CMS- Cardiorespiritory and dental and GIT Flashcards
upper respiritory tract disease in horses
Nasal and Paranasal-
Rhinitis
Sinusitis - 1o or 2o
Sinus cysts
Ethmoid Haematoma
Nasal/sinus neoplasia
Trauma
Guttural Pouch-
Tympany
Empyema
Mycosis
Neoplasia - rare
Temporohyoid Osteoarthropathy
Laryngeal/Pharyngeal-
Recurrent Laryngeal neuropathy (RLN)
Dorsal displacement of the soft palate (DDSP)
Epiglottic entrapment
Sub-epiglottic cysts
Arytenoid chondropathy
4-Branchial arch defects
Infectious-
Strangles
Influenza, EHV etc
Lower Respiratory Tract disease in horses
Pneumonia
Pleuropneumonia
Haemothorax
Pneumothorax
Pulmonary/pleural neoplasia
Equine Asthma
Exercise induced Pulmonary haemorrhage (EIPH)
Interstitial disease
Pulmonary oedema
Guttural Pouch
Not present in any other domestic species other than horses
Very large air-filled spaces ( 300- 500 ml in adult horse)
Floor of GP forms dorsal roof of nasopharynx
Contain numerous important structures
Entrance through the ostia from the nasopharynx
Ostia meet in the midline when the horse swallows to equalise pressure
Medial and lateral compartments divided by the styohyoid
Medial compartment is larger
(2/3 of total size)
what structures are assosiated with the medial compartment od the gutteral pouch
Glossopharyngeal (IX)
Vagus (X)
Accessory (XI)
Hypoglossal (XII)
pharyngeal branches of (IX and X)
Sympathetic trunk
Internal carotid
+ Retropharyngeal LN’s
what structures are assosiated with the Lateral Compartment
of the gutteral pouch
Facial nerve (VII) (short distance over the caudodorsal aspect.
External carotid artery (continues as the maxillary artery along the roof of the guttural pouch)
The vestibulocochlear nerve (CN VIII) does not enter the guttural pouch directly but may be involved in guttural pouch diseases
Guttural Pouch Empyema
Something you will come across
Most commonly secondary to streptococcus equi var equi
Occasionally strep zooepidemicus
Clinical Signs-
Dullness/pyrexia (not always)
Bilateral/unilateral nasal discharge
Occasionally neuropathies dysphagia/dyspnoea
Diagnosis -
Endoscopy
Radiography
Culture/PCR
Treatment-
Acute- liquid pus
Feed from floor
Flush with indwelling foley
Crystalline penicillin mixed with gelatin instilled into guttural pouch (care with penecillin and horses - has huge effect on bacterial flor and causes diarrhoea)
Chronic (chondroids)-
Lavage
Endoscopic basket
numerois condriods- Surgical removal
Guttural pouch mycosis
Rare but very serious
Often one non-fatal bleed before catastrophic episode
No age, breed sex dispositions
Aspergillus and Candida species commonly involved.
Attach to neurovascular structures
Most commonly ICA
Clinical signs
May be found dead due to epistaxis
Unilateral epistaxis
Dysphagia
Facial paralysis
Diagnosis
Clinical signs
Endoscopy
Treatment
Topical antifungals (mild disease with no severe epistaxis)
Surgical correction- referral
Vessel ligation
Balloon catheter
Embolisation
in horses with dyshpagia as opposed to epistaxis treatment is less rewarding. neuro signs harder to treat
Guttural Pouch Tympany
occurs when the guttural pouch becomes abnormally filled with air, causing nonpainful swelling just behind the jaw
congenital
Uncommon disorder of foals
Breed and gender risk (fillies and Arabs)
Unilateral or bilateral distension of pouches with air/ otherwise healthy foal
Causes-
Mucosal flap acting as a one-way valve
Inflammation from an upper airway infection
Persistent coughing/muscle dysfunction
Clinical signs-
Air filled swelling of the parotid area
Snoring noises when suckling
Rarely dyspnoea / Acute respiratory distress
Diagnosis-
Clinical signs
Endoscopy – distinguish between unilateral and bilateral disease and plan treatment
Radiography
Treatment-
Temporary relief achieved by catheterising the affected guttural pouch or pouches- short and long term
Surgical treatment to create a permanent means of evacuating air, either through the unaffected guttural pouch or
through an artificially created opening into the pharynx (salpingopharyngeal fistula)
usually undertaken in referal
Temporohyoid Osteoarthropathy
horses
Quite uncommon
Arthritis
Infection - Secondary to middle ear infection
Lead to fusion of the temporohyoid joint
Pathogenesis-
Bony changes may be exacerbated by:
movement of the tongue and larynx during swallowing
vocalising
combined head and neck movements
oral or dental examinations
Fused temporohyoid joint can fracture injuring adjacent CN VII
& CN VIII
Clinical signs
Vestibular disease
Head tilt
Facial paralysis
Head shaking
Pain on palpation of base of ear
Diagnosis
Endoscopy
Radiography
Computed tomography (choice)
Treatment-
NSAIDs
Antibiotics
Surgery
Ceratohyoidectomy ( removal of whole ceratohypid bone)
Partial Styloidectomy
Laryngeal/Pharyngeal Disorders of the horse
Recurrent Laryngeal neuropathy (RLN)
Dorsal displacement of the soft palate (DDSP)
Epiglottic entrapment
Sub-epiglottic cysts
Arytenoid chondropathy
4-Branchial arch defects
Recurrent Laryngeal Neuropathy (laryngeal hemiplegia)
Common cause of poor performance in racehorse
Degenerative disorder of the recurrent laryngeal nerves (RLn) of breeds such as Thoroughbreds and Drafts.
Preferential degeneration of the left RLn over the right RLn that causes paresis or, in severe cases, paralysis of the left intrinsic laryngeal muscles preventing arytenoid movement
Horse height is reported as a significant contributor to RLN-status, with taller horses being at greater risk
Clinical signs -
Inspiratory noise (‘Roar’)
Exercise intolerance
Diagnosis -
Clinical history and signalment
Laryngeal palpation (asymmetry noted – severe cases)
Resting endoscopy: Havemeyer scale
Exercising Endoscopy
Laryngeal ultrasonography (Chalmers et al, 2006)
Treatment-
Dependant on use of horse and severity
Prosthetic laryngoplasty
Hobday’ procedure (via laryngotomy
or standing laser)- less severly effected and not high activity horse removal of the horse’s left vocal cord along with two adjacent pouches, to reduce or stop the vibration induced noise.
Arytenoidectomy -
Neuromuscular pedicle graft - rarley done in uk, more usefulll in young horses
Tracheostomy- can race a horse with tracheostomy tube
Laryngeal pacemaker
Complications post-surgery? - aspiration pneumonia
Dorsal Displacement of the Soft Palate (DDSP)
Most common NP disorder of horses presenting with respiratory noise and poor performance.
Horses that undergo fast competitive work
Precise aetiology unknown (2 theories)
Neuromuscular dysfunction of the intrinsic soft palate muscles (Holcombe et al, 1998)
Positioning of laryngohyoid apparatus – factor? Larynx held in a more dorsal and caudal position.
Leads to Abnormal position of soft palate and larynx - theory behind “Tie forward” procedure
Pathophysiology
Severe exertion → billowing at junction of hard and soft palate → wave moves caudally along soft palate towards free edge.
Concurrent caudal retraction of larynx and irregular breathing → soft palate slips out from under epiglottis and obstructs the rima glottiis.
Clinical signs
“Choking” “Gurgling” “Swallowing of the Tongue” at exercise
Often suggestive respiratory noise together with a dramatic drop in exercise tolerance which may then resolve
Can be “silent”
Diagnosis
Resting endoscopy is usually normal
Many horses will displace their soft palate on endoscopy – as longs as they can replace in 1-2 swallows this should not be considered abnormal.
Ulceration of caudal border may suggest displacement at exercise
Exercising endoscopy is normally required for diagnosis
Many treatments available - reflects lack of clear understanding
Conservative-
Eliminate predisposing factors and concurrent disease.
Get the horse fit.
Allow time as may improve with age.
Tack changes -
Nose bands
Tongue ties (regulations apply)
Medical-
Systemic and topical corticosteroids to reduce upper airway inflammation
Staphylectomy - Resection of caudal border of soft palate- stops obtruction, too much of border removed causes worse issues with displacment
Myectomy - reduces caudal retraction of larynx.
Combined staphylectomy and myectomy (Llewellyn Procedure)
Tension palatoplasty (Ahern procedure) -attempts to tighten palate
Epiglottic augmentation to help keep soft pallet bellow
Thermocautery / laser cautery – “firing”
‘Tie-forward’ procedure with sternothyroid tenectomy– treatment of choice
Tracheostomy – last resort
Epiglottic Entrapment
Loose sub epiglottic mucosal tissue becomes persistently or intermittently entrapped over the dorsal surface of the epiglottis.
Unknown aetiology -
Two studies have shown a shorter epiglottic length or excessive sub-epiglottic tissue as potential cause (Lindford et al, 1983; Tulleners 1991)
Clinical signs-
Respiratory noise
Exercise intolerance
Some asymptomatic found incidentally at endoscopy
Diagnosis-
Resting endoscopy
Exercising endoscopy (some can be intermittent and occur only at exercise)
Around 45-50% are ulcerated (Ross et al, 1993)
Treatment: division of entrapping membrane
Axial division with laser
Axial division with a curved bistoury
Nasally
Orally
Division via laryngotomy
Sub-epiglottic Cyst
Uncommon -
May be inflammatory, traumatic or congenital in origin
Congenital (abnormality of thyroglossal duct)
Clinical signs -
Foals – nasal reflux of milk
respiratory noise (inhalation and exhalation)
poor performance, coughing, dysphagia, nasal discharge
Diagnosis -
Endoscopy
If below level of palate – oral endoscopy/ palpation
Treatment-
Excision via laryngotomy (can be standing)
Electrocautery snare
Laser Excision
Formalin injection
Arytenoid Chondropathy
Inflammatory/infectious/dystrophic changes of one or both arytenoid cartilages
Most common in young TB’s
Rare in UK
Aetiology
Unknown? secondary to mucosal disruption
leading to infection/ inflammation of arytenoid
Clinical signs
Acute : can present in respiratory distress (inspiratory noise)
Chronic: Poor performance and inspiratory noise
Diagnosis
Endoscopy
Treatment
Medical
NSAIDs and antibiotics (long term) +/- Steroids
Tracheostomy
Surgical- IF MEDS UNSUCESSFUL
Arytenoidectomy
Debridement via laryngotomy
Prognosis- variable
4-Branchial Arch Defects (4-BAD)
Developmental malformation of laryngeal structures formed from the 4th and, occasionally 6th, branchial arches.
Horses affected to varying degrees
The most common cause of apparent RIGHT sided RLN
Most common findings are:
Right sided laryngeal dysfunction
Rostral displacement of palatopharyngeal arch
Abnormalities of the laryngeal cartilages and associated muscles
which can lead to aerophagia
Vary depending on deformity
Poor performance
Dysphagia / aspiration pneumonia
“Burping”
Respiratory obstruction
Diagnosis-
Endoscopy
Radiography - may indicate the presence of a column of air
extending into the oesophagus.
Treatment-
None
Laryngeal surgery / tracheostomy
Characteristics of Infectious uper respiritory tract disease in horses
Nasal discharge
Pyrexia
Cough
Depression/anorexia
Lymphadenopathy
Limb oedema
Ocular discharge
Abortion/ acute onset neurological disease / (EHV-1
Infectious Respiratory viruses in horses
Common Viral causes-
Equine Influenza
Equine Alphaherpesviruses (EHV-1 and 4)
Uncommon Viral causes-
Equine picornaviruses – Equine Rhinitis A and B (ERAV and ERBV) Role unclear. Mild disease
Equine gammaherpesviruses (EHV-2 and EHV-5) ? role in development of equine multinodular pulmonary fibrosis (EMPF)
Adenovirus – usually only a problem in animals with immunodeficiency (SCID in Arab foals)
Equine Viral Arteritis – reproductive/respiratory disease conjunctivitis; dependent, especially limb oedema, abortion, neonatal pneumonia, enteritis.
Hendra virus and African horse sickness virus – geographically limited can cause severe systemic disease which can manifest as respiratory disease
common bacterial respiritory pathogens in horses
Streptococcus equi equi (Strangles)
EIv- equine influenza virus
high morbidity, low mortality, commom in young horses
incubation- 1-3 days
rapid spread
transmission- close contact and extended distances
shedding time- 7-10 days
can be subclinical shedder
Orthymyxovirus, single stranded RNA virus
Haemagluttin (H) and Neuraminidase (N) glycoprotein surface antigens determine subtype.
2 subtypes H7N7 (no recent outbreaks) and H3N8
H and N mutations lead to antigenic drift allowing the virus to escape immunity
H3N8 diverged into European and American lineages
American lineages diverged into antigenically and genetically different lineages, sub-lineages and clades
Worldwide distribution ( Exceptions NZ and Iceland)
Young horses in big groups – highest risk
Endemic in the UK
Risk factors Poor ventilation, high humidity, poor vaccination status
Subclinical shedders can infect naïve populations
Spread primarily by respiratory route aerosol and direct contact
Inhaled virus attaches to respiratory mucosal cells
Penetrates the epithelial cells of the URT
Virus Replicates in epithelial cells leading to…
Desquamation, denudation and clumping of cilia on respiratory epithelium
Denuding of respiratory epithelium leads to increased risk of secondary bacterial infection
Can take up to 32 days for mucociliary transport to recover
Horses need protracted recovery time- interuption of training
1 week off for each day of pyrexia
clinical signs-
Pyrexia
Nasal discharge – serous > mucopurulent (2° infection)
Cough (cough initially dry and harsh and frequent, can change with secondary pneumonia)
Inappetence / anorexia
Muscle soreness
Complications-
Development of secondary opportunist bacterial infections (e.g. pharyngitis, sinusitis, pneumonia)
treatment-
Largely symptomatic
Nonsteroidal anti‐inflammatory drugs (NSAIDs)
Air hygiene- to prevent secondary infection
Adequate rest- exersise can draw pathogens down deeper into the weakened epithelium
Antimicrobials in case of secondary infections
Antiviral drugs
Available but not regularly used – mixed evidence/
resistance concerns / cost
diagnostics-
cough and rapid disease spred characteristic
paired serology (acute and convelesent sample)
virus idolation form np swab- shedding breif so tricky
nasal swab elisa
EHV 1/4- equine herpes
high morbidity, low mortality, commom in young horses
incubation- 3-10 (up to 21)days
rapid spread
transmission- close contact and extended distances/ prodicts of abortion
shedding time- 3 weeks
can become latent
Alpha herpesvirus, double stranded DNA virus
Foals, weanling and yearlings
Widespread – high seroprevalence ( approaching 90%)
Latent infection occurs following primary infection
EHV 4 – Respiratory only
EHV 1 – Respiratory, Abortion, Neurological
Inhaled and attaches and replicates in mucosal epithelial cells of nasal passage, pharynx and tonsillar tissues
EHV 1 can also infect via the conjunctival epithelium
Both EHV-1/4 lead to upper respiratory tract inflammation (rhinitis, pharyngitis and tracheitis)
Allows secondary invasion of mucosa by bacteria
EHV 4 limited to the respiratory tract but EHV-1 cell associated viraemia
Transported by T‐lymphocytes to other tissues
Latent infection in CD8+ T‐lymphocytes and trigeminal neural ganglion
EHV 1-
Following infection through the respiratory system, some virulent strains of EHV-1 demonstrate endotheliotropism
> Endothelial cell replication and infection
> Vasculitis & thromboischaemia of small arterioles
Nervous System > Ischaemic neuronal death >Myeloencephalopathy
Uterus > Placental disease > Abortion/Stillbirth or Foetal Infection
Sudden onset neurological signs:
Ataxia – particularly in the hind limbs
Caudal spinal cord segments often affected;
Bladder distension & urinary incontinence
Penile protrusion in males
Flaccid tail & anus
Abortion or foetal infection
Treatment of EHV associated respiratory disease
As for EIV, symptomatic +/- antibiotics for secondary bacterial infection.
Respiritory signs-
Mild disease in adults
Can be fatal in neonatal foals / foals infected in utero
Older foals, outbreaks of rhinopneumonitis
Biphasic pyrexia, depression and anorexia
Nasal discharge – serous > mucopurulent (2° infection)
Swelling of LN’s
Oedema and hyperaemia of mucous membranes
Coughing in some cases
Inflammatory airway disease in young racehorses
Complications-
Development of bronchopneumonia
*Viral recrudescence generally leads to no clinical signs
diagnostics-
paired serology- though high seroprevelance
viris isolation from np swabs
virus isolation from whole citrated blood
pcr of np swab (too sensitive)
Streptococcus equi equi (Strangles)
high morbidity, low mortality, commom in young horses
incubation- 3-8
rapid spread
transmission- close contact and extended distances/ prodicts of abortion
shedding time- 4-6 weeks
can become chronic carrier
Lancefield Group C Streptococci
Worldwide prevalence
Commonly affects young horses
4-6 times more common than influenza in UK
High morbidity/ low mortality
Highly contagious – spread by direct contact & fomites
Spread in water and feed buckets
Recovered animals may shed for months
Infection by inhalation or ingestion
Attachment to crypt of tonsils
Local rhinitis and pharyngitis (sore when swallowing)
Translocation to local lymph nodes ( SMLN or RPLN)
Abscess formation – drain either outside or into GP’s
clincical signs-
Pyrexia, inappetence
Nasal discharge generally mucopurulent
Swelling of LN’s and abscessation.
Abscesses rupture and resolve within 2 weeks.
Swelling can be dramatic > respiratory distress, cough, dysphagia
Shedding up to 4 weeks
complications-
Dyspnoea due to URT obstruction - tracheotomy
Carrier State (guttural pouches – lasts for many months)
Metastatic strangles (Bastard strangles) systemic spread > abscesses formation at any other site in the body. Difficult to treat
Purpura Hamorrhagica
Can occur after any respiratory disease
Antibody-antigen complex (type 3 hypersensitivity)
Results in a vasculitis and severe illness. This must be treated with corticosteroids to suppress the hypersensitivity inflammatory response.
treatment-
Symptomatic pain relief (NSAID’s) – to help the horse feel better and improve its appetite
Hot pack abscesses – this helps to mature the abscesses
Lance mature abscesses and collect the pus so that it does not contaminate the environment
A tracheostomy is necessary in horses with respiratory distress (rare)
Antibiotics
Reserve for very sick/compromised patients.
S. equi equi usually sensitive to Penicillin (20-25mg/kg IM BID)
Will have benefit in early disease, but may interfere with development of natural immunity
Can slow maturation of abscesses and may lengthen disease course
No influence on development of “bastard” strangles
Guttural pouch empyema / chondroids -
Purpura haemorrhagica
Goal is to eliminate underlying infection (Penicillin)
Limit immunologic response ( Corticosteroids e.g. dexamethasone 0.05-0.1 mg/kg IV SID/ Prednisolone 0.5 – 1 mg/kg)
Provide analgesia (NSAID’s)
Reduce oedema
Nursing care
diagnostics-
absessation of LN diagnostic
paired serology
pcr of np swabs and gp wash
culture (less sensitive)- np swabs, abcess content, gp wash
Confirmation of Freedom from Disease form equine influenza
When all clinical signs have resolved &
Repeat nasopharyngeal swabbing confirms negative PCR tests
Most horses stop shedding virus about 10 days after initial uncomplicated infection.
Confirmation of Freedom from Disease form EHV-1/4
When all clinical signs have resolved
Endemic in UK: Total freedom from disease can never be confirmed
Confirmation of Freedom from Disease form strep. equi
When all clinical signs have resolved &
Three negative nasopharyngeal swabs
OR
negative on bilateral guttural pouch samples (PCR)
Clearance testing should commence approximately four weeks after the last clinical signs of strangles have been observed.
Specific disease testing for nasopharyngeal disease in small animals
Expensive - only perform where high index of suspicion
Feline
PCR on a conjunctival/nasal swab
Chlamydia felis, Calicivirus, herpesvirus, M. felis, B. bronchiseptica
Canine
PCR on a swab
Adenovirus, parainfluenza virus, herpes virus, distemper virus, B. bronchiseptica, Mycoplasma spp.
Small Mammals
B. bronchiseptica PCR and culture; Guinea pigs and rabbits.
Rabbits – B. bronchiseptica, P. multocida, Chlamydia spp.
Reptiles
Tortoises – herpesvirus, Mycoplasma spp, picornavirus; PCR on a swab.
Snakes - Adenovirus, Reovirus, Arenavirus, Paramyxovirus/Ferlavirus, Nidovirus; PCR and EDTA blood sample.
Chlamydia psittaci
Nasal flush in small animals
Can sometimes be done conscious with the head directed towards the floor.
Otherwise do under GA – protect the airway!!!
Collect material into a sterile kidney dish for cytology and culture (bacterial, fungal)
Can be therapeutic e.g. with disinfectant or to flush out a FB.
Nasal swabs in small animals
Not as useful for sample collection as a nasal flush.
Deep swab better sensitivity – around the level of the medial canthus of the eye in rabbits.
Generally done under deep sedation or GA to get deep enough sample.
Radiographs for nasopharyngeal isease in small animals
Poorly sensitive for nasal passage and sinus changes; often subtle.
Useful to assess dental disease
computed tomography for nasopharyngeal disease in small animals
Cross-sectional images avoid superimposition of structures much better assessment of the nasal cavities and sinuses.
Useful for SOL where and endoscpe cannot be passed.
Necessary for surgical planning e.g. for neoplasia.
Requires GA
rhinoscopy for nasopharyngeal isease in small animals
Can use a rigid endoscope; flexible preferred for pharyngoscomy.
Requires deep plane of GA.
May ned to flush nasal passages first to facilitate visualisation.
Risk of haemorrhage.
Uses:
Visualize masses, fungal plaques, foreign bodies
Biopsy
Sample for fungal culture
May be therapeutic:
Removal of foreign body or polyp
Aspergilloma debulking
Targeted flushing with treatment e.g. antifungal.
pharyngoscopy for nasopharyngeal isease in small animals
Usually done as extension of rhinoscopy.
Flexible endoscope retroflexed behind the soft palate for inspection of the caudal nasopharynx.
Uses:
Evaluate length of soft palate.
Look above soft palate for mass, polyp, foreign body, stenosis etc.
Emergency management of epistaxis
Can be dramatic.
Emergency management:
Reduce BP - cage rest, sedation
Reduce bleeding - ice packs on, packing of the nose with adrenaline soaked sponges.
Ongoing management
Severe cases may require treatment for hypovolaemic shock or even blood transfusion
Need to identify and treat underlying disease
Common underlying causes:
Coagulopathy
Invasive nasal diseases, eg Aspergillosis, neoplasia blood vessel rupture.
Trauma e.g. FB, penetrating I jury
viral upper respiritory tract dissease in small animals
Dogs: See Canine infectious respiratory disease lecture
Cats: Calicvirus and herpesvirus
Tortoises: Herpesvirus
Snakes: adenoviruses, herpesviruses, ranaviruses, iridioviruses, reovirus and picornaviruses.
Ferrets: Influenza
Some have a very poor prognosis e.g. snake viral diseases.
Usually rely on the immune system clearing the infection
May lifelong carrier status (calicivirus, herpesvirus etc.)
treatment-
Supportive treatment:
Anti-inflammatory drugs (NSAIDs most common)
Nebulisation (F10, saline, mucolytics)
Mucolytic (e.g. Bromhexine)
Fluid therapy
Supportive feeding
Specific treatment:
Feline herpesviruses – ocular topical preparations (human preparations off license) or systemic (famiciclovir or feline omega interferon) reported
Chelonia – acyclovir reported for use in herpesvirus infection
bacterial upper respiritory tract dissease in small animals
Primary bacterial disease = rare:
Bordetella bronchiseptica (Dogs, cats, G. pigs)
Pasteurella multocida (rabbits)
Mycoplasma spp. (birds, chelonia, rats)
Chlamydia (birds, cats)
Also commensals; require a stressor to induce disease.
Also common as 2o infections
Treatment:
Systemic antibiosis
TMPS, tetracyclines and fluorquinolones all effective against P. multocida and B. bronchiseptica.
Chlamydia and mycoplasma have no cell wall so tetracyclines and fluoroquinolones indicated.
Systemic mucolytics (bromhexidine)
Anti-inflammatory drugs (NSAIDs most common)
penicilin and cyclosporins effective against pasturella- but mainly a pathogen of rabbits and these antibiotics caise dibiosis in rabbits
Supportive care:
Nebulisation
Saline and/or mucolytics (e.g. acetylcysteine) to aid removal of exudate.
Antiseptics e.g. F10
Assisted feeding (rabbits, G. pigs)
Fluid therapy
Prevention of primary bacterial disease
Vaccination:
B. bronchiseptica - dogs and cats, intranasal administration.
P. multocida – rabbits (commercial situations)
Reduces symptoms but doesn’t prevent disease.
Reduce stressors
Bacterial infection usually 2o to underlying pathology:
Viral or fungal infection
Dental disease (esp rabbits)
Foreign body
Neoplasia
Trauma
Hypovitaminosis A- birds
Treatment:
As for primary disease
Treat underlying condition
upper respiritory fungal disease in small animals
Aspergillosis most common by far in the UK.
Dogs = usually immunocompetent (cf disseminated aspergillosis), birds = usually an underlying condition
Forms granulomas in the nasal cavity (dogs), syrinx (birds) and lower airways.
Granuloma debulking essential to success of treatment – often done at time of rhinoscopy.
Topical treatment:
Irrigation post-debulking +/- nebulisation with antifungal agents.
Antifungals - Amphotericin B, terbinafine, azoles (clotrimazole, enilconazole)
F10
Systemic treatment:
Azoles (itraconazole, voriconazole, ketoconazole)
Amphotericin B
Terbinafine
Supportive care:
Treat 2o infections
Liver support (SAMe and silybin)
GI support (diet, probiotics)
Monitoring
Bloods (hepatic enzymes, WBC count)
treatment for fungal disease in small anials
Topical treatment:
Irrigation post-debulking +/- nebulisation with antifungal agents.
Antifungals - Amphotericin B, terbinafine, azoles (clotrimazole, enilconazole)
F10
Systemic treatment:
Azoles (itraconazole, voriconazole, ketoconazole)
Amphotericin B
Terbinafine
Supportive care:
Treat 2o infections
Liver support (SAMe and silybin)
GI support (diet, probiotics)
Monitoring
Bloods (hepatic enzymes, WBC count)
upper respiritory foreign bodies in small animals
Common FB:
Cats: Grass blades
Dogs: Grass seeds, stones?
Small mammals and chelonia: Hay
Primary treatment = removal.
Tx of 2o infections
Systemic anti-inflammatory (NSAIDs)
trauma to upper repiritory tract in small animals
Pharyngeal trauma e.g. stick injury
External trauma e.g. bite wounds to muzzle
Symptomatic treatment:
Removal of stick if present - will require GA if penetrating.
Analgesia
Tx 2o infections
Nasopharyngeal polyp
Rare in dogs; result of chronic inflammation hyperplasia.
Common in cats
Benign masses arising from the lining of the middle ear.
Can extend up into the external ear canal or down into the nasopharynx.
Removed via traction in the first instance.
Surgical access – Incision through the mid-line of the soft palate (avoiding the distal 5 mm) or bulla osteotomy.
Malignant neoplasia of the upper respiritory tract of small animals
Adenocarcinoma = most common.
Other epithelial tumours (carcinoma, squamous cell carcinoma) also relatively common.
Radiotherapy = treatment of choice
Surgical resection/reduction and chemotherapy reported, may be suitable for some cases.
Median survival time 10-18 months
imaging for laryngeal disease in small animals
Radiographs = poorly sensitive; possibly useful for mass or FB; best without ET tube
CT = better sensitivity, may be used to assess airway lumen.
MRI = useful for soft tissue lesions airway narrowing.
laryngitis- small animals
May be due to infection (e.g. KC complex), irritation (e.g. smoke inhalation), trauma etc.
Treatment usually symptomatic:
Anti-inflammatory drugs (NSAIDs for mild cases, steroids for severe).
Treat any underlying infection where possible.
In very severe cases, inflammation may laryngeal oedema and complete or partial obstruction.
Oxygen supplementation, sedation, or GA with intubation or tracheotomy may be required.
Laryngoscopy for laryngeal disease in small animals
Most useful test in most cases.
Larynx evaluated for:
Normal function (bilateral abduction during inspiration)
Thickening
Masses associated with arytenoids or vocal folds
Presence of everted laryngeal saccules
Extraluminal masses compressing airway
Laryngeal collapse
laryngeal trauma- small animal
Internal (e.g. from FB) or external (e.g. bite wound, choke chain injury).
Commonly partial or complete obstruction due to oedema.
Need to check for cartilage fractures
Complications:
Laryngeal paralysis or collapse.
Fibrotic and granulomatous tissue secondary to severe or chronic damage stenosis.
lower airway foreign body- small animals
Less common than nasopharyngeal or tracheal.
May -> complete or partial obstruction, or just irritation.
Treatment: Removal and anti-inflammatory drugs, treatment of 2o infections.
In acute obstruction tracheostomy may be indicated – see later
frequently present as emergancies etih as inncident took place or after tissus have swolen and obstruction has occured
Emergency treatment:
Oxygen administration.
Sedation/anesthesia.
Intubation/tracheostomy
Corticosteroids to reduce oedema
Antibiotics (if infected)
Surgical treatment:
To repair severe soft tissue damage, including removing foreign bodies e.g. penetrating stick injuries.
To repair discontinuous laryngeal cartilage fractures (high risk of granulation tissue stenosis)
To manage 2o laryngeal paralysis
Laryngeal paralysis
common in older dogs
roaring noise
Failure of arytenoid and vocal fold movement during the respiratory cycle, particularly decreased or absent abduction during inspiration.
Result of:
Intrinsic laryngeal muscle innervation disease or damage.
Disease or injury of the dorsal crico arytenoid muscles or the arytenoid cartilages.
Generalised neuropathy (cats)
usually ideopathic
The rima is progressively obscured by the collapsing corniculate (upper arrows) and cuneiform (lower arrows) processes of the arytenoid cartilages. The epiglottis may also collapse towards the rima.
Symptoms:
Inspiratory stridor (“roaring”, dysphonia (altered bark), and exercise intolerance most common symptoms.
Cyanosis and collapse in severe cases.
Dysphagia also reported.
Diagnosis
Clinical signs, signalment, laryngoscopy
treatment of laryngeal collapse
Emergency management:
As per trauma
Medical management:
Anti-inflammatory drugs (NSAIDs in mild cases, steroids in severe)
Rarely successful
Surgical management:
Laryngoplasty (“tie back”)
Laryngoplasty (“tie back”)
Surgical abduction of the arytenoid cartilage -. enlargement of the rima glottidis .
Unilateral generally provide sufficient increase in glottis diameter to reduce symptoms.
May be performed bilaterally if needed but increases risk of aspiration.
NEOPLASIA OF larynx in smal animals
Rare
Advanced imaging, biopsy and histopathology required for diagnosis.
Benign masses may be removed (care re:larynx function); malignant masses may be managed surgically, or via radiotherapy or chemotherapy depending on type.
Radiographs and CT for tracheal disease in small animals
Neck radiographs used to evaluate for tracheal collapse, foreign body, hypoplasia,and stenosis.
Thoracic radiographshelp rule out pulmonary or cardiac disease.
CT more sensitive for structural abnormalities, masses etc.
fluroscopy for tracheal disease in small animals
Useful in evaluating tracheal collapse.
Shows real time changes in tracheal diameter.
Can be done conscious (observation of dynamic changes as the dog breaths or coughs) or under GA (negative pressure applied to the ET tube)
Tracheobronchoscopy for tracheal disease in small animals
Used for:
Evaluating dynamic disease e.g. tracheal collapse.
Diagnosis of extraluminal or intraluminal masses.
Diagnosis and removal of foreign bodies.
Obtaining cytology and biopsy samples.
Endoscope usually passed through ET tube to maintain airway patency under GA.
Tracheal wash for tracheal disease in small animals
Small volume of sterile saline instilled into trachea then re-aspirated.
Samples can be used for cytology, culture, and to identify parasitic organisms.
May be performed via the oral cavity under GA, either blind or via endoscopic visualisation.
Conscious technique also described.
or
Small volume of sterile saline instilled into trachea then re-aspirated.
Samples can be used for cytology, culture, and to identify parasitic organisms.
May be performed via the oral cavity under GA, either blind or via endoscopic visualisation.
Conscious technique also described.
Tracheitis in small animals
As per laryngitis; due to infection, irritation, trauma etc.
Treatment usually symptomatic:
Anti-inflammatory drugs (NSAIDs for mild cases, steroids for severe).
Treat any underlying infection where possible.
Small FB can irritation without obstruction and may require removal.
Tracheal obstruction in small animals
Can be complete or partial obstruction.
Common in small psittacines e.g. cockatiels (millet seeds)
Can be very dramatic e.g. dogs and rubber balls!
Treatment: Removal and anti-inflammatory drugs, treatment of 2o infections.
In acute obstruction tracheostomy (mammals) or air sac tube (birds) may be indicated.
Tracheal trauma in small animals
Internal (e.g. from FB or inappropriate ET tube use) or external (e.g. bite wound, choke chain injury).
All cervical bite wounds should be assessed for airway damage.
Penetrating injuries:
Require surgical repair
Minor injuries – debridement, primary closure +/- fasciomuscular repair.
Major injuries (non-viable tissue or excessive size) – tracheal resection and anastomosis.
Iatrogenic tracheal tears and pressure necrosis:
Usually from ET tube cuff overinflation and/or excessive repositioning without disconnecting GA circuits during procedures.
May resolve with strict cage rest (esp cats).
Surgery may be primary closure (tears) or anastomosis (necrosis)
Supportive care: Analgesia, antibiosis if needed, airway maintenance.
Tracheal stenosis = common sequale, esp for anastomosis.
Tracheal stenosis in small animals
Usually secondary to injury (iatrogenic, traumatic) or neoplasia, rarely congenital.
Initial treatment = symptomatic (oxygen, anxiolytics)
Mild cases: Dilation with balloon catheter or bougie under endoscopic of fluoroscopic guidance.
High risk of recurrence
Stent placement
Used to retain opening of stenotic area and for palliative management of malignancies
Placed under fluoroscopic guidance.
Antitussives (e.g. butorphanol)
Same procedures in tracheal collapse
Surgical resection and anastomosis
As for trauma
Low dose pred may help prevent stricture formation following surgery.
Tracheal collapse in small animals
In dogs can be acquired or congenital.
Due to chondrodystrophy collapse of the tracheal cartilage rings.
Toy breeds esp Yorkshire terriers predisposed.
Note: Also occurs in horses (Shetland ponies and mini-horses predisposed); Can be 1o or 2o, very rare.
treatment of trachela colapse in small animals
Emergency management:
Place animal in a cool, dark environment
Supplemental oxygen
Light sedation to reduce stress
Cough suppression
Corticosteroid
Symptomatic treatment and management:
Exercise restriction
Maintain (or obtain!) good BCS
Harness instead of collar and lead
Treat concurrent respiratory disease.
Remove respiratory irritants (e.g. cigarette smoke)
Sedatives in stressful circumstances
Conservative management:
Coticosteroids- long term needs tapering
Antitussives
Antisecretory drugs
Bronchodilators
Antibiotics if indicated
Surgical management:
Extraluminal propylene ring prostheses.
Intraluminal stent placement – see prev
Brachycephalic Obstructive Airway Syndrome (BOAS)
Pathogenesis:
Abnormal respiratory anatomy due to shortened faces and reduced skull size without proportional reduction of soft tissues.
Features of BOAS:
Stenotic nares and nasal passages
Overlong soft palate
Laryngeal saccule eversion +/- ccollapse
Tracheal hypoplasia
Acute collapse may occur, especially in hot weather.
Emergency management:
Supplemental oxygen
Sedation
Corticosteroids
Emergency intubation or tracheostomy
Cool, dark environment +/- active cooling if hyperthermic.
treatment of BOAS
Management
Weight management
Avoid walks at hot times of day.
Anti-inflammatory drugs may be used to control airway oedema and maintain patency.
Management of GI signs (thought to be induced by constant aerophagia)
Surgery
Indicated in all cases where CS persist despite medical management, and any animal presenting with acute respiratory distress as a direct result of BOAS.
Variety of procedures which can be performed in isolation or combination, depending on the individual presentation.
Correction of stenotic nares
Resection of aberrant turbinates
Soft palate resection
Laryngeal sacculectomy
Laryngeal tie-back
Prevention – this is an entirely human made problem!
Breed for respiratory function:
The Kennel Club/ University of Cambridge RFG Scheme was introduced in January 2019
Grades BOAS severity to guide breeding choices- 0 to 3.
Validated in the Bulldog, French bulldog and Pug so far
Consists of a clinical assessment of the upper airway with an exercise stress test.
Dogs must be over 1 year of age prior to assessment; results are valid for 2 years then reassessment required.
No analogous scheme currently for cats.
important history questions for sudden death in calves
immune state- what are they vaccinated agianst? how are they vaccinated, collostrum managment
housing- housed togther? quality of housing? housing system
age of calves?
timeline- onset, progression conclusion
history of disease
changes in behaviour
managment- dry cow, partuition and post- partum
clinical assesment on a farm with sudden death of two calves
post mortem dead calves
asses sickly live animals
asses non diseased animals
calf factors= respiritory defences
assess housing- bedding, ventilation, clenliness, size, shared housing, maixed age groups?
important history questions for respiritoey disease in a large beef feedlot
were they bought in? raised on farm? relationship farmer has with suppliers?
biosecurity measures for cows that are bought in?
housing
managment
age
timeline of disease
Important cardiac Diagnostic Tests
Blood pressure
Blood tests-
Haematology/biochemistry
Cardiac biomarkers
Electrocardiography (ECG)
Ultrasonography (focused/emergency thoracic ultrasound, echocardiography)
Radiography
blood pressure as a diagnostic for cardiac disease
Assess cardiac output
Hypotension (particularly in DCM)
Hypertension (cats, MMVD)
(Be aware of stress/white coat effect)
Therapeutic considerations
Antihypertensives
Risks/contraindications e.g. ACEIs in hypotension
Doppler/Oscillometric/Invasive
haemotology and biochemistry as a diagnostic for cardiac disease
Haematology/Biochemistry
Not directly useful in evaluating cardiac disease
Systemic conditions
Therapeutic considerations
Renal values/electrolytes
cardiac biomarkers
Cardiac Biomarkers
NT-proBNP
Troponin
Aims
Screening
Differentiating cardiac v respiratory
Prognostication
Less useful for
Staging
Assessing cardiac function
Diagnosing specific disease
NT-proBNP
Evaluate cardiac stretch
Natriuretic peptides synthesised by the brain (BNP), heart (ANP) and other organs (CNP). Release stimulated by atrial/ventricular stretch
Two major pathways of effects:
Vasodilatory – reduce BP
Renal - natriuresis and diuresis
(Actions generally oppose those of RAAS)
Can measure concentrations of N-terminal portions (NT-proANP/BNP)
BNP used more often, commercial assays available
Increase with severity of disease
Elevated values associated with worse outcome
Can be assessed quantitatively or qualitatively
qUANTITATIVE nt-ProBNP
Quantitative – numerical value
External lab – useful for screening, not emergencies
In house quantitative machines also available (Woodley Vcheck)
Cats:
<100pmol/L – not compatible with increased myocardial stretch/stress
>100pmol/L – increased stretch/stress, further investigations indicated
>270pmol/L – respiratory signs are likely secondary to CHF
Dogs:
<900pmol/L – not compatible with increased myocardial stretch/stress
900-1800pmol/L – increased stretch/stress, further investigations indicated
>1500pmol/L in MMVD – increased risk of CHF in the next 12 months
>1800pmol/L – likely to have clinical signs of heart disease
Breed variation
Dobermans >735pmol/L – increased risk of DCM
Labrador up to 2000pmol/L may be normal
qualitiative NT-proBNP
Qualitative – positive/negative
Use: Differentiating cardiac from respiratory disease in dyspnoeic patients
Good for emergencies
Especially if unable to image
Idexx Feline ProBNP snap
99.5% accuracy for >100pmol/L
95% accuracy for >270pmol/L
troponin
Troponin complex involved in actin-myosin interaction (C, T and I subunits)
Troponin-I (cTnI) is normally bound to troponin-T, detaches in response to sarcomeric injury
Elevated circulating cTnI is a specific indicator of myocardial injury/hypoxia or cellular necrosis
Increases with severity of disease
Elevated values associated with worse outcome/prognosis
Extremely high values seen in myocarditis, sustained ventricular arrhythmias
Day to day utility – unclear
Limited use in myxomatous mitral valve disease, congenital disease
Of some use in patient with unusual presentation
Dilated phenotype in a non-typical breed (or in a cat)
Hypertrophic phenotype in a young cat
May suggest acute inflammatory process
Electrocardiography as a diagnostic for cardiac disease
Arrhythmias
Physical exam critical
Remember arrhythmias can be present in non-cardiac disease, especially in dogs
Also preclinical disease, especially dobermanns, boxers
Ultrasound/Echo as a diagnostic for cardiac disease
Ultrasound is the gold standard test for diagnosing cardiac disease
Thoracic ultrasound (TFAST/POCUS)
Emergency
Dyspnoeic patients
Differentiate cardiac from respiratory conditions
Left atrial enlargement
Identify pleural effusion, pericardial effusion, B-lines?
Measurements?
Subjective?
Ultrasound is the gold standard test for diagnosing cardiac disease
Thoracic ultrasound (TFAST/POCUS)
Emergency
Dyspnoeic patients
Differentiate cardiac from respiratory conditions
Left atrial enlargement
Identify pleural effusion, pericardial effusion, B-lines?
Measurements?
Subjective?
Radiography as a diagnostic for cardiac disease
Aims
Presence of CHF
Cardiomegaly/staging
Concurrent disease
Cough
Less useful for:
Risk of impending CHF
Cardiac function
Diagnosing specific disease
Looking for CHF
Stabilise!
In emergencies ultrasound better
If uncertain but unstable trial medication?
Sedation
MMVD patients are usually safe to sedate/anaesthetise
Usually have good cardiac output/blood pressure/systolic function
Cats, patients with DCM
Ideally assess function
Butorphanol 0.1-0.3mg/kg IM,IV
Alfaxalone/propofol
Cardiomegaly/staging
Very useful if echocardiography not available
Subjective/objective
Vertebral heart score (VHS)
Vertebral left atrial score (VLAS)
VLAS: Vertebral Left Atrial Score
Objective assessment of LA size
Draw from the centre of the ventral aspect of the carina to the most caudal aspect of the LA
Measure the length of this line in vertebral body units, starting at T4
normal equine heartrate
28-44 (lower end for athletes)
Bradydysrhythmias in the horse
MOST ARE NORMAL
Physiological, due to high Parasympathetic (VAGAL) tone
Atrioventricular Block
Sinus arrhythmia
Sinus bradycardia
Siniatrial Block
Sinoatrial Arrest
Abolished with increased sympathetic tone- light exersise, slight stress
profound cases ARE abnormal
Tachydysrhythmias in the horse
ABNORMAL
Pathological
Supraventricular or Ventricular-
Premature depolarisations
Tachycardia
Fibrillation
Inflammatory, degenerative, metabolic, toxic aetiologies
heart sounds in the horse
s1- lub- start of systoly, av valves- qrs
s2- dub- end of systole, sl valves closing- t
s-3 very small squeek sound- ventricles recoiling
s4- contraction of the atria- comes in just before s1- p
Yearling colt presents for castration under standing sedation.
On auscultation, a regularly irregular bradysrhythmia is detected
Regular diastolic pauses
Isolated S4 audible in diastolic pause- missed lub dub
What is the likely diagnosis?
How could you confirm this diagnosis?
What considerations exist for sedating this colt?
regularly ireegular heart rhythm
1)second degree AV block- blocked p waves without qrst complex
p-p interval is the same- san firing fine but avn not transmiting to ventricles
2)The most common physiological dysrhythmia of horses
40% of horses have 20-AV block on 24-hour ECG monitor
3)Long pauses (SA block/arrest) and variation in length of diastole (Sinus bradycardia and sinus arrhythmia) are less common, but can all occur in normal horses
When is it not normal?
If present during exercise (not abolished by inc. sympathetic tone)
Advanced 20-AV block - RARE
- Pathological process creating conduction block at AV node
- Horse will demonstrated exercise intolerance or collapse
Pathological heart blocks are usually associated with inflammatory or degenerative changes at the AV node
Third-Degree AV Block in horses
ventricles not contracting with signals from san
avn will fore them independantly every 20 seconds or so
will show on ECG as random qrs complexes independent of P waves
AV-dissociation:
Rapid SA discharge (due to reduced cardiac output)
Slower rate of Ventricular ‘escape’ complexes (approx. 20/min)
Horses present with severe exercise intolerance and frequent collapse
Treatment
Anti-dysrhythmic medication – used with caution (with 24-hour ECG monitoring)
Anti-inflammatories (dexamethasone 0.1 – 0.2 mg/kg IV) if evidence of inflammatory cause
Definitive long-term therapy - Placement of Pace-maker
4-year-old Thoroughbred racehorse – pulled up during race
An irregularly irregular tachydysrhythmia is detected on auscultation immediately after the race
What differentials exist for tachydysrhythmias in horses at exercise?
Tachydysrhythmias-
Pathological
Supraventricular or Ventricular
Premature depolarisations
Tachycardia
Fibrillation
Inflammatory, degenerative, metabolic, toxic aetiologies
Supraventricular (SVPD)- supraventricular premature depolarisation
Originate in atria - signal came form somewhere separate to SA node
Usually conducted through AV- normal QRS complex seen on ECG
Isolated SVPD at rest not uncommon
eloctrolite imbalence post exersisse
seen as a normal qrs without p wave that interups regular interval- shows they are atrail in nature
Ventricular (VPC)= ventricular premature complex
Originate in ventricles- follows different pathway through heart
Abnormal QRS complexes- different to surrounding ones
Isolated VPCs can occur at rest, during exercise or in the immediate recovery phase post-exercise
Frequent VPCs, or ‘runs’ of VPCs are abnormal
4-year-old Thoroughbred racehorse – pulled up during race
An irregularly irregular tachydysrhythmia is detected on auscultation immediately after the race
Very irregular diastolic pauses
Absence of S4
Loud S1
1)What is the likely diagnosis?
2)How could you confirm the diagnosis?
1) Atrial Fibrillation- most common
2) ecg- irrecular intervals between qrst complex with no p waves and varience on baseline. the atria are fibrilating creating F waves (bumpy apearence of base line)
atrail contraction into ventricles is lost and so cardiac output slightly reuced- ventricular contraction good but irregular
Atrial Fibrillation in horses
1) Atrial Fibrillation- most common
2) ecg- irrecular intervals between qrst complex with no p waves and varience on baseline. the atria are fibrilating creating F waves (bumpy apearence of base line)
atrail contraction into ventricles is lost and so cardiac output slightly reuced- ventricular contraction good but irregular
Lone (primary) AF
Horses are predisposed to AF due to;
High resting vagal tone
Large atrial mass
In combination with any of the following;
Shortening of the effective refractory period
Atrial inhomogeneity Presence of SVPDs
0.3% Prevalence in Thoroughbred racehorses
Clinical Signs of Lone AF-
Reduced athletic performance
Prolonged respiratory recovery after exercise
Normal resting HR
Low grade cough
Typical findings on auscultation
Irregularly irregular rhythm, absence of S4
Sustained AF
Persistent AF which presents at rest and during exercise
Paroxysmal AF
Sudden and transient AF that spontaneously reverts to normal sinus rhythm when not exersising- hard to diagnose- in exersise ecg
Paroxysmal AF
Usually occurs during strenuous exercise
Will revert to normal within 24-48 hours post-exercise
Diagnosis
Definitive = resting ECG recording at time of paroxysm
Post-reversion;
Exercising ECG
24hr Holter ECG
Frequent SVPDs at rest, or during exercise provides supportive evidence for AF
Secondary Atrail Fibrilation
AF that occurs as a consequence of underlying structural cardiac disease;
Mitral Valve insufficiency ->Left atrial enlargement-> increases capacity of electrical signals
Primary myocardial disease
Clinical Signs
More profound exercise intolerance
Resting tachycardia
Other signs of heart disease – loud cardiac murmurs
Structural remodelling of myocardium and
inability to treat underlying condition means
AF will be permanent
Cardioversion
Horses with sustained, uncomplicated lone AF may be candidates for conversion to sinus rhythm.
Success of cardioversion will depend on;
Duration of AF-
Prolonged AF -> Structural and electrical remodelling of atria
Horses with AF > 4months have significantly higher rate of recurrence
Presence of underlying disease:
Horses with existing cardiac disease are poor candidates for conversion, evidenced by;
Resting HR > 60bpm
Loud cardiac murmurs (significant regurgitation)
Structural changes on echocardiography
Only ever done in hospital environment with continual ECG monitoring
Quinidine - Prolongs the effective refractory period
Given orally (via NGT) @ 22mg/kg every 2hrs for max 4 doses
Conversely can be Proarrhythmic (severe tachycardia)
Severe GIT, respiratory and neurological complications can occur- colic common
Electrocardioversion-
Transvenous cardiac electrodes placed across atria, prior to defibrillation under GA
Only available in a couple referral centres in UK
electrode plcaed via jugular vein
shock administered as ventricles depolarising- r wave
if delivered at any other time horse may be killed
Atrial Fibrillation - Management
Horses with - prolonged, sustained AF
- mild underlying heart disease
- refractory AF
Can be successfully managed
Require regular exercising-ECG recordings
Absence of frequent or sequential premature depolarisations
Evidence of regularity of R-R interval during exercise
Level of exercise dictated by maximal HR achievable – often moderate
Severe cases should be retired.
regular ecgs every 6-12 months. check for ventricular changes
Valvular Regurgitation in horses
Physiological regurgitation-
Some degree of regurgitation can be found in horses with normal valves,
or in horses without murmurs
Atrioventricular regurgitation is recognised in fit athletic TBs
No association with racing performance
Pathological regurgitation-
Congenital - valvular dysplasia
Degenerative - endocardiosis
Inflammatory/infectious- endocarditis
Idiopathic
how can you distinguish between systolic and diastolic heart murmers
diastolic murmenrs will completely cover over other heart sounds and murmer will be there fro most of the cycle
systolic murmers will be shorter
Valvular Regurgitation - Diagnostics in horses
Examination-
Historic or clinical indicators of cardiovascular insufficiency
Murmur characteristics – localisation
Echocardiography- When to investigate?
Valves – Position, shape, movement
Regurgitant jet – Doppler; size, direction & velocity (severity of regurgitation)
Cardiac structure – Chamber size; evidence of compensatory change.
Electrocardiography-
Investigate for the presence of any concurrent dysrhythmias
aortic regurgitation in horses
diastolic
Most common – high prevalence (5-8%)
Common in middle age
Usually degenerative form
blood leaks into ventricles and usually dosent effect horse too badly
Assessing severity:
Loudness of murmur
Quality of arterial pulse - Hyperkinetic pulses- cardiac output increased due to increased blood in ventricles
Monitor progression with serial echocardiography
If no structural change – good prognosis for general riding, may need to be retired at wors
Poor prognosis;
Compensatory left ventricular overload
Higher risk of ventricular dysrhythmias
mitral regurgitation in horses`
Second most common regurgitation
Prevalence of 2.9 – 3.5%.
Higher in Thoroughbreds
Most likely form of valve regurgitation to lead to congestive heart failure
Due to pulmonary hypertension (increased atrial pressure)
Also risk factor for AF
Investigate if - higher grade murmur
- loud 3rd heart sound
- in high level exercise
Ventricular Septal Defect (VSD) in horses
Most common congenital cardiac defect in horses
Common in Welsh mountain ponies
Defect (‘Hole’) is normally in membranous portion of septum
Blood flows from left right
Loud & course pansystolic murmur audible on right side (4th ICS)
Also often a murmur audible on left side associated with increased flow out of pulmonary artery
louder murmer indicates smaller hole and therefore better prognosis
Prognosis
Depends on size and position of defect
Horses with small defects can have successful athletic careers
Poor prognosis associated with;
Larger defects;
As measured on echocardiography
Evidence of right ventricular overload
Reduced velocity of shunt flow
Increasing pressure in right ventricle
murmers and dhysrhythmias in the horse
Dysrythmias
2nd-degree AV block is very common and completely normal at rest
Atrial Fibrillation is the most common dysrhythmia in horses and will affect athletic performance
Dysrhythmias should be thoroughly assessed in any active horse
Murmurs
Aortic and mitral regurgitation are relatively common
Often exist in normal horses, functioning at high athletic ability
Mitral regurgitation more likely to cause significant secondary changes
Loud murmurs, progressive murmurs or murmurs associated with clinical signs should definitely be investigation
Staging – Myxomatous Mitral Valve Disease
A- At risk (e.g. CKCS, chihuahua, etc)
B1- Degenerative mitral valve changes present, normal LA and LV dimensions
B2- Degenerative mitral valve changes present, LA and LV dilation
C- Congestive heart failure (past or present)
D- Congestive heart failure refractory to standard therapy
Staging – Feline Cardiomyopathies
A- At risk (e.g. CKCS, chihuahua, etc)
B1- Subclinical – normal left atrium/mild enlargement
B2- Subclinical – moderate/severe atrial enlargement (i.e. increased risk of CHF/thromboembolic disease)
C- Congestive heart failure (past or present)
D- Congestive heart failure refractory to standard therapy
Staging – Dilated Cardiomyopathy
A- At risk (e.g. CKCS, chihuahua, etc)
B-Occult DCM – morphological or electrical changes. No evidence of CHF but may experience syncope
B1- Electrical abnormalities (suspected to be due to DCM)
B2- Left ventricular systolic dysfunction +/- chamber enlargement
+/- electrical abnormalities
C- Congestive heart failure (past or present)
D- Congestive heart failure refractory to standard therapy
Management of Acquired Heart Disease- preclinical
Pimobendan-
Phosphodiesterase III inhibitor, calcium sensitiser
“Dual-action inodilation”
Improved inotropy (muscle contraction) and vasodilation
Improved cardiac output
Delays onset of clinical disease (MMVD, DCM)
Improves survival (MMVD, DCM)
DCM – PROTECT study (2012)
MMVD – EPIC study (2016)
Pimobendan group had longer time to endpoint
Pimobendan also improved survival
Pimobendan
Stage B2 DCM/MMVD
0.1-0.3mg/kg BID
anecdotally used TID in advanced CHF (off label)
One hour before food/empty stomach
Food decreases bioavailability
Rapid peak effect
Pimobendan
What about cats?
Limited evidence supporting a clear benefit
Consider in CHF
Be careful in patients with obstructive cardiomyopathy
Pimobendan
given in Stage B2 DCM/MMVD
0.1-0.3mg/kg BID
anecdotally used TID in advanced CHF (off label)
One hour before food/empty stomach
Food decreases bioavailability
Rapid peak effect
Pimobendan
What about cats?
Limited evidence supporting a clear benefit
Consider in CHF
Be careful in patients with obstructive cardiomyopathy
Thromboembolism in cats
Stage B2
Spontaneous echo contrast (smoke)
Increased left atrial size
Reduced left atrial function
Clopidogrel 18.75mg SID
NB: very bitter
Aspirin 81mg every 2-3 days
Rivaroxaban 2.5mg SID
Management of Acquired Heart Disease- clinical disease
Largely same for dogs and cats
Control congestion (backwards failure): diuretics
Improve output (forwards failure): pimobendan
Suppress RAAS: ACE Inhibitors/spironolactone
diuretics use in aqiread heart disease
Loop diuretics (ascending loop of Henle):
Furosemide
Torasemide- good for patients with right sided heart faliure due to higher bioavailability than furosemide
Thiazides (distal convoluted tubule):
Hydrochlorthiazide
Potassium-sparing (collecting duct):
Spironolactone
Amiloride
Diuretics
Most important part of CHF therapy
Furosemide – first line?
Start around 1-2mg/kg BID (can give TID)
Maximum total dose around 12mg/kg/day
(8mg/kg/day helpful cutoff for refractory/stage D?)
Furosemide for heart disease
Short duration of action
Long term tolerance (diuretic resistance)
Not completely absorbed (~50%)
Torasemide for heart disease
Long duration of action (SID dosing)
Reduced likelihood of resistance?
High bioavailability (~100%)
good for patients with right sided heart faliure due to higher bioavailability than furosemide
First line vs refractory
Personal choice?
Upcard: licensed product, about 20x more potent than furosemide
transition from furosomide once refractory
Torasemide transition
1/20 of the total furosemide daily dose
e.g. if a dog is receiving 20mg BID (i.e. 40mg/day), the equivalent dose is 2mg/day
0.1-0.6mg/kg SID
Management of Acquired Heart Disease- RAAS
Aldosterone antagonists- spironolactone
ACE Inhibitors-benazepril etc
Angiotencin receptor blockers RBs-telmisartan(somitra)- no cardiac license but licenced for renal disease
Management of Acquired Heart Disease- ACEIs
ACE Inhibitors
Benazepril most common in UK
Enalapril, ramipril, etc
Long history of use, limited evidence base?
Theoretical benefit in opposing RAAS
Combined with spironolactone (Aldosterone antagonists)_ (Cardalis)
May reduce the rate of CHF progression
May reduce LA pressure
Risks:
Decreases systemic blood pressure
Decreases the GFR
Can cause hyperkalaemia (theoretically)
Use with caution in azotaemic/hypotensive patients
dual therapy vs tripple therapy- possible lack of support for using this
Spironolactone
Aldosterone antagonist – opposes RAAS
Potassium-sparing “diuretic” (very limited diuretic effect)
Alone or combined with ACEI
Shown to improve survival in dogs with MMVD and CHF
Evidence of benefit in cats
Quadruple therapy (furosemide, pimobendan, ACEI, spironolactone) currently recommended for patients in CHF – MMVD, DCM
Cats: furosemide + clopidogrel +/- ACEI, spironolactone, pimobendan
what is the current rtreatment recomendation for patients in CHF – MMVD, DCM
Quadruple therapy (furosemide, pimobendan, ACEI, spironolactone)
what is the current rtreatment recomendation for cats in chf
furosemide + clopidogrel +/- ACEI, spironolactone, pimobendan
dogs in B2 MMVD Treatment
Pimobendan
May be a candidate for valve repair under bypass
May be a candidate for transcatheter edge-to-edge repair (TEER)
dogs in C MMVD Treatment
Diuretic (furosemide or torasemide)
Pimobendan, benazepril, spironolactone
May be a candidate for valve repair under bypass
May be a candidate for TEER
dogs in D MMVD Treatment
Diuretic (torasemide) +/- hydrochlorothiazide
Pimobendan, benazepril, spironolactone
May be a candidate for valve repair under bypass
Likely not a good candidate for TEER
May benefit from transseptal puncture
Management of Acquired Heart Disease- mitral valve disese Surgery
Surgery preferred in humans with mitral regurgitation due to primary valvular disease
“When surgery is considered, mitral valve repair is the surgical intervention of first choice when the results are expected to be durable according to the Heart Team evaluation since it is associated with better survival compared to mitral valve replacement”
Medical treatment is palliative in its nature
Reduction in clinical signs; can reduce or stop diuretics
93% survival at 38 months postop
Transcatheter edge-to-edge repair
(Mitraclip, V-clamp)
“Transcatheter mitral valve implantation for severe PMR is a safe alternative in patients with contraindications for surgery or high operative risk.”
Patients for whom repair is not an option (finances, few centres)
V-Clamp
Chinese group (Hongyu Medical Technology) manufactured a device (V-Clamp), similar to human Mitraclip
Excellent results in Shanghai
CSU are having great success in USA (70 cases, 90% 12m survival)
Few centres in Europe; Willows the only hospital in the UK
Transseptal Puncture
Management of Acquired Heart Disease
paliative procedure
Left atrial decompression
Minimally-invasive, reduces LA pressure
Reduction in pressure in dogs reported
for dogs ith advanced refractive heart failure
Bovine Respiratory Disease Complex (BRDC)
CAUSE OF MORTALITY
Multi-factorial disease complex – infectious agents, environment, stress on the host (c.f. triad of disease causation!)
Younger animals mostly, but adult cattle can also be affected
Main cause of mortality in young cattle globally
Probably the highest economic impact of any infectious condition of cattle in UK – est. cost of £60-80M per year
Risk (trigger) factors involved
housing-Inadequate ventilation and high stocking densities. Mixing of ages in same air space.
transport- Major stressor. Strong association between transport and BRD morbidity. Passage through a livestock market – mixing of animals. ‘Shipping fever’.
weather conditions- Sudden or extreme temperature changes. Lack of wind affecting air movements and ventilation in housing in Autumn/Winter.
husbandry practices on farm- Stressors such as castration, dehorning, weaning, mixing batches, market purchases and mixing of cattle from different sources.
Vaccination/Immune status-Initial colostrum intake and quality. Use of vaccine and according to data sheet. Improper storage of vaccine rendering ineffective.
Genetics- Some breeds may have more resistance to BRD. Sucklers calves may have more resistance than dairy
BRDC: Antibiotic + NSAIDs = better treatment outcomes? Short-term perhaps, but seemingly not longer-term
Bovine Respiratory Disease Complex (BRDC) clinical signs
Dull, lethargic - pyrexia
Lack of appetite - reduced feed intake - low rumen fill (‘look empty’)
Increased respiratory rate (tachypnoea), difficulty breathing (dyspnoea)
Coughing often a feature (but not for ‘shipping fever’)
Nasal and ocular discharges
Upper and lower respiratory tract may be involved, but we are usually focussed on LRT
Common viral and bacterial pathogens in BRDC:
have synergistic effects
Bovine herpese virus 1
bovine respiritory syncytial virus
bovine diarrhoea virus
bovine adenovirus
bovine corona virus
mannheimia haemolytica
pasturella multiocida
hisophilus somni
mycoplasma bovis
ureaplasma spp.
Mycoplasma (Class Mollicutes): The organism
More than 125 named Mycoplasma species
Generally host-specific, a few are opportunist zoonoses
Small: cell = 300-800nm
Nutritionally fastidious, dependent on host.
TCA cycle is absent, cannot synthesise own amino acids, nucleotides or fatty acids.
No cell wall – very unusual- affects antibiotic use
in cattle-
Respiratory infections - pneumonia
Mastitis
Eye infections
Joint infections
Reproductive infections
Otitis (inner ear – head tilt) / Meningitis
calf pneumonia, arthritis, mastitis, infective keratoconjunctivitis
Many Mycoplasma species can produce biofilms:
This helps them to survive:
Host immune responses
Disinfectant treatments
Antimicrobial treatments
In the environment
Also no cell wall – limits Tx options
Mannheimia haemolytica – ‘shipping fever’
M. haemolytica bacteria part of the normal bacterial flora of the bovine resp. tract
If conditions are right for the bacteria they can invade the lungs and set up a severe inflammatory response and bronchopneumonia – aged 1 month to 2 yrs generally
Often associated with prior/concurrent infection with viruses or Mycoplasma bovis
M. haemolytica is particularly associated with ‘shipping fever’ or ‘transit fever’ in cattle (formerly also known as pasteurellosis – NB name change for the bacterium)
Clinical signs often seen about 2 weeks after sale and transport
Similar clinical signs seen with Histophilus somni infections in cattle
Infectious bovine rhinotracheitis (IBR)
Bovine herpesvirus 1 (BHV-1)
Can affect adults as well as youngstock i.e. all ages
Severe outbreaks occur where the disease enters a non-immune herd for the first time
Highly contagious disease with severe inflammation of the upper respiratory tract may lead to serious primary or secondary pneumonia
clinical signs-
High morbidity in group – spreads fast – sudden onset
Copious (quickly purulent) nasal and ocular discharges
Erosions on nasal septum – severe nasal inflammation
Conjunctivitis
Pyrexia – inappetence
Animals very depressed
Halitosis – trachea severely affected
Frequent coughing
Reluctant to allow handling of larynx/trachea
Differentiate URT from LRT signs – rhinotracheitis, no lung sounds
Adult cows may abort and there is often a reduced fertility until herd immunity develops
Animals suffering from IBR are highly susceptible to secondary bacterial infections
Acute disease in milking cows usually accompanied by a severe and prolonged drop in milk production (up to 10 days)
Differentials – Mannheimia, Malignant Catarrhal Fever (MCF), [bluetongue]
Once infected, the majority of cattle in the herd become carriers (even if vaccinated) and can excrete the virus when stressed (Herpes virus)
Herds where IBR is endemic suffer mainly from low-grade problems associated with calf pneumonia, decreased fertility and occasional abortions
Vaccines available e.g. Bovilis® IBR Marker Live (MSD), Hiprabovis IBR Marker Live (Hipra), Rispoval IBR-Marker Live (Zoetis), Tracherine (Zoetis)
Vaccinate to prevent or in the face of an outbreak
Procaine penicillin for supportive therapy in clinical cases; NSAIDs
lungworm in cattle
Dictyocaulus viviparus) – ‘husk’ – coughing - vaccine available (Bovilis Huskvac, MSD) – initial vaccination protocol and then exposure to low levels on pasture boosts immunity, which should preclude need for boosters
fog fever
(Atypical Interstitial Pneumonia) - an intoxication from lush pasture after poor plane of nutrition – adult cattle in late summer/autumn
- Sudden onset resp. distress with pulmonary oedema – tachypnoeic, not coughing, temperature normal, salivation, outstretched neck with mouth breathing, usually multiple animals – deaths possible
- Conversion of amino acid L-tryptophan in rumen to 3-methylindole by microbes – enters bloodstream and damages lung tissue
Ovine respiratory complex (ORC)
ORC tends to be the term used in sheep rather than ORDC
Same principles apply – complex mix of aetiological agents present in natural microbial flora, triggered into causing disease due to stressors
Ovine respiratory symptoms - causes-
Bacterial agents:
Mannheimia haemolytica
Bibersteinia trehalosi
Pasteurella multocida
Mycoplasma ovipneumoniae
Viral agents:
Parainfluenza 3 (PI3)
Ovine pulmonary adenocarcinoma (Jaagsiekte)
Maedi-Visna
Ovine respiratory symptoms - causes
Bacterial agents:
Mannheimia haemolytica
Bibersteinia trehalosi
Pasteurella multocida
Mycoplasma ovipneumoniae
Viral agents:
Parainfluenza 3 (PI3)
Ovine pulmonary adenocarcinoma (Jaagsiekte)
Maedi-Visna
Others – e.g. lungworm – Dictyocaulus filaria in sheep (milder than in cattle – chronic cough)
‘Pasteurellosis’ in sheep
Mannheimia haemolytica (formerly P. haemolytica)
Most important respiratory pathogen in sheep – septicaemic and systemic forms
Often acute – sudden deaths – (in lambs up to 3 months - septicaemia)
Pneumonia in adult sheep – rare unless predisposing factor such as OPA
Temperature +41°C, dull, respiratory signs
Also Pasteurella multocida Type A – rare in UK, mostly septicaemia in young lambs
Systemic ‘pasteurellosis’ due to M. haemolytica: Major economic importance in UK
Acute onset depression, lethargy and inappetence in adults - apart from flock
Pyrexia
Septicemic ‘pasteurellosis’ – sudden death in lambs up to 12 weeks old
At post-mortem – often overlying fibrinous pleuritis with lung consolidation
Vaccines – often combined with Clostridial disease protection: Ovivac P Plus (MSD), Heptavac P Plus (MSD). Also Ovipast Plus (MSD).
Note Clostridial disease as differential for sudden death in unvaccinated lambs.
Systemic pasteurellosis: Bibersteinia trehalosi
Bibersteinia trehalosi (formerly known as Pastuerella trehalosi) – sheep only
Most common form in recently-weaned (older) lambs - August to December, aged 5-12 months
Sudden deaths after moving onto weaning/sale/movement and turn out onto brassicas or improved pasture after poor plane of nutrition e.g. weaned off hill ground, moved to lowland for fattening
Treatment – oxytetracycline
Vaccines – may be combined with Clostridial disease protection: Ovivac P Plus (MSD), Heptavac P Plus (MSD) ; Ovipast Plus (MSD)
Parainfluenza 3 (PI3) in sheep
Most infections are mild or non-clinical
Mainly young and growing lambs affected
Enzootic pneumonia in sheep
(atypical Mycoplasma pneumonia)
Mycoplasma ovipneumoniae
Mild to severe respiratory disease – primarily coughing, reduced weight gain
Probably mixed infections (Mannheimia, PI3) – respiratory complex
Often housed / intensively kept sheep
Ovine pulmonary adenocarcinoma (OPA)(Jaagsiekte)
Contagious tumour – respiratory transmission
Jaagsiekte sheep retrovirus (JSRV) – no cure – one of the ‘iceberg diseases’
Causes the development of tumours in the lung
Lungs become very heavy and produce large quantities of fluid
Incubation period: Several months up to 2 yrs
Secondary bacterial infection common e.g. M. haemolytica - pneumonia
Clinical signs:
Weight loss
Laboured breathing, especially during exercise – lagging behind
‘Wheel-barrow test’ – large quantities of fluid drain from the nose
Spread from animal to animal via infected expired air droplets and fluid
Maedi-Visna in sheep
Viral disease of adult sheep that can cause two syndromes:
Maedi – respiratory (most common) – interstitial pneumonia
Visna – neurological signs - encephalitis and wasting – rarer form
Incubation period: 2 – 5 years
Mainly transmitted from dam to lamb via colostrum; air-borne indoors between adults; highly infectious
No vaccine and no cure – fatal. Also causes Caprine Arthritis Encephalitis (CAE) in goats
Notifiable disease in Northern Ireland; endemic in GB – test and cull – accreditation scheme
Porcine Respiratory Disease Complex (PRDC)
Mainly growing and finishing pigs – huge global economic impact
Main organisms involved:
Mycoplasma hyopneumoniae (Enzootic pneumonia)
Pasteurella multocida
Actinobacillus pleuropneumoniae
Porcine circovirus (PCV)
Swine influenza viruses (SIV)
Porcine reproductive and respiratory syndrome virus (PRRSV)
Global distribution - important economically
Causal organism: Mycoplasma hyopneumoniae (as part of PRDC)
Clinical signs mainly seen at 8 – 20 weeks, although infection contracted much younger (often around 2 wks)
Normally low grade chronic soft cough; unless get secondary infection
Very high morbidity, low mortality - bronchopneumonia
Incubation period about 2 weeks
Barking cough – especially when disturbed in the pen
Gradual spread between pigs, unless a naïve herd become infected – c/s in all ages of pig, including adults
Lasts +/-50 days
Depression of growth rate and feed conversion
Outcome - uneven size depending on clinical impact and recovery rate
lung leasions-
reactive lympnodes
Streptococcal pneumonia in pigs (Streptococcus suis)
menigitis and pneumonia in pigs
leaison covers whole lung
Enzootic pneumonia in pigs - epidemiology
Infected sow can pass on infection to piglets around 14 days of age
Carrier pigs
Aerosol transmission for up to 3 km
Direct contact and aerosol transmission within herds
Disease in non-immune herds – importance of vaccination
Treatment/control:
Diagnosis based on: clinical signs, ELISA tests, post-mortem findings, lung scoring at slaughter
Antibiotics active against M. hyopneumoniae (NB no cell wall)
Vaccination e.g. Suvaxyn M. hyo (Zoetis); Stellamune Once, (Elanco)
Vaccination reduces clinical signs, lung lesions and antibiotic use, with improved performance in terms of FCR
Infectious Pneumonia in horses
LESS COMMON cause of pneumonia in horses
Viral Pneumonias
Equine Influenza
Equine Herpes Virus
Equine Arteritis Virus
Rhodoccocus equi equi infection in weanlings
Complications from URT viral URT infections
