or viral DNA or viral isolation
○ Nasopharyngeal swab, buff coat
Pathogenesis
- Infection via respiratory tract
○ Virus attaches and replicates within mucosal epithelium of the URT
○ Lymphocyte- associated viraemia
- Latent infections are common - initiating new outbreaks
○ Lymph nodes
20
Q
EHV-1 and 4 treatment and control
A
Treatment
- Symptomatic (anti-inflammatories to control fever)
- Rest from exercise essential
- Antibiotics
○ Typically not indicated
○ Prolonged (>7 days) or persistent severe clinical signs
Control
- Isolation of affected horses
- Immunity following natural infection not strong
- Vaccine immunity poor (required q3-6monthly booster)
21
Q
Equine influenza what ages susceptible and typical clinical signs
A
- All ages susceptible
○ Young (1-3 years) adults commonly affected
○ Weanlings are also particularly susceptible when stressed
○ All age likely affected in naïve population
Clinical signs
○ Sudden onset, short (48 hour) incubation (spreads rapidly)
○ Biphasic fever (up to 41 degrees)
○ Cough: easily elicited by tracheal palpation
○ Serous nasal discharge
○ Pharyngitis, tracheitis, myalgia (muscle pain) - Disease usually restricted to the URT
22
Q
Equine influenza diagnosis and treatment
A
Diagnosis
- History of multiple affected horses, rapid spread
- Clinical signs (coughing)
- Rising serum antibody titre
- Viral isolation or PCR detection confirms diagnosis
Treatment
- REST
○ Horses recovering from EI might be unfit for competition for 50 to 100 days
○ Mucociliary clearance might be impaired for over 30 days
- Antibiotics
- Reportable
23
Q
Hendra virus what need to do if suspect a case and diagnosis
A
What to do if you suspect a case
- Contact appropriate state department or emergency animal disease hotline
- Personal protective equipment (PPE)
○ Overalls, protective boots, safety eyewear, gloves and respirator or mask
Diagnosis
- PCR and virus isolation of blood, nasal swabs, and tissue
- Samples to submit
○ Nasal swab (preferable in virus transport media)
○ 10ml blood in plain tube
○ 10ml blood in EDTA
24
Q
Hendra virus outbreak recommendations
A
- Quarantine affected horses
- Avoid returning to exercise too early
○ Secondary bacterial infection
○ Rest sick horses “one week for every day of fever” - Consider vaccination in future
○ Reduce severity of clinical signs
○ Reduce viral shedding
25
What are the 5 differentials for Bilateral nasal discharge, lymphadenopathy and fever and which want to rule out first
1. Strangles - WANT TO RULE OUT FIRST AS VERY CONTAGIOUS
2. Pneumonia
3. Sinusitis
4. Viral infection
5. Pharyngeal/retropharyngeal/pulmonary abscess
26
Streptococcus equi ssp equi (strangles) type of bacteria, age, how contagious and transmission
- Gram (+) cocci - ALWAYS A PATHOGEN - should not be present
- Mostly affects horses ages 1-3 years
○ However any age can be affected
- VERY CONTAGIOUS
○ Spread by inhalation or ingestion
- Fomites are very important in epidemiology
○ Buckets, water troughs, humans (veterinarians)
○ Does not persistent in the environment
- Some horses will become persistent shedders
○ Reservoir in guttural pouches
○ Asymptomatic
27
Strangles what are the main clinical signs and diagnosis
Clinical signs
- Lymphadenopathy
○ Submandibular and/or retropharyngeal (harder to see swelling- need to scope and go into the guttural pouch as present on the floor - will be puss present if infected - if don't treat can get chondroids (puss balls - need to remove))
- Nasal discharge
- Fever
- +/- depression, inappetence - variable but does indicate severity and shape treatment
Diagnosis
- Complete blood count
- FNA of submandibular lymph nodes or sample discharge if ruptured - PCR, culture and cytology
- Endoscope - to look a guttural pouches and ensure don't have retropharyngeal lymphadenopathy
- Nasopharyngeal swab or lavage - PCR or culture
28
Strangles treatment for mild fever, anorexia and no respiratory distress - IMPORTANT
○ Drain abscesses (hot packing - will rupture (once rupture very contagious particles released), lancing)
○ Cautious NSAID use -> in general with horses and gastric ulceration, possible dehydration for renal issues as well
○ Antibiotic therapy probably contra-indicated in mild cases and typically of little value once abscessation has occurred
§ Would use penicillin which is inactivated with puss
29
Strangles treatment for severe respiratory distress with systemic signs of disease - IMPORTANT
○ Often indicates retropharyngeal lymphadenopathy
§ +/- guttural pouch empyema
○ Antibiotics usually required
§ Penicillin is drug of choice
○ Tracheostomy might be required - if very extreme lymphadenopathy
○ Drain abscesses and treat guttural pouch empyema if present
§ Lavage, surgical drainage
○ Feeding tube, oesophagostomy etc might be required if severe, longstanding dysphagia present
30
Control and prevention of strangles what are the 4 important steps within
1) Strict quarantine
○ Feed/groom horse last
○ Muck out stall last and care with bedding
○ Separate clothing and boots
○ Gloves and wash hand
2) Confirm negative before mixing with other horses
○ PCR/culture of GP washes or nasopharyngeal swabs - 3 x negative then confident
3) Environmental
○ Isolate infected horses until negative
○ Human important fomites -> excellent personal hygiene
○ Care with shared feeding and cleaning equipment, track
○ Identify carriers -> culture/PCR of GP lavage samples
4) Vaccination: 75% are immune after infection
○ Intramuscular -> not very effective but might reduce severity of disease
○ Intranasal (MLV) more efficacious but not available in Australia
31
List the 4 main complications of strangles
1) metastatic S. equi
2) bastard strangeles
3) pupura haemorrhagica
4) streptococcal myositis
32
Metastatic S. equi what is it and what does it lead to
Complication of strangles
○ Bastard strangles - approx. 10% of cases
○ Abscesses in the abdomen, brain, liver, spleen, kidneys
○ Guttural pouch empyema - chondroids
33
Basatrd strangles what is it, diagnosis and treatment
```
Complication of strangles
○ Diagnosis
§ Increase strep M protein titre (antibodies detected against SeM)
§ Inflammatory blood work
§ History
§ Ultrasound, abdomenocentesis, CSF tap
○ Treatment
§ Long term antibiotics (1-6months)
```
34
Purpura haemorrhagica what is it, what does it result from and result in and treatment
Complication of strangles
Type III hypersensitivity reaction
○ Immune complex deposition -> vasculitis
§ Severe distal limb oedema -> skin sloughing
§ Petechiation or ecchymosis
§ Glomerulonephritis reported
○ Has been associated with vaccination
○ Treatment - corticosteroids and penicillin
35
Streptococcal myositis what is it, how common and the 3 main mechanisms
```
Complication of strangles
○ Rare
○ Various mechanisms
§ Infarcts
§ Immune mediated
§ Bacterial invasion of muscle
```
36
Oesophageal obstruction what differential for, cause of, main clinical signs, treatment and what need to do afterwards
○ Differential diagnosis for nasal discharge in horses
○ Cause of aspiration pneumonia - particularly if obstruction is prolonged
Clinical signs - quite obvious
- Gagging or retching
- Bilat, frothy nasal discharge - saliva and food material
Treatment
- lavage with nasogastric tube
- if failure to respond oesophagostomy
AFTERWARDS - need to endoscope to assess pathology that may have caused obstruction - gradual re-feeding with soft feed
37
What are the 4 paranasal sinuses in the horse
1. Conchofrontal sinus (includes the frontal, ventral conchal and dorsal conchal sinuses)
2. Caudal maxillary sinus
3. Rostral (also called ‘cranial’) maxillary sinus
4. Sphenopalatine (also called ‘palatine’) sinus
38
Paranasal sinus empyema (sinusitis) clinical signs and management fr primary or secondary causes
Clinical signs
- Unilateral nasal discharge
○ rostral to where the nasal septum finishes
- +/- facial distortion - If pressure in sinus from fluid of mass
- +/-ocular discharge (epiphora) - nasolacrimal duct runs on the underside of the bone that may become compressed
Management
- Primary (respiratory tract infectious process) - lavage (flush twice daily) and systemic antibiotics (penicillin)
- Chronic or secondary (dental disease, formation of cysts within sinus, occasionally neoplasia)
○ Bone flap = explore, debride, treat the cause (teeth extraction), lavage
○ Systemic antibiotics
39
What are the 7 diagnsotic tools for diagnosing paranasal sinus empyema (sinusitis)
1. Clinical signs
2. Percussion: should sound dull as should be hollow
3. Endoscopy: discharge from nasomaxillary opening into middle meatus of nasal passage - cannot go in
4. Radiograph: fluid lines in sinuses, masses
- Hold the radiograph horizontally so able to see lines parallel to the ground
5. Oral examination - for dental disease -> last 4 from 6 cheek teeth roots go into maxillary sinus
6. Trephine: a hole to allow aspiration of fluid or biopsy
- Direct endoscopy via trephine hole to visualize what is happening within
7. CT, MRI: useful for superimposition
40
Sinunasal cysts at what age, colour, cause and clinical signs
- Any age
- Single or multiple fluid filled cysts
- Yellow, relatively acellular, cystic fluid is contained in a membrane or capsule.
Aetiology - Unknown
Clinical Signs
- Signs attributable to expanding masses within the sinus and nasal passage:
○ nasal airflow obstruction, abnormal respiratory noise at rest, facial swelling/distortion, epiphora (indicating compromise of the nasolacrimal duct).
○ Unilateral nasal discharge – mucoid to mucopurulent material - or serous
41
Sinunasal cysts what are the 4 diagnostic techniques, what seeing there
1. Percussion of affected sinuses usually results in a dull sound
2. Endoscopy of the nasal passage often reveals narrowed nasal meati and may reveal a cyst bulging into the caudal nasal passage
3. Aspiration of the sinus through a small opening made with a Steinmann pin usually produces a characteristic clear yellow, acellular fluid
4. Radiography reveals a mass in the sinunasal region - soft tissue opacity
○ There may also be fluid lines, nasal septum deviation and distortion of the tooth roots.
42
Sinunasal cysts treatment and prognosis
Treatment - Removal of cysts via a bone flap approach
○ CT - can be good for surgical planning - able to determine the severity and location of cyst
Prognosis - Good after surgery
43
Progressive ethmoid hematoma (PEA) what is it, how common, age, cause and clinical signs
mass (NOT A TUMOUR)
- Mass that grows via repeated hemorrhage - slowly expand
- Uncommon but important differential for epistaxis
- Typically middle aged to older
Cause - unknown
Clinical signs
- Low-volume, intermittent, unilateral epistaxis (rostral to nasal septum) or a serosanguineous nasal discharge unassociated with exercise.
44
What are the 4 diagnostic tools for Progressive ethmoid hematoma (PEA) and what usefulf for
1. Clinical signs plus:
2. Endoscopy:
○ Haemorrhagic mass ethmoid turbinates varying in colour from red/purple to green/yellow.
○ Occasionally bilateral so always examine both nasal passages.
○ Less commonly, the mass is confined to the paranasal sinuses - Direct endoscopy via a trephine hole over the sinus is useful in these cases.
3. Radiography:
○ Useful to confirm the extent and location of the lesion (ie. paranasal sinus involvement)- aids in making a prognosis and planning for surgery.
4. CT:
○ Very useful for identifying location and extent of lesions but cost
45
Progressive ethmoid hematoma (PEA) what needed for a definitive diagnosis, is this done and prognosis
Definitive diagnosis:
Histopathology
- But usually not biopsied as characteristic endoscopic appearance
Prognosis
- Good for a small lesion but poor for extensive lesions.
- Recurrence is not uncommon so warn owner that treatment is not curative in all cases and that annual or twice yearly endoscopic examinations are therefore recommended
46
Progressive ethmoid hematoma (PEA) what are the 2 treatment ptions and which recommended and why
1) Chemical ablation via endoscope – inject lesion with 4% formalin on repeated occasions (every 2-4 weeks until the lesion is obliterated
- recommended due to reduced cost and avoidance of hemorrhage
2) Surgical resection of the lesion via a frontonasal bone flap approach -> uncommon due to risk of haemorrhage - laser better
47
Gluttural pouch mycosis how common, why significant, cause and clinical signs
- Can lead to death within 3 weeks
- Very uncommon
Cause - fungal growth within guttural pouch involved internal carotid artery (medial compartment) and/or external carotid and maxillary artery (lateral compartment)
Clinical signs
· Epistaxis - varies in severity from a minimal to litres of blood and is spontaneous
- Other signs associated with damage to the various nerves - not as common
48
Guttural pouch mycosis what important to consider before diagnosis and diagnosis
may be wise to consider referring the horse before endoscopic examination and prepare the surgery facility in case the clot over the artery is dislodged during the endoscopic examination
Diagnosis - endoscopy
49
Guttural pouch mycosis treatment what is and isn't effective and prognosis
Treatment
1. Surgical treatment is the only effective treatment and is an emergency as fatal bleeding can occur.
○ Refer promptly: 1st to fatal haemorrhage - 3 weeks or days
§ Involved occluding blood flow to the affected artery to cause regression
2. Medical treatment with antifungals is not effective if used alone
Prognosis with surgical treatment
- Good for survival (about 80%) but may be worse if nerve dysfunction is present (especially dysphagia) as this may not resolve.
50
When need a tracheostomy and how to perform and what important things to remember
- Stridor
- Difficulty breathing at rest
Technqiue
○ Ideally be in midline, third of the way down the neck where trachea easily palpable
○ Clip and prep and local anesthetic line block
○ Vertical incision through layers of skin, subcut, muscle onto trachea
§ ALWAYS make horizontally between tracheal rings (allows for easy healing)
§ Never extend excision a third of the way around
○ Range of tracheostomy tubes that can be used
51
What causes a nasal flutter, what can it lead to, why need to know about it and what if significant
Alar fold redundancy "nasal flutter"
- Due to vibration inside the tissue of the false nostril (alar fold)
- "buzzing" or "snoring" noise
- Uncommon to cause a problem in exercise
- BUT need to exclude as a potential cause of noise or PP by mattress suture of alar fold before exercise test
- IF significant -> can surgical remove alar fold
52
Why does airway obstruction become more significant and worsen with exercise intensity
- On inspiration during intense exercise the forces acting to collapse the walls of URT are considerable
-> when exercising large increase in flow and need to have same resistance so the pressure changes -> strong collapsing force on the airways which is blocked by dilation of nostrils, pharynx, larynx and stabilization of soft palate
§ Dysfunction of any of these structures results in their collapse into airway during exercise
53
How does head and neck position have an effect on performance
- Has an effect on pharyngeal diameter
○ Flexion may compromise pharyngeal diameter an may be important in horses that exercise in a flexed position
§ To optimise for performance -> stretch out the neck
54
What are the 8 diagnostic tools to use when horse present for poor performance
1. History
2. Physical examination
3. Endoscopy at rest
○ Best for abnormal respiratory noise at rest
4. Endoscopy during exercise-treadmill or over ground
○ Essential when only occurs due to forces on the airways during exercise as explained above
○ FOR DYNAMIC COLLAPSE
5. Tracheal wash
6. BAL
7. Radiography
8. Ultrasound
55
Dynamic collapse what are the 7 structures that can cause collapse
1) alar fold of the nostrils
2) soft palate
3) pharyngeal wall and roof
4) arytenoid cartilage
5) aryepiglottic fold
6) vocal cords
7) epiglottis
56
Palatal instability and intermittent DDSP what is it a common cause of, clinical signs, 3 possible causes and proposed contributing factors
- Common cause of dynamic collapse
- Abnormal noise in most BUT NOT ALL CASES
○ Typically a gurgling noise loudest on expiration -> will flap at this point
Cause - incomplete understanding -> numerous treatment options
1. Physical abnormalities - epiglottis or soft palate that seen on endoscope
2. Degree of URT inflammation
3. Most cases - neuromuscular dysfunction and inappropriate intrinsic muscle contraction
- Probably multifactorial
Proposed contributing factors
- Caudal retraction of tongue
- Opening of mouth
- Position of larynx and hyoid during exercise
57
Palatal instability and intermittent DDSP diagnosis and how reliable
- Challenging as type of noise can be unreliable and may only occur under intense exercise
1. History
2. Endoscopy during exercise - ONLY WAY TO GET DIFFERENTIAL DIAGNOSIS
○ looking at displacement of soft palate that is hard to replace even when swallowing (some will displace and it is normal but can replace easily)
○ At rest with nasal occlusion - create the negative pressure that may be needed
○ Only 50% detected to not reliable
58
Palatal instability and intermittent DDSP what are the 2 main management techniques and when use
1. Conservative management - first step - most respond
○ Rest and treatment of URT inflammation if present
○ Improved conditioning may help in certain cases
○ Gear changes -> tongue ties, corneal collar (pressure under hyoid bone to stabilise)
2. Surgical treatment - if don't respond to conservative
○ Laryngeal tie-forward -> most popular
Larynx pulled dorsal and proximal relative to hyoid apparatus
59
Recurrent laryngeal neuropathy (laryngeal hemiplegia - roarer) cause and pathogenesis
Cause - unknown - possible genetic bases
Pathogenesis
- Chronic neuropathy and distal axonopathy recurrent laryngeal nerves - more commonly the left
○ Left has longer route than right
- Spectrum of dysfunction and denervation atrophy of adductor and abductor muscles innervated by recurrent laryngeal nerve
- Cricoarytenoidous dorsalis muscle - ONLY ABDUCTOR muscle - IMPORTANT CLINICALLY
○ Innervated by recurrent laryngeal nerve
60
Recurrent laryngeal neuropathy (laryngeal hemiplegia - roarer) main clinical signs and 6 diagnostics
Clinical signs
- Exercise intolerance and respiratory noise with exercise ○ Inspiratory whistle or roaring
Diagnosis
1. Signalment (TB, WB, Draft breeds)
2. History and nature of noise
3. Palpation of larynx
4. Endoscopy at rest - asymmetry and asynchrony of left arytenoid
○ Is full abduction achieved and maintained -> do this by covering nostril to create negative pressure
○ Apply a grading system - 4 grade system with subgrades
5. Endoscopy at exercise
○ Apply a grading system - which need surgery (if can maintain abduction then doesn't need surgery)
6. Ultrasound for muscle change - not common
61
Recurrent laryngeal neuropathy (laryngeal hemiplegia - roarer) management for low grade and non-racing/performance horses
○ Ventriculocordectomy (bilateral) alone for some grade 2-3 RLN sport horses
§ Noise reduction
§ Standing, few complications
○ Manage any small airway disease
62
Recurrent laryngeal neuropathy (laryngeal hemiplegia - roarer) management for perofrmance horses with complications
will dramatically impact there exercise tolerance
○ Laryngoplasty (tie-back) + Ventriculocordectomy - unilateral or bilateral (helps with the noise as above)
§ Suture to act as Cricoarytenoidous dorsalis muscle (abductor muscle)
§ Prognosis for racing - 70% even higher in horses that perform less strenuously
§ Complications possible
□ Possible to get aspiration -> coughing
□ Dynamic collapse of other structures during exercise
□ Persistence of noise
□ Seroma
□ Infection of prosthesis
63
Epiglottic entrapment what occurs and clinical signs
- Subepiglottic tissues enveloping epiglottis -> become redundant and move ups and traps the epiglottis
- Can't see epiglottis with its scalloped edge and vascular pattern
- Can cause obstruction or association with DDSP
Clinical signs
- +/- exercise intolerance
- +/ noise
- +/- cough
- Sometimes an incidental finding
64
Epiglottic entrapment treatment and what if complicated case
Treatment
- Transection of tissue entrapping the epiglottis using a hock or laser
○ Nasal approach (within nasal cavity standing via endoscope
○ Oral approach under GA
Complicated case
- Some cases have secondary ulceration of the entrapping tissue and/or distortion of the epiglottis
- May need to treat with systemic +/- tropical anti-inflammatory and antibiotic therapy per-operatively
65
Arytenoid chondritis what involved, clinical signs and 2 diagnostic techniques
- Range in severity
○ Small lesions on arytenoids to dramatic lesions
Clinical signs
- Progressive exercise intolerance and noise
- Advanced cases-dyspnoea at rest requiring tracheostomy
Diagnosis
1. Endoscopy at rest
2. Ultrasound - extraluminal lesions can also occur - this needed to examine that
- Both good to evaluate extent of lesion and guide surgical planning
66
Arytenoid chondritis treatment for mild case, focal lesions and affected cartilage
- Medical treatment for very mild cases
○ Anti-inflammatory, topical throat spray with anti-inflammatory and topical antibiotics
§ Cartilage is AVASCULAR so no systemic treatments will work
- Surgical or laser debridement of focal lesions
- Surgical removal of affected cartilage (partial artenoidectomy)
Will compromised the protective mechanism of the airway - possible aspiratio
67
What are the 2 parts of equine asthma
1) inflammatory airway disease
| 2) recurrent airway obstruction (RAO)
68
Inflammatory airway disease what age, how common and clinical signs (differentiate from RAO)
- Young to middle-aged horses
- Extremely common
- Airway disease second only to musculoskeletal injury in wastage
- 11-50% of THB and STB racehorses
Clinical signs
- Cough
- Tracheal mucus
- Exercise intolerance
- Generally well and bright and happy - no increase in respiratory effort or rate (unlike RAO)
69
Recurrent airway obstruction (RAO) what also called, main types where common, age and clinical signs
- Also called Heaves
- uncommon
- Mostly indoor housing associated - moulds etc - not as common in australia as we don't house inside
- Summer pasture associated - possible pollens - more seen in australia
§ Feeding out from round bail hay - after been sitting there and have to move their muzzle all the way
- Older horses
Clinical signs - how to differentiate from inflammatory airway disease
- Episodic (attacks) dyspnoea
- Increased expiratory effort -> increase RR and HR
- Cough
- Heave line - abdominal muscle hypertrophy (increase) due to increased abdominal movement during expiration
- +/- nasal discharge
70
Pathophysiology of equine asthma
- Environmental respiratory irritants
○ Dust, mold spores
○ Ammonia
○ Endotoxin (manure)
- Summer-pasture associated heaves -> pollens (?)
- Genetics
○ Certain families of warmblood have higher rates of heaves
- Airways become inflamed
○ Neutrophils and mucus (pus) collect in small airways
- Airway are hyper-reactive
○ Triggers cause more severe bronchospasm than expected
○ Bronchospasm increases work of breathing
71
Equine asthma diagnosis and what not to diagnose with
Bronchoalveolar lavage - diagnose via percentage of neutrophils, eosinophils and mast cells
DON'T use skin testing or serum allergy testing as variable and not useful
72
List the 3 main treatment options for equine asthma
1) environmental management - decrease dust/hay allergens
2) corticoeroids
3) bronchodilators - not as sole treatment
73
Environmental management for treatment of equine asthma what is involved
```
○ Decrease dust, hay allergens
§ Full-time turnout
§ Shavings or cardboard bedding rather than straw
§ Out for >2 hr after cleaning stall
§ Soak hay, feed pelleted diet - less dusty
§ Optimise stall ventilation
□ End stall by the door
□ No hay storage overhead
§ Avoid summer pasture
```
74
Corticosteroid use for treatment of equine asthma what disease needed in and types
○ IAD -> complete resolution once removed from the offending environment
○ RAO -> progressive, usually require medical treatment eventually
1. systemic - try to get under control
-> prenisolone (side effects of immunosuppresion and lamainits)
2. inhalaed steroids - to main remission
- expensive but fewer side effects
75
Bronchodilators use for treatment of equine asthma what used for
ineffective as sole treatment
1. Inhaled bronchodilators
§ Albuterol, slameterol, ipratroprium
§ 30 mins before exercise or before steroid puffer - open up
2. atropine as resuce therapy only - GIT slow so only emergency
76
Rhodoccus equi what type of bacteria where found, trnasmission, age generally present and how common on farms
- Gram positive pleomorphic coccobacillus
- Present in the:
○ Soil of most geographical areas
○ Faeces (in relatively low numbers) of normal adult horses
§ Foals pass large numbers in faeces -> quickly contaminate the paddock especially foaling paddocks
Epidemiology
- Affects foal between 1 and 6 months of age
○ Infection often acquired in the first days to weeks of life
- Disease often endemic on well-established horse farms with lots of foals
77
Rhodoccus equi clinical signs and otehr sites of infection
```
- Severe bronchopneumonia with granuloma and/or abscess formation
○ Inappetence
○ Lethargy
○ Fever
○ Tachycardia
○ Increased respiratory effort (nostril flaring, increased abdominal effort)
- SOME - no-clinical signs - able to deal with the disease by themselves
- mortality in severely affected
- Extra-pulmonary sites of infection
○ GIT abscess, ulcerative
○ Joints and uveitis (immune mediated)
○ Osteomyelitis
```
78
What are the 4 diagnosis technqiues for rhodoccous equi infections
- Consider in any young horse showing signs of respiratory disease
1. Clinical pathology indicating chronic inflammation
○ Hyperfibrogenaemia, leucocytosis
○ Increased platelet count
2. Culture (and cytology) of appropriately collected tracheal wash samples
3. Thoracic radiographs
○ Prominent alveolar pattern
○ Poorly defined regional consolidation and/or abscessation
4. Ultrasonography
a. Pulmonary abscesses in peripheral pulmonary parenchyma
b. Very useful screening tool on endemic farms
79
Rhodoccous equi treatment for mildly affected vs severely affected and treatment duration
MILD - Self-cure common
○ Screen weekly and ensure abscesses don't get any bigger -> about 10cm below wouldn't treat
SEVERE
- Macrolide antimicrobial
○ Erythromycin or clarithromycin
○ Adverse side effects - NOT IN ADULT HORSES
§ Colitis (often self-limiting), hyperthermia (erythromycin)
- Supportive care
○ Intranasal oxygen
○ Intravenous fluid therapy
○ Nutritional support
Treatment duration ranges from 4 to 10 weeks
80
Rhodoccous equi prevention and prognosis
Prevention
- Management practices thought to be important
○ Manure removal
○ Prevent overcrowding
○ Reduce dust
- Hyperimmune plasma
○ Administered in the first week of life and then at 30 days
Prognosis
- Outcome difficult to predict in individual animals
○ Mildly affected foals (early detection) usually respond to therapy
- Fair to good overall
○ Many foals perform as expected as athletes
81
Pleuropneumonia/bacterial pneumonia what age, history of, clinical presentation and cause
- Usually young adults
- Often history of travel
○ Shipping fever
- Clinical presentation
○ Dull, depressed, febrile, tachypnoea
○ Often no COUGH
○ Horses with pleurodynia can present with sign of colic
- Causative bacteria are often opportunistic invaders from URT - why need to do trans-tracheal wash
82
Why is a history of travel predisposing for pleuropneumonia and therefore how can you improve
○ Other stresses (viral disease) can be predisposing, dehydrated - don't like to drink when on truck (clogged mucociliary clearance)
○ Poor ventilation, unable to move head downwards and so get rid of bacteria, close proximity to other horses
○ CAN PREVENT VIA ADDRESSING THESE THINGS -> not hay in-front of horse, increase ventilation, stop every few hours to allow horse to drink and put head down to graze
83
pleuropneumonia what are the 5 diagnostic techniques
1. Physical examination
○ Re-breath if not distressed
2. Complete blood count
○ Fibrinogen concentration
○ Consider serum/plasma biochemistry - going to treat with NSAIDS so need to know whether able to take it
3. Radiography, ultrasonography
4. Trans-tracheal wash
○ Cytology and culture
§ Examples of bacteria -> strep equi ss zooepidemicus - MOST COMMON, Klebsiella pneumoniae
5. Thoracocentesis -> pleural fluid
○ Often a different organisms when compared to TTW - degenerate neutrophils present (worse prognosis)
○ L and R sides of the chest often different despite fenestrated mediastinum in most adults
84
pleuropneumonia what are the 4 things needed for treatment
1) antibiotics - broadspectrum and change for culture results - pencillin and aminoglycoside +/ metronidazole (anaerobic - abscess present)
- need long-term treatment
2) NSAIDS - care with GIT renal
3) thoracic drains if necessary - until effusion stops
4) supportive care - IV, intra-nasal oxygen, nutritional, laminitis prophylaxis (ice boots)
85
pleuropneumonia what are 4 complications and when do you stop treating
Complications
- Abscess formation (pleural, pulmonary)
- Pleural adhesions
- Jugular vein thrombosis
- Laminitis
When do you stop treating?
○ Re-check with radiographs and/or ultrasound
○ Normal fibrinogen and white cells count
○ Afebrile off all drugs for several days
- Mild cases usually require 1-3 weeks treatment
- Abscesses/necrotic lung/anaerobic infections will need 1-6 months
○ Need to switch onto oral antibiotics for this length of time will not handle intramuscular injection of penicillin for this timeframe
86
Epistaxis what are 8 common causes and most common
1. Exercise induced pulmonary haemorrhage (EIPH) - most common
2. Trauma - common
○ Passage of an NGT or endoscope
3. Ethmoid haematoma
4. Guttural pouch mycosis
5. Abscess
6. Foreign body
7. Tumours/neoplasia
8. Nasal polyps
87
Unilateral vs bilateral epistaxis where originate and examples
Unilateral - typically originates from URT
- Nasal passage
- Sinuses
- Guttural pouches (mild haemorrhage)
Bilateral - typically originates from LRT
- Exercise induced pulmonary haemorrhage
- Guttural pouches (moderate to severe haemorrhage)
- Larynx/pharynx
- Also consider systemic disease causing coagulopathies
88
Exercise induced pulmonary haemorrhage
| what is it and additional clinical signs
```
- Blood in the airways following strenuous exercise
○ Approx 10% of affected horses present with epistaxis
- Additional clinical signs include:
○ Impaired athletic performance
§ Slowing toward the end of the race
○ Prolonged recovery after exercise
○ Abnormal breathing
○ Excessive swallowing after exercise
```
89
Exercise induced pulmonary haemorrhage diagnosis, cause and treatment
Diagnosis
- Endoscopic examination of trachea within 90 min of exercise
Cause - unknown - capillary stress failure due to high vascular pressure most common
Treatment - large numbers few beneficent
- Furosemide reduces the severity of EIPH
○ Reduces vascular pressures although exact mechanism of action is unclear
- Management (reduction) of airway inflammation probably important
○ Very difficult to eliminate in race horses
