Respiratory Flashcards
* Percussion
* Endoscopy at rest: discharge from nasomaxillary opening
* Radiogrpahy: fluid lines in sinuses
* Oral examination teeth
* Sinus centesis (trephine)
* direct endoscopy
Primary sinusitis management
*Lavage and systemic antibiotics
Chronic primary sinusitis or seconadry sinusitis management
* bone flap- expore, debride, treat the cause (e.g. tooth root infection), lavage
* Systemic antibiotics
Severe URT obstruction- emergency tracheostomy indications
DDX Epistaxis
* Trauma, progressive ethmoid haematoma, Exercise induced pulmonary haemorrhage (EIPH), mass (FB, neoplasia, abscess), guttural pouch mycosis (severe or fatal epistaxis)
Diagnosis of progressive ethmoid haematoma
PEH Treatment
Guttural pouch mycosis sequelae
Guttural pouch mycosis treatment
Abnormal respiratory noises in horses
Alar fold redundancy
Differentiate from normal high blowing at canter
Treatment of alar fold redudancy
Change in airway dynamics at exercise
Airway Dynamics
•
Many causes of airway obstruction become clinically
significant and worsen with increasing exercise intensity
•
On inspiration during intense exercise the forces acting to
collapse the walls of the URT are considerable
•
Air movement is achieved by creation of pressure
gradients during inspiration and expiration
•
During exercise
↑↑ RR (6x), ↑↑airflow (15x), ↑↑trans
-upper
airway P (10x),
but impedence to flow is normally not reduced
due
to
- Structural features of nostrils, nasal passages, pharynx & larynx, and
trachea act to withstand collapsing force
- Dysfunction of any of these structures results in their collapse into
airway during exercise
Narrowing of lumen does what to flow?
VO2 max in a race horse
Structural and functional features important in stabilising against airway collapse
How does head and neck position effect amount of air coming in?
Diagnostic plan for poor performance in race horse
Structures that may collapse into the airway during exercise
Palatal dysfunction- palatal instability and intermittent DDSP
Signs and symptoms of IDDSP
PI and IDDSP: Challenges in diagnosis and management
Aetiopathogenesis of PI and IDDSP
Experimental models
– bilateral resection thyrohyoid m.
- distal hypoglossal n. block
Some cases are preceded by PI during exercise and/or
increased frequency of swallowing
Proposed contributing factors
•
Caudal retraction of tongue
•
Opening of mouth
•
Position of larynx and hyoid during exercise-
Caudal descent of larynx
IDDSP management
IDDSP gear changes
IDDSP surgical management
Challenges in management of palatal dysfunction
Recurrent laryngeal neuropathy aetiopathogenesis
RLN Signs
RLN diagnosis
Havemeyer grading system?
Management of RLN affected horses non-performance
Management of performance RLN clinically affected horses
Potential complications post RLN surgery
Epiglottic entrapment signs
Surgical treatment of epiglottic entrapment
Important aspects of signalment and history respiratory disease
Respiratory clinical exam in horses
Nasal discharge presentation in respiratory disease– clues?
Is it URT?
Thoracic auscultation
* Quiet room
* Not 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 for…
- regions where bronchovesicular sounds are dull or absent especially in horses with tachypnoea
- adventitial sounds (crackles, wheezes, friction rubs) indicate pulmonary pathology
** The green sections in the photo– hard to hear the lungs, a lot of muscle covering those areas e.g. triceps
Re-rebreathing examination
U/S evaluation for??
When would radiographic evaluation be helpful?
* RG of the URT
- primarily used to evaluate the sinuses and guttural pouches
- look for the presence of fluid lines or soft tissue opacities
- dorsoventral view very useful to evaluate the sinuses but can be difficult to obtain
Why do TTA (TTW) over BAL?
Trans-tracheal aspirate or wash
STERILE SAMPLE FOR CULTURE!
* Technique:
- aseptically prepare site
- pass stylet trans-cutaneously into trachea
- introduce long catheter
- deposit small volume of sterile saline at carina via catheter
- pooled sample from entire lung– good for focal disease BECAUSE of the mucociliary escalator everything ends up moving up the trachea
- appropriate for culture
** Can be performed trans-endoscopically using “guarded” catheters, but samples often contaminated with URT commensals
Cytology of Trans-Tracheal Aspirate or Wash
Why do we use BAL? Bronchoalveolar Lavage Technique
Why do we use it? Better idea of what is going on in the alveoli… very focal area
*Moderate sedation and twitch
* Pass BAL tube (or endoscope) via nasal passage into trachea
* Wedge in bronchus and inflate cuff
* Infuse and then aspirate sterile fluids (e.g. LRS)
-Variable volumes used (e.g. 3 x 120 mL)
* Mix final sample
* Samples a random, relatively small region of the lung
- better reflext alveolar inflammation
- good for global lung disease (RAO, IAD, EIPH… etc.)
* NOT appropriate for culture (pharyngeal contamination)
BAL Cytology DDX
Other diagnostic tests aside from TTW and BAL
*Biopsy uncommon as major vessels– haemorrhage into the area– distressing for the owner
Bilateral serous nasal discharge, high fevers, multiple animal affected with rapid spread
Epi of EHV1 and EHV 4
What does a comet tail on an U/S mean?
Comet tails- pleural surface is irregular. A few is normal. Lots of comet tails abnormal
Clinical signs of EHV1 and 4
Clinical Signs…
EHV-1 is also associated with…
Abortion storms (late gestation)
Birth of weak neonates and neonatal death
Myeloencephalopathy
EHV-4 typically causes less severe respiratory disease
Very rarely causes abortion or neurological disease
Diagnosis confirmed by:
Rising serum titre (or very high initial titre)
PCR identification of viral DNA or viral isolation
Nasopharyngeal swab, buffy coat
Pathogenesis EHV1 and 4
Treatment of EHV 1 and 4
Equine Influenza Epi
Clinical signs of Equine Influenza
Clinical signs of Equine Influenza
Equine Influenza Treatment
What do you do if you suspect Hendra?
Diagnosis of Hendra Virus
EHV Outbreak Recommendations
Viral v. bacterial
* Viral- serous nasal discharge
* Common things happen commonly
* Rapid spread (though Strangles could)– but also Lower Resp Tract is infected, not URT (crackles & airway inflammation)
* Predisposing factors for bacterial disease not present
* Young horses
* Additional diagnostics as you can’t rule out bacterial disease
EI– differentiating from other viral dx?
* dry hacking cough often… however can’t rule out completely
Pleuropneumonia in horses background
Standard diagnostic plan in pleuropneumonia in horses
Typical treatment protocol in pleuropneumonia in horses
Pleuropneumonia
in Horses
Typical Treatment Protocol
NSAIDS
Care with GIT and renal toxicity
Additional analgesia required in some cases
Thoracic drains if necessary
Leave in place until effusion stops (requires one-way valves)
Supportive care
IV fluids if water intake decreased
Intra-nasal oxygen
Nutritional support
Diagnosis and therapeutic plan in bacterial pleuropneumonia
Culture results in pleuropneumonia
Complications in pleuropneumonia
Pleuropneumonia
When do you stop treating pleuropneumonia?
Epistaxis definition and where it might come from
Epistaxis common causes
Unilateral v. bilateral epistaxis
EIPH
EIPH diagnosis
EIPH pathogenesis
EIPH treatment
RBCs v. Haemosiderophages
Haemosiderophages– can indicate EIPH– v. iatrogenic trauma. Lung macrophages gobbled up RBCs– now just the break down products in them. Common finding in EIPH– because process that recurs repeatedly. Chronic haemorrhage into the lungs.
TTW vs. BAL
* Guarded catheters in small animals
* Collect the TTW first, if you do the BAL first drag all the URT commensals up through the area where you’re going to do the TTW
What samples do you take for PCR if you suspect viral and want to get a definitive diagnoses?
Nasopharyngeal swab or blood sample
(Serology useful to figure out what is going on, to convince the owners to isolate the horses and figure out what is going on– looking for antibodies or antigen– ELISA)
Number one DDX- Strangles (strep equi ssp equi)–always a pathogen, it should not be there (Strep equi zooepidemicus– NOT THE SAME– doesn’t mean anything it is a URT commensal)
Guttural pouch empyema (Guttural pouch empyema is defined as the accumulation of purulent, septic exudate in the guttural pouch. The infection usually develops subsequent to a bacterial (primarily Streptococcus spp) infection of the upper respiratory tract.)
Could be viral, could be LRT– Pneumonia
* Sinusitis- bacterial most common (primary or secondary)–TOOTH ROOT ABSCESS
* Pharyngeal, retropharyngeal, pulmonary abscess
*** CBC (fibrinogen because WCC is unreliable in horses), FNA of LN, check the lungs with an U/S
** Very contagious– inhalation or ingestion
Why are antibiotics (penicillin) C/I in mild cases of Strangles?
Cause the edges of the abscess to dry up and leaves viable bacteria in the middle
Exception would be guttural pouch empyema on top of Strangles
16 yr old Morgan mare, exercise intolerant for 12 months, coughs occasionally during exercise, mucopurulent nasal discharge
BAR
HR 44/ min- normal rhythm, grade II diastolic musical murmur on the left
RR 20/min- normal effort, auscultation normal, cough with re-breathing and prolonged recovery
Temperature 37.8 C
Mare in ideal condition 4/9
grade II diastolic muscal murmur–Regurgitation through aortic or pulmonic valve– aortic valve regurg because really common
* Problem list: exercise intolerance, coughing during exercise, mucopurulent discharge, diastolic murmur– mild and common but perceived exercise intolerance??, didn’t tolerate rebreathing, tachycardia, tachyopnoeic
* DDX: bacterial pneumonia/ pleuropneumonia (unlikely sick for 12 months), viral resp dz (unlikely sick for 12 months), heart failure (rare), inflammatory airway disease
* Additional tests: CBC (fibrinogen, inflammatory markers), biochem, U/S lungs, BAL might give us a more accurate idea in the alveoli vs. TTW (but could suggest both because TTW– could this be a secondary bacterial infection), Echo from U/S (NOT AN ECG because would help us with murmur), Lung functioning test (but less likely)…….
Cost constrained client– BAL, CBC (fibrinogen)
* CBC- normal fibrinogen; thoracic U/S unremarkable; BAL- 16% neutrophils (normal 5%)
* TTW- increase in non-degenerate neutrophils, no bacteria observed, no growth on bacterial culture
** Inflammatory airway disease
Inflammatory Airway Disease
Recurrent Airway Obstruction
Probably the more severe form of Inflammatory airway disease
Pathophysiology of Inflammatory Airway Disease
* Airways become inflamed
- neutrophils and mucus (e.g. pus) collect in the small airways
* Airways are hyper-reactive
- Triggers cause more severe bronchospasm then expected
- Bronchospasm increases work of breathing
What will you see with cells with Inflammatory Airway Disease with a BAL?
Role of Allergies in IAD and RAO
Treatment #1 in Inflammatory Airway disease
Treatment option 2 Inflammatory Airway Disease
* Inhaled steroids an option (MDI puffer or nebulizer)
- Maintain remission
- Expensive (requires delivery device)
- Fewer side effects
- Fluticasone or beclomethasone
Treatment #3 in Inflammatory Airway Disease
* Connection between RAO and IAD unclear
- IAD typically resolves when horse is removed from environment
* Like asthma, RAO is managed but not cured
- Horses will need to be treated and managed for life
- May see some waxing and waning of clinical signs with change in seasons
Epi of Rhodococcus equi
* Gram positive pleomorphic coccobacillus
* Present in the: soil of most geographical areas, faeces (in relatively low numbers) of normal adult horses
* Pathogenic strains of R. equi contain plasmids that code for virulence proteins
- VapA best known
- inhibit macrophage function
* Many foals (up to 50%) have extra-pulmonary sites
- eyes, GI tract, joints (immune mediated), osteomyelitis
IAD v. RAO
Clinical signs of Rhodococcus equi
* Cough and nasal discharge are inconsistent
* extra-pulmonary sites of infection
- GI tract abdominal abscesses, ulcerative colitis
- Joints (immune mediated?)
- Uveitis (immune mediated?)
- Osteomyelitis
Diagnosis of R. equi
* Consider any youn horse showing signs of respiratory disease
* Thoracic radiographs
- prominent alveolar pattern
- poorly defined regional consolidation and/or abscessation
* Ultrasonography
- pulmonary abscesses in peripheral pulmonary parenchyma
- very useful screening tool on endemic farms
* Macrolide AMs are associated with some adverse side effect including
- colitis (often self-limiting)
- Hyperthermia (erythromycin)
* Severe, fatal colitis has been described in some mares of foals being treated with oral erythromycin
Prevention of R. equi
Prognosis of R. equi
* Has there been a fever? Have you tried to treat it? Vaccine history? Other horses ill?
* Problem list: Recent transport (LRT pleuropneumonia risk factor), haemodynamic derrangements and inflammation (MM), fever, tachypnoeic, dull sounds ventrally (fluid in the chest likely), crackles, cough, off feed, depressed….
clear indicators LRT
* Infectious– fever and really sick horse (not IAD or RAO)
** Viral resp disease horses won’t be as sick as bacterial pneumonia horses– it could start with viral (Fungal is very uncommon)– it is a sliding scale, subjective but helps you decide
* Diagnostic plan– suspicious of bacterial pneumonia or pleuropneumonia…. things to monitor to gauge if therapies are working, how sick is this horse?
* TTW because we want to culture the sample, CBC and biochem– to look at electrolyte abnormalities, thoracic U/S, Fibrinogen (or Serum Amyloid A), Thoracocentesis and thoracic drainage if significant drainage, serum chemistry– LIVER function, RENAL function (IMPORTANT BECAUSE GENTAMYCIN– sick horse, not drinking as much as should do)
** Penicillin (gram pos, anaerobes) + Gentamycin (gram neg, synergy with penicillin, inexpensive)– fairly inexpensive broad spectrum coverage
** U/S good monitoring esp. with fluid in the chest
Results: Azotaemia (careful of Gentamycin), fibrinogen is high (takes 2-3 days to increase), neutropenia– massive tissue demand for the white cells, band neutrophils– bone marrow trying to catch up, severe suppurative inflamm, large number of degenerate neutrophils, and intra- and extra cellular bacteria onthe TTW
** U/S– pleural effusion, consolidation/ atelectasis of the lung, fibrin strands
** Thoracocentesis: fenestrated mediastinum BUT still the different sides are different–marked increase in leukocytes in both samples, predominately neutrophils, toxic neutrophils, bacteria seen
Background of Pleuropneumonia in horses
Pleuropneumonia Diagnostic Plan
Typical Treatment Protocol of Pleuropneumonia
Typical Treatment Protocol
NSAIDS
Care with GIT and renal toxicity
Additional analgesia required in some cases
Thoracic drains if necessary
Leave in place until effusion stops (requires one
-
way valves)
Supportive care
IV fluids if water intake decreased
Intra
-
nasal oxygen
Nutritional support
Therapeutic plan pleuropneumonia
Tx for strep equi zooepidemicus? Klebsiella pneumoniae? What does Metronidazole do?
Metronidazole- increases anaerobic coverage
Complications of Pleuropneumonia
Pleuropneumonia in horses
When do you stop treating pleuropneumonia?
Common causes of epistaxis
Epistaxis: Unilateral v. Bilateral
EIPH
Diagnosis of EIPH
Pathogenesis of EIPH
EIPH Treatment
