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Respiratory Flashcards

1
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3
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* Percussion

* Endoscopy at rest: discharge from nasomaxillary opening

* Radiogrpahy: fluid lines in sinuses

* Oral examination teeth

* Sinus centesis (trephine)

* direct endoscopy

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4
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Primary sinusitis management

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*Lavage and systemic antibiotics

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6
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Chronic primary sinusitis or seconadry sinusitis management

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* bone flap- expore, debride, treat the cause (e.g. tooth root infection), lavage

* Systemic antibiotics

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7
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8
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Severe URT obstruction- emergency tracheostomy indications

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9
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10
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DDX Epistaxis

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* Trauma, progressive ethmoid haematoma, Exercise induced pulmonary haemorrhage (EIPH), mass (FB, neoplasia, abscess), guttural pouch mycosis (severe or fatal epistaxis)

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11
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Diagnosis of progressive ethmoid haematoma

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12
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PEH Treatment

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13
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Guttural pouch mycosis sequelae

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14
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Guttural pouch mycosis treatment

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15
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Abnormal respiratory noises in horses

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16
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Alar fold redundancy

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Differentiate from normal high blowing at canter

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17
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Treatment of alar fold redudancy

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18
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Change in airway dynamics at exercise

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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

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19
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Narrowing of lumen does what to flow?

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20
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VO2 max in a race horse

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21
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Structural and functional features important in stabilising against airway collapse

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22
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How does head and neck position effect amount of air coming in?

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23
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Diagnostic plan for poor performance in race horse

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24
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Structures that may collapse into the airway during exercise

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25
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Palatal dysfunction- palatal instability and intermittent DDSP

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26
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Signs and symptoms of IDDSP

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27
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PI and IDDSP: Challenges in diagnosis and management

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28
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29
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Aetiopathogenesis of PI and IDDSP

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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

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30
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IDDSP management

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31
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IDDSP gear changes

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32
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IDDSP surgical management

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33
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Challenges in management of palatal dysfunction

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34
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Recurrent laryngeal neuropathy aetiopathogenesis

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35
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RLN Signs

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37
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RLN diagnosis

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38
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Havemeyer grading system?

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39
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Management of RLN affected horses non-performance

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40
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Management of performance RLN clinically affected horses

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41
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Potential complications post RLN surgery

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42
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43
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Epiglottic entrapment signs

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44
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Surgical treatment of epiglottic entrapment

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45
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47
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48
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Important aspects of signalment and history respiratory disease

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49
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Respiratory clinical exam in horses

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50
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Nasal discharge presentation in respiratory disease– clues?

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51
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Is it URT?

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52
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Thoracic auscultation

A

* 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

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53
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Re-rebreathing examination

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54
Q

U/S evaluation for??

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55
Q

When would radiographic evaluation be helpful?

A

* 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
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56
Q

Why do TTA (TTW) over BAL?

Trans-tracheal aspirate or wash

A

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

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57
Q

Cytology of Trans-Tracheal Aspirate or Wash

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58
Q

Why do we use BAL? Bronchoalveolar Lavage Technique

A

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)

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59
Q

BAL Cytology DDX

A
60
Q

Other diagnostic tests aside from TTW and BAL

A

*Biopsy uncommon as major vessels– haemorrhage into the area– distressing for the owner

61
Q

Bilateral serous nasal discharge, high fevers, multiple animal affected with rapid spread

A
62
Q

Epi of EHV1 and EHV 4

A
63
Q

What does a comet tail on an U/S mean?

A

Comet tails- pleural surface is irregular. A few is normal. Lots of comet tails abnormal

64
Q

Clinical signs of EHV1 and 4

A

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

65
Q

Pathogenesis EHV1 and 4

A
66
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Treatment of EHV 1 and 4

A
67
Q

Equine Influenza Epi

A
68
Q

Clinical signs of Equine Influenza

A
69
Q

Clinical signs of Equine Influenza

A
70
Q

Equine Influenza Treatment

A
71
Q

What do you do if you suspect Hendra?

A
72
Q

Diagnosis of Hendra Virus

A
73
Q

EHV Outbreak Recommendations

A
74
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75
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76
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77
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78
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86
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87
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88
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89
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90
Q

Viral v. bacterial

A

* 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

91
Q

EI– differentiating from other viral dx?

A

* dry hacking cough often… however can’t rule out completely

92
Q

Pleuropneumonia in horses background

A
93
Q

Standard diagnostic plan in pleuropneumonia in horses

A
94
Q

Typical treatment protocol in pleuropneumonia in horses

A

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

95
Q

Diagnosis and therapeutic plan in bacterial pleuropneumonia

A
96
Q

Culture results in pleuropneumonia

A
97
Q

Complications in pleuropneumonia

A
98
Q
A

Pleuropneumonia

99
Q

When do you stop treating pleuropneumonia?

A
100
Q

Epistaxis definition and where it might come from

A
101
Q

Epistaxis common causes

A
102
Q

Unilateral v. bilateral epistaxis

A
103
Q

EIPH

A
104
Q

EIPH diagnosis

A
105
Q

EIPH pathogenesis

A
106
Q

EIPH treatment

A
107
Q

RBCs v. Haemosiderophages

A

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.

108
Q

TTW vs. BAL

A

* 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

109
Q

What samples do you take for PCR if you suspect viral and want to get a definitive diagnoses?

A

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)

110
Q
A

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

111
Q
A
112
Q

Why are antibiotics (penicillin) C/I in mild cases of Strangles?

A

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

113
Q

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

A

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

114
Q

Inflammatory Airway Disease

A
115
Q

Recurrent Airway Obstruction

A

Probably the more severe form of Inflammatory airway disease

116
Q

Pathophysiology of Inflammatory Airway Disease

A

* 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
117
Q

What will you see with cells with Inflammatory Airway Disease with a BAL?

A
118
Q

Role of Allergies in IAD and RAO

A
119
Q

Treatment #1 in Inflammatory Airway disease

A
120
Q

Treatment option 2 Inflammatory Airway Disease

A

* Inhaled steroids an option (MDI puffer or nebulizer)

  • Maintain remission
  • Expensive (requires delivery device)
  • Fewer side effects
  • Fluticasone or beclomethasone
121
Q

Treatment #3 in Inflammatory Airway Disease

A

* 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
122
Q

Epi of Rhodococcus equi

A

* 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
123
Q

IAD v. RAO

A
124
Q
A
125
Q

Clinical signs of Rhodococcus equi

A

* Cough and nasal discharge are inconsistent

* extra-pulmonary sites of infection

  • GI tract abdominal abscesses, ulcerative colitis
  • Joints (immune mediated?)
  • Uveitis (immune mediated?)
  • Osteomyelitis
126
Q
A
127
Q

Diagnosis of R. equi

A

* 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
128
Q
A

* 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

129
Q

Prevention of R. equi

A
130
Q

Prognosis of R. equi

A
131
Q
A
132
Q
A

* 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

133
Q

Background of Pleuropneumonia in horses

A
134
Q

Pleuropneumonia Diagnostic Plan

A
135
Q

Typical Treatment Protocol of Pleuropneumonia

A

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

136
Q

Therapeutic plan pleuropneumonia

A
137
Q

Tx for strep equi zooepidemicus? Klebsiella pneumoniae? What does Metronidazole do?

A

Metronidazole- increases anaerobic coverage

138
Q

Complications of Pleuropneumonia

A
139
Q
A

Pleuropneumonia in horses

140
Q

When do you stop treating pleuropneumonia?

A
141
Q

Common causes of epistaxis

A
142
Q

Epistaxis: Unilateral v. Bilateral

A
143
Q

EIPH

A
144
Q

Diagnosis of EIPH

A
145
Q

Pathogenesis of EIPH

A
146
Q

EIPH Treatment

A

Equine (4 decks)

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