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Equine BCM > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Name the common and uncommon causes of non-infectious airway diseases in the horse

A

Common: equine asthma, inflammatory airway disease (IAD), exercise induced pulmonary hemorrhage (EIPH)

Uncommon: neoplasia (granular cell tumor most common), silicosis (associated with housing near dusty road), equine multinodular pulmonary fibrosis (caused by EHV 5), multisystemic eosinophilic epitheliotropic disease (MEEDS)

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2
Q

Describe the growth of granular cell tumors in the lungs of horses

A

They grow out of the interstitium and into the airways
-block the entire airway
-easily diagnosed through endoscopy

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3
Q

What would you find through biopsy or BAL of a horse with equine multinodular pulmonary fibrosis?

A

Evidence of equine herpes virus 5
-might also be found in a normal horse though

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4
Q

What is the pathophysiology of MEEDS?

A

Unknown
-can affect many different body systems

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5
Q

What are some other names for equine asthma?

A

-equine chronic obstructive pulmonary disease (COPD)
-equine recurrent airway obstructive disease (RAO)
-lay names: heaves, broken wind

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6
Q

T/F: humans are the experimental model for understanding asthma in horses

A

TRUE!

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7
Q

Describe some general characteristics of equine asthma

A

-usually affects middle aged (7) and older horses
-recurrent chronic and seasonal disease
-often a response to exposure to respirable debris
-progressive clinical signs over time
-horses can achieve remission but there is no cure

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8
Q

What are the most common symptoms of equine asthma?

A
  • moderate exercise intolerance in early disease
    -cough and mucoid nasal discharge with moderate disease
    -nostril flare and abdominal push with severe disease
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9
Q

In the worst cases of equine asthma, how do the nostrils appear?

A

Fixed and dilated
- don’t move when the horse breaths

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10
Q

What are the two different forms of equine asthma?

A

Typical equine heaves: associated with exposure to barn dust, hay dust or hay mold. More commonly observed in winter

Summer pasture airway obstructive disease (SPAOD): observed in southeastern states, associated with pasture, humidity and hot temperatures

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11
Q

Describe the mechanics of deposition of material in the airways

A

-if material is >5 microns there will be insertional impaction (ex: dirt, pollen). Mainly get trapped in nose and sinuses
-if material is 1-5 microns it will undergo sedimentation (mold spores, bacteria). Get stuck in trachea and upper bronchial tree (can ride the airstream for a while)
-if <1 micron, will undergo diffusion (gasses, moisture, endotoxin). Get into deep airways and can be very irritating

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12
Q

What is believed to be one of the main culprits of asthma in horses?

A

Aspergillus
-prominent hay and affects mid range of airways

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13
Q

Describe the inflammatory response that occurs with asthma

A

-exposure to the inhaled irritant drives airway neutrophilic inflammation (non-degenerative)
-this inflammation then leads to bronchoconstriction and mucous hypersecretion

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14
Q

How do you diagnose asthma?

A

First must determine if infectious or non infectious
-complete physical (including rebreathing if indicated), auscultate larynx, trachea and thorax as well as heart
-observe horse in work

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15
Q

How do you determine if a horse is suffering from infectious or noninfectious airway inflammation?

A

-infectious: history of exposure to infectious organism or initial event. Feverish, other animals affected, acute onset

-non-infectious: exposure to new environmental factor, seasonal onset, recurring. No fever, not contagious, gradual onset, chronic or recurring

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16
Q

T/F: clinical signs of asthma correlate with the severity of disease

A

False- horses can fool you
- try rebreathing bag for better indication of severity
-if you see clinical evidence of disease, the horse is very compromised

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17
Q

Why might a CBC/chem be helpful in an asthma case?

A

CBC: can help to determine if infectious or not (infectious- leukocytosis, neutrophilia, hyperfibrinogenemia, hyperproteinemia. Non infectious- stress leukogram- neutrophils and monocytes increase, leukocytes go down)
Chem: hyperglobulinemia would be more suspect of infectious or neoplastic disease

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18
Q

What are some additional diagnostics that may be beneficial in an equine asthma case?

A

-airway endoscopy- mucous scoring, transtracheal wash, thorough airway exam
-thoracic ultrasound or rads to rule out other causes

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19
Q

What are the two options for transtracheal aspirates?

A

-transendoscopic or percutaneous
-sterile so can culture, gram stain, PCR, cytology

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20
Q

What are the pros and cons of BAL?

A

Can be somewhat therapeutic
-gets to site of infection, but is not sterile
-good to determine success of treatment
-can do PCR, cytology and gram stain

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21
Q

If a horse is experiencing airway inflammation, what should you always do during your first exam?

A

-obtain a transtracheal wash or brush

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22
Q

T/F: it is not uncommon to see some bacteria on transtracheal wash in an asthma case

A

True- often not causing the inflammation though
-may be an indication for a round of antibiotics
-asthma may predispose to infection due to mucous presence

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23
Q

Describe some advantages and disadvantages to Transtracheal washes

A

Advantages: sample is more representative of what is happening in the whole airway and the lung, samples are sterile so can be submitted for culture

Disadvantages: may not represent the current state of the lower airways since it is a sample of everything

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24
Q

When should you perform a BAL?

A

Recheck exam

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25
Q

What percent neutrophils are commonly seen with TTW and BAL in NORMAL patients?

A

TTW: up to 15% normal
BAL: 5% is normal

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26
Q

What are the main goals of treatment in asthma cases?

A

-resolve airway inflammation, bronchoconstriction and hypersecretion
-maintain remission

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27
Q

What is the first thing you should do when determining your plan in a patient diagnosed with asthma?

A

Perform an inspection of the animals environment
- round bales? excessive dust? lots of old dusty hay?
-can this horse be maintained on pasture? Is the pasture free of a lot of weeds?

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28
Q

When should you turn to medications?

A

When environmental management has failed

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29
Q

What are the main treatments available for equine asthma?

A

-corticosteroids is main treatment
-can layer on bronchodilators (beta 2 agonists)

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30
Q

Why are bronchodilators contraindicated as the primary treatment?

A

-not addressing primary issue (inflammation)
-inflammation can make the bronchodilators less effective
-horse may become refractory to treatment
-condition will come back as soon as meds are stopped

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31
Q

What are the main functions of bronchodilators?

A

-relieving bronchoconstriction
-reducing airway resistance- promoting mucociliary clearance, reducing secretions
-reduces the work of breathing

  • does not resolve inflammation
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32
Q

T/F: NSAIDS can be helpful in asthma cases

A

False- they don’t do much
-need something stronger (steroids)

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33
Q

Describe the use of corticosteroids for equine asthma

A

Often given orally (inhaled meds not as effective when horse is struggling to breath) for systemic effects
-beware of risk of laminitis

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34
Q

Which system has direct innervation into the smooth muscle of the respiratory system: sympathetic or parasympathetic?

A

Parasympathetic
-releases Ach which binds to muscarinic receptors
-causes bronchoconstriction

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35
Q

Describe the pharmacologic characteristics of M3 receptor antagonists

A

-main 3 are atropine (ok for 1 time use), ipratropium bromide (primary one used for long term use) and buscopan
-antagonist binds to Ach receptors which promotes bronchodilation
-sympathetic administration decreases gut motility and leads to colic (buscopan)
-can decrease secretions and mucociliary beating (atropine)

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36
Q

Describe the features of Ipatropium bromide

A

-effect remains localized to the lung and is rapidly degraded in blood
-nebulize with 1-3 ug/kg
-metered dose: 180-360 ug total (10-20 activations)
-peak response in 15 minutes, effect lasts 6 hours
-administer up to 4 times daily
-effective in the presence of inflammation

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37
Q

Describe how Buscopan is used

A

-0.3 mg/kg IV
-leads to rapid bronchodilation (10 min)
-effect lasts about 1 hour
-can be used for a single rescue dose
-significant side effects: increased HR, decreased gut motility

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38
Q

Describe the pharmacology of alpha 2 receptor agonists?

A

Cause bronchodilation through binding a pre-junctional receptor which decreases Ach release and reduces contraction of bronchial smooth muscle
-increases mucous and water transport and promotes smooth muscle relaxation

Xylazine and detomidine fall in this class

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39
Q

How does sympathetic innervation affect the tone of smooth muscle in the airways?

A

-circulating epinephrine and NorE from adrenals binds to beta 2 receptors on smooth muscle
-results in bronchodilation, increase mucous secretions and increased mucociliary clearance
-examples of beta 2 agonists include clenbuterol and albuterol

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40
Q

Describe some of the features of clenbuterol for treating asthma

A

-dose is 0.8 -3.2 mcg/kg PO BID
-can result in increased HR, sweating, excitability
-most effective if inflammation is under control as inflammation down regulates beta 2 receptors (start steroids before this for more effective response)

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41
Q

What are the main corticosteroids used to control airway inflammation in horses?

A

Systemic: dexamethasone, prednisolone (NOT PREDNISONE- horses cant convert to active form)
Inhaled: fluticasone, ciclesonide
- safer option- less systemic side effects

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42
Q

When should systemic therapy be pursued in asthma cases?

A

-with severe airway disease
-when abnormal respiratory pattern may not allow for deep deposition of the drug

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43
Q

T/F: you can use the injectable form of dexamethasone orally

A

True- just be sure what is drawn from that bottle never goes IV
-cannot give IM

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44
Q

What are the advantages and disadvantages of systemic corticosteroids?

A

Advantages: much less expensive than inhaled, less labor and equipment intense than inhaled

Disadvantages: systemic distribution affects overall immune response, horses are more susceptible to infection, heavy parasite load, skin disease, laminitis

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45
Q

What are the inhaled steroid options for horses?

A

-Flexineb (more expensive), equihaler (only works for metered dose drugs)
-nebulized or metered dose administration
-good for maintenance of mild-moderately affected horses

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46
Q

Describe the use of inhaled ciclesonide in horses

A

-delivered in an inactive form
-drug is inactivated in the lungs when it reaches the airway epithelium
-has minimal effect on serum cortisol levels (minimal systemic distribution)

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47
Q

What are the main advantages and disadvantages of inhaled therapy?

A

Advantages: local effect, rapidly degraded when enters blood, minimal side effects, best choice for long term maintenance

Disadvantages: more expensive, more labor and equipment intense

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48
Q

What treatment should you recommend with mild asthma cases (grade 1-2)? More severe (grade of 3 or greater)?

A

Mild: start with environmental management (mow pasture, wet the hay). If horse fails to respond make more changes (remove hay from diet, switch to chopped hay or pellets)

Severe: start with IV corticosteroids at 0.05 mg/kg following with descending dose regime. Consider oral bronchodilators like clenbuterol

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49
Q

T/F: you should still taper the steroid dose even if the horse is not fully responding

A

FALSE
-dont automatically drop the dose, drop based on clinical picture

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50
Q

When should you stop corticosteroids when using for asthma control?

A

-when horse is on a very low dose (4 mg or 1 tab per day) and there is no evidence that clinical signs are returning
-environmental modifications are still in place
-recheck BAL confirms that airway inflammation has resolved

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51
Q

What are your options if you are on low dose dex and neutrophilic inflammation is still present in the BAL?

A

-continue dexamethasone at a low dose or switch to inhaled drugs
-revisit environment and make farther changes
-if horse remains normal, recheck BAL in 3 weeks
-some horses stay on low dose for a long time, but check parasite fecal egg counts and monitor for lameness, skin diseases and other infections

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52
Q

What is important to communicate to the client in order to maintain remission?

A

Make sure they know to call you when there is any evidence of problems
-have regular consults discussing clinical signs, temp, any other affected horses or any changes in management

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53
Q

What are some reasons for poor response to treatment?

A

-weight loss due to high energy demands of increased respiratory effort
-bronchial malacia resulting in bronchiectasis

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54
Q

Describe some of the features of inflammatory airway disease

A

-commonly found in racetrack horses
-often resolves with time
-may be due to viral infection- prolonged healing due to high respiratory demands of racing
-affects young horses
-can resolve, does not recur
-less neutrophils

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55
Q

What is the most common virus that affects horses?

A

Flu

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56
Q

How can viruses contribute to IAD?

A

-causes injury to airway epithelium leading to decreased clearance and accumulation of debris
-bacteria rarely plays a role

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57
Q

What are the clinical signs associated with IAD?

A

-cough, lethargy, mucous secretions

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58
Q

Which airway aspirate is preferred in IAD cases?

A

BAL- gives more accurate view of what is happening in terms of inflammation in the deep airways
-can be associated with eosinophil and mast cell inflammation in addition to neutrophils

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59
Q

What is the best course of treatment for IAD cases?

A

-get horse away from dust and tack environment
-modify bedding, feed, etc to minimize dust
-turnout on pasture
-medicate with oral prednisolone if no response to environmental management
-dont need antibiotics unless seen on cytology

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60
Q

What contributes to exercise induced pumonary hemorrhage?

A

-horses performing frequently at a high level (racehorses)
-occurs more in older horses
-occurs more in females

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61
Q

Describe the pathophysiology of EIPH

A

Extreme expansion of diaphragm when undergoing high exercise leads to negative pressure in the alveoli
- capillary beds with high pressure near alveoli leads to rupture
-areas around past hemorrhage become weak and more predisposed to future injury (fragile neovascular nets)
-hemorrhage leads to inflammation leading to neovascularization and easier ruptures (vicious cycle)

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62
Q

What are some ways to diagnose EIPH

A

-scintigraphy- can evaluate distribution of blood flow in the lung
-radiolabeled RBCs- to map at rest and during exercise (main redistribution of blood flow occurs in dorsocaudal lung field)
-endoscopy, BAL or TTW
-radiographs and echo have limited value
-necropsy: stains areas in dorsocaudal lung

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63
Q

What are the treatment options for EIPH?

A

Furosemide: leads to reduction in plasma and blood volume
-reduces RA, PA, pulmonary wedge and pulmonary capillary pressure
-bronchodilator

Nasal dilators: open up nostrils to reduce resistance

Equine concentrated serum doesn’t show great efficacy as treatment

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64
Q

How are equine respiratory viruses usually transmitted?

A

Horse to horse transmission aka contact with an infected shedding horse
-contact with recently expelled secretions (fomites)
-recrudescence of latent viral infections (herpes virus)

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65
Q

Describe the pathology of how viruses usually affect horses

A
  1. Virus enters track, attaches to respiratory epithelium
  2. Virus enters epithelial cells and uses cell apparatus to replicate
  3. Virus is released from the epithelial cells, killing cells
    4.Viral shedding begins within 48 hours of infection
  4. Damages the epithelium and mucociliary clearance mechanism
  5. Virus can spread systemically through viremia
  6. Epithelium can take a month or more to fully recover
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66
Q

How long does it take for epithelial cells lining the airways to regenerate after damage?

A

2-3 weeks
-if down to the basement membrane it will be replaced with scar tissue

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67
Q

What is the equine immune response to viral infection?

A

Innate response: secretion of soluble factors into mucous including complement, cytokines, macrophages, NK cells

Humoral immunity: in upper respiratory tract IgA response, in lower respiratory tract IgG response

Cell mediated immunity: viral antigen presented locally by dendritic cells, viral replication inhibited by NK cells and cytotoxic T cells

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68
Q

What are the main clinical signs of respiratory disease in horses?

A

-young horses most often affected
-acute signs include high fever, general malaise, cough that persists for several weeks, nasal discharge that is clear or mucoid (mucous usually with secondary bacterial infection)
-some can cause local lymph node swelling, tenderness, limb or ventral edema (common with influenza)
-chronic signs include diminished performance, chronic nasal discharge, chronic pharyngitis (due to pharyngeal lymphoid hyperplasia), cough

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69
Q

What are some secondary syndromes that can occur with viral infections?

A

-predisposition to bacterial infection
-pleural pneumonia/pleuritis- can lead to severe fibrin deposition and infection
-lower airway hyperreactivity and inflammation
-pericarditis
-generalized vasculitis which can affect many organs
-purpura type response-can stimulate immune reaction in multiple organ systems

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70
Q

Where should you start with your diagnostics in a suspect respiratory virus case?

A

CBC- mild normocytic normochromic anemia, acute leukopenia with mild to moderate lymphopenia, after several days mild to moderate neutrophilia, early convalescence- monocytosis, fibrinogen normal

Chem- +/- elevated CK, AST< LDH

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71
Q

How do you treat equine viral respiratory disease?

A

-cant treat the virus, treat the signs
-NSAIDS for fever, general malaise, bronchodilators (clenbuterol) and nebulizers (saline, acetylcysteine, bronchodilators) for cough
-acyclovir and oseltamivir moderate viral replication and protect against neuro response, can add in steroids, antibiotics if secondary bacteria, fluids

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72
Q

How should you monitor respiratory virus cases?

A

-ask owners to monitor temp, resp rate, pleural pain
-make sure fluid intake is adequate, monitor fecal consistency and output
-consider soaking feed or feeding softer feed
-place in a “clean” environment (pasture) if the horse is clinically stable and does not require close monitoring
-rest for at least three weeks past resolution of fever and other clinical signs

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73
Q

What steps should you take in terms of biosecurity in viral cases?

A

Isolate horse, use dedicated clothing, footwear, tools, monitor others for clinical signs, remove and isolate additional affected horses
-submit samples for specific diagnosis (PCR) and advise against movement on or off of farm

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74
Q

Describe the principles of vaccination against equine viral respiratory disease

A

Goals: to stimulate cell mediated immunity and antibody response

Types: modified live (stimulates cell mediated response), killed vaccines (mainly stimulate humoral response)

-all of these tend to be incomplete and short lived, but they are still reccomended

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75
Q

What general tests are available for viral detection?

A

Equine respiratory panel for PCR identification of common viruses and bacteria (submit nasopharyngeal swab or lavage, transtracheal wash, bronchoalveolar lavage (does not need to be sterile)

Viral isolation: best method for identifying viral strain. submit nasopharyngeal swab

Viral titers: pre and post antibody titers, collect and freeze acute and convalescing samples from serum
-not used much anymore

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76
Q

What are the common equine respiratory viruses?

A

-equine influenza (ssRNA, orthomyxovirus)
-equine herpes virus 1 & 4 (dsDNA)
-equine viral arteritis (ssRNA, arteriviridae)

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77
Q

T/F: DNA viruses are much more fragile than RNA viruses

A

False-other way around

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78
Q

What are some less common, less severe or age specific viruses that need to be considered?

A

-Equine rhinovirus: affects foals >3-4 weeks of age
-equine adenovirus 1: affects foals, severe if immunocompromised
-equine herpes virus 2: immunosuppression in weanlings
-equine herpes 5: equine multinodular pulmonary fibrosis

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79
Q

What is the most common cause of upper respiratory tract infection in the horse?

A

Equine influenza
-causes the most damage in the upper respiratory tract

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80
Q

What is antigenic drift and shift that occurs with influenza?

A

Drift: mild shift in surface antigens
Shift: development of a new viral subtype

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81
Q

What is the most common strain of influenza in horses in US?

A

H3N8

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82
Q

What is the most popular vaccine against influenza?

A

Modified live intranasal
- causes profound local IgA response and IgG
-frequency depends on the horses use

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83
Q

Describe some of the main clinical features of equine herpes virus 1 and 4

A

-double stranded DNA virus
-distributed worldwide
-most horses are infected by 2 years of age
-transmission can occur vertically (especially herpes virus 1)
-incubation of 2-10 days
-may become latent and reside in respiratory lymphoreticular system or trigeminal ganglion- shedding recurs with stress or steroids

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84
Q

What clinical manifestations are seen with herpes virus infection?

A

-upper respiratory tract infection
-pulmonary vasculotropic infection (can be lethal- endothelial cells necrose and fluid rushes into lung parenchyma)
-late term abortion
-neonatal foal death
-myeloencephalopathy
-neuropathogenic disease (mutation of EHV 1)

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85
Q

What are the main clinical signs seen with equine herpes virus?

A

-URT is most common form- older horses less severely effected

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86
Q

When does abortion tend to occur with herpesvirus infection?

A

Late term- at least 5 months into gestation
-fetus has minimal autolysis
-fetus and placenta contain high viral loads- infectious source
-usually several mares abort but abortion typically follows respiratory signs (a month or two later)

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87
Q

How do you prevent against equine herpes virus?

A

-vaccinate: first vaccine at 6 months with 2 boosters, then every 4 to 6 months thereafter
-usually use modified live (as it stimulates some cellular immunity)
-vaccine prevents abortion but not completely protective for other forms of disease

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88
Q

What is the infectious agent responsible for strangles?

A

Strep equi ssp equi

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89
Q

What are the characteristics of strep equi equi?

A

-gram positive, chain forming, beta hemolytic (completely lyses RBCs) streptococcus
-facultative anaerobe present worldwide

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90
Q

Why does being a facultative anaerobe make strep such a good pathogen?

A

It can spread through aerosolized particles and can live in any part of the body

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91
Q

Describe the pathogenesis of strep equi equi

A

-spread via the nasal or oral route, aerosolized or fomite
-bacteria adhere, colonize URT epithelium
-invades through the epithelium, lamina propria and enters lymph within hours of exposure
-evades neutrophils and replicates in the lymph nodes of the head
-may spread through lymphatics and cause bastard strangles
-may elicit immune response (purpura reaction and other immune mediated diseases)

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92
Q

Which horses are the most at risk for strangles infections?

A

-young horses that are naiive to the bacteria
-old debilitated horses
-but all horses are at risk (100% morbidity, 2-3% mortality)

93
Q

How can horses go into a carrier state?

A

They harbor the bacteria as chondroids in the guttural pouch

94
Q

What are the classic clinical signs associated with strangles?

A

-incubation of 1-14 days after exposure
-fever, nasal discharge (2-4 weeks)
-swollen lymph nodes (palpable 2-3 days after exposure)
-mature abscess at 2-3 weeks
-submandibular drain ventrally, retropharyngeal drain to exterior or rupture into the medial floor of the gutteral pouch
-abscesses are a primary source of environmental contamination
-bacteria do not survive in the environment long, especially if hot and dry

95
Q

T/F: strangles is the only disease in horses that can cause swollen lymph nodes

A

False- other viruses such as influenza can cause this as well
-they are the only one to populate in and cause rupture of the lymph nodes however

96
Q

Describe the immune mediated disease that can result due to strangles

A

-circulating strep equi antigens form immune complexes
and cause leukocytoclastic vasculitis (purpura hemorrhagica)
-other organs may be directly affected or affected secondarily to vasculitis such as the kidney heart and lung
-can lead to autoimmune mediated thrombocytopenia, anemia or myositis
-agalactia is normally the result of fever and anorexia

97
Q

What is the difference between bastard strangles and atypical strangles?

A

Bastard strangles: dissemination and abcess formation in other viscera (all tissue at risk)
-general signs include weight loss, low grade fever, elevated WBC and fibrinogen

Atypical strangles: subclinical disease or mild/self limiting disease. May be due to bacterial load and pathogenesis, prior exposure or horse specific characteristics

98
Q

How do you diagnose strangles?

A

-bacterial culture or PCR -nasal, nasopharyngeal or abscess swab, nasal or guttural pouch washes or abscess aspirate
-must keep sample cool, process quickly, wash samples are superior, pellet fluid samples and submit pellet
-false negatives can occur so you should do both culture and PCR to increase sensitivity

99
Q

Why is serology probably not the best diagnostic for strangles?

A

-not very sensitive, has cross reactivity with other strep antigens
-have to take 2 samples days apart to see rise in titers in order to determine if infection is active

100
Q

How do you manage the horses on a farm during a strangles outbreak?

A

Horses with obvious signs: do not treat abscesses with antibiotics, NSAIDs. Use hot pack, bring to head and drain. Can use antibiotics or NSAIDS if uncomfortable, depressed, unable to eat, or after abscess has ruptured

Horses at risk (have been exposed) with no apparent disease: take temp daily, if febrile start antibiotics immediately and place into quarantine

Unaffected horses: keep separate from affected horses and fomite exposure
-handlers need to use separate clothing, tools, lead lines, etc

101
Q

What antibiotic would you start a horse on that had evidence of strangles?

A

Beta lactams- procaine penicillin G
- causes horses to be sore
-can give ceftiofur IV and follow up with excede- might be a better option

102
Q

What vaccines are available against strangles?

A

Intramuscular- minimal protection and high risk of SE
Intranasal- also poorly protective, abscesses if other vaccines are given at the same time
-risk of contaminating the other vaccines and causing abscesses - spread out vaccines

103
Q

How long should you isolate affected horses?

A

Perform culture/scope gutteral pouch exams until negative on PCR and culture- every 2 weeks
-can also do nasopharyngeal swab- not quite as good but doesnt require fancy equipment

104
Q

What does the normal recovery look like from a strep equi equi outbreak?

A

<10% develop persistent guttural pouch infection
-up to 50% may become carriers

105
Q

How does strep zoo become pathogenic?

A

Part of the normal flora but can cause opportunistic infections following viral disease or high loads in foals

106
Q

What should you do whenever you are suspicious of a bacterial infection in the respiratory tract?

A

Perform transtracheal aspirate and submit for gram stin, cytology, culture and sensitivity

107
Q

T/F: fungal pneumonia is rare in horses

A

True

108
Q

What fungal organisms are most common in lower airway infections? What treatments are available?

A

Aspergillus, fusarium
-usually from the gut or inhaled
-occurs in immune compromised, young, or very sick horses

Treatments: amphotericin B (expensive, poorly absorbed, nephrotoxic), fluconazole (inexpensive but poor efficacy against aspergillus or fusarium), miconazole (inexpensive, good topical treatment)

109
Q

What are the main parasitic diseases that affect the lungs of horses?

A

Lung worm: dictyocaulus arnfeildi
- not a primary lungoworm of horses, but can occur in young horses housed with donkeys
- can see eosinophilia in TTW
-responds to ivermectin

Parascarid infection
- migrating larvae
-responds to ivermectin, moxedectin, fenbendazole

110
Q

What are the causes of pleural effusion in horses?

A

-often can be secondary to pulmonary lymphatic blockage by pneumonic exudate
-secondary to thoracic neoplasia
-penetrating wound/trauma
-pleuritis: inflammation of pleural membrane. most common in young thoroughbred or standardbred racehorses or other performance horses with a history of stress, transport, recent viral infection, strenuous exercise or general anesthesia

111
Q

What are the main clinical signs associated with pleuropneumonia?

A

-depression, inappetence, acute weight loss
-maybe fever
-tachycardia
-variable dyspnea, pain associated with respiration (grunting)
-soft reluctant cough
-mucopurulent discharge +/- fetid breath
-ventral edema
-scant dry feces
-reluctance to move or lie down, wide base stance with abduction of forelimbs (may be confused with colic signs)
-auscultation may reveal absent lung sounds or amplified lung sounds depending on region
-percussion can cause a dull sound starting at fluid line and going ventrally

112
Q

What sample is the most ideal to get in a pleuropneumonia case?

A

TTW
- submit for everything

Can also do radiographs and look for a pleural fluid line or ultrasound

Can also get thoracocentesis which can be both diagnostic and therapeutic. Perform on both sides (IC or 8 on left, 6 or 7 on right- use ultrasound to find best place), chest tube if large amount of fluid, suture in place and cover with one way valve

113
Q

What antibiotics should be reached for in a pleuropneumonia case? What other therapies are indicated?

A

-broad spectrum (penicillin or gentamycin, aminoglycosides, metronidazole)
-can use systemic and aerosolized administration

Others: NSAIDs, Pemtoxyfilline, DMSO
- laminitis prophylaxis with ice boots
-fluid and nutritional support

114
Q

What can be done in super severe cases of pleuropneumonia?

A

Thoracoscopy if incomplete mediastinum
- used to evaluate necrotic tissue and abscess capsule
-attempt to assess risk of pneumothorax
-insert scope at rib space 8-12 at site of proposed thoracotomy
-if pneumothorax develops, close entry site and re-inflate lung

115
Q

What is the prognosis in pleuropneumonia cases?

A

-related to chronicity and extent of disease
-good in acute cases with pleural defects but minimal effusion or fibrin
-poor if chronic disease with significantly consolidated lung, effusion or fibrin tags

Other indications of poor prognosis: malodorous breath with serosanguinous discharge indicating anaerobic infection and necrotic lung, malodorous pleural effusion that contains mixed bacteria, anaerobic bacteria or Ecoli in tracheal or pleural fluid, poor response to therapy

116
Q

What virus is equine multinodular pulmonary fibrosis associated with?

A

Equine herpes 5
-treatment options limited- corticosteroids
-poor prognosis

117
Q

What is MEEDs?

A

Multisystemic eosinophilic epitheliotrophic disease
- causes respiratory disease, weight loss, skin lesions
-treat with steroids

118
Q

What can cause pneumothorax? Clinical signs?

A

-penetrating wound, dissecting subQ emphysema, bullae or ruptured bronchi, necrotic process causing bronchopleural fistula

Signs: restlessness or severe anxiousness, tachypnea or tachycardia, flared nostrils, abdominal component to respiratory effort, symmetric thoracic movement

Treat with teat canula and suction to remove air, but can recur. Can cause cascade of inflammation

119
Q

What is the airflow that horses need to maintain their oxygen requirements?

A

90 L/second

120
Q

What is the normal approach to an upper airway case?

A

Start with physical, then move onto upper airway endoscopy
-if you still don’t have your answer can pursue radiographs, dynamic endoscopy, MRI, CT, oral exam, bloodwork or biopsy
-then develop working diagnosis and treatment plan

121
Q

T/F: a noise from the upper airway can refer down to the lungs

A

True- need to listen to larynx and trachea for this reason

122
Q

T/F: inspiratory noise is not always pathologic

A

False- it is
- it indicates narrowing of the upper airway lumen

123
Q

What is the difference between stridor and stertor? Roaring/whistling?

A

Stridor is high pitched, stertor is low pitched (snoring)

Roaring/whistling may range from low to high pitched wheezing and is inspiratory sounds during exercise.

124
Q

Are expiratory sounds normal during canter/gallop?

A

YES

125
Q

What is the common order for performing upper airway endoscopy?

A

Larynx, trachea, dorsal pharyngeal recess and pharynx, guttural pouch 1, ethmoid turbinate’s, sinus drainage angle, nasal passage 1, then change sides and do second guttural pouch and second nasal passage

** do unsedated unless there is a clinical indication to sedate. Sedation can change ability of arytenoids to move. You can use a twitch

126
Q

Where is the sinus drainage angle located?

A

Just rostral to the ethmoid turbinates

127
Q

How should you focus your exam if you narrow down the region from your physical exam and resting endoscopy?

A

Sinus/nasal passages: head radiographs, dental exam (head CT or MRI)

Larynx/Pharynx: watch during exercise, dynamic endoscopy/treadmill endoscopy, laryngeal ultrasound

128
Q

When should a tracheotomy be pursued? How is it performed?

A

In cases of life threatening URT obstruction
-can be used prophylactically or as an emergency procedure
-hesitation can lead to pulmonary edema and asphyxiation
-complications: cellulitis, emphysema, cartilage damage, stricture

Procedures: local block, feel for the 3rd-6th tracheal rings, make a vertical incision and cut down to trachea, then make horizontal cut through tracheal rings. Place finger through and keep it in place until you have an opening to place in there (can use end of 60 cc syringe)

129
Q

Describe the different types of nasal discharge

A

Serous: from viral infection, allergic rhinitis
Mucoid to purulent: from primary or secondary bacterial respiratory infection, sinusitis
Hemorrhagic: fresh- GP mycosis, trauma, EIPH; old- ethmoid hematoma, necrotizing pneumonia
Feed contamination: choke (saliva), dysphagia due to pharyngeal dysfunction
Fetid odor: dental or chronic

130
Q

If discharge originates rostral to nasal septum, where will it come out? What about if its from the lungs? Guttural pouches?

A

Unilateral on side of origin
-ex: sinus drainage angle

Lungs- bilateral

Guttural pouches- can be unilateral or bilateral depending on speed of ejection from the pouch

131
Q

What is an epidermal inclusion cyst?

A

Atheroma of false nostril
-fluid filled cystic lesion that contains squamous and keratin debris
-primarily cosmetic
-rarely obstructs airway and is usually unilateral but can be bilateral

COSMETIC

132
Q

How do you remove an epidural inclusion cyst?

A

-remove surgically in the standing sedated horse with local anesthesia
-can use external or internal approach (internal with laryngeal burr)
-remove with the lining intact as drainage alone causes recurrence

133
Q

Describe alar fold collapse

A

The alar fold is a mucocutaneous fold separating the false from the true nostril attached to alar cartilage
-rare enlargement or failure of the transversus nasi muscle allows for collapse during exercise
-most common in standardbreds and saddlebreds
-vibrates and makes noise during inspiration and expiration (can cause reduced performance)

134
Q

How do you diagnose alar fold collapse?

A

-place large mattress suture over gauze to hold alar folds open to see if noise goes away
-rule out other causes of noise and exercise intolerance by resting and/or dynamic endoscopy
-can occur in conjunction with other problems

135
Q

How do you correct alar fold collapse?

A

Surgically resect alar fold: incision through latera alar GA, standing removal with ligasure device
-return to exercise when incision is healed in 2-3 weeks
-should improve performance and noise, if not there is likely another problem

136
Q

Describe nasal fold collapse and its treatment

A

-collapse of both the nasal and alar folds
-can use adhesive nasal strips on horses during intense exercise to reduce peak inspiratory pressure and resistance
-pulls dorsal conchal fold laterally and expands dorsal meatus, may reduce work of breathing and alleviate noise

137
Q

T/F: if a laceration or wound of nares is closed by primary closure then a scar can cause secondary stenosis

A

False- if it is not closed primarily this can occur
DO NOT LET HEAL BY SECOND INTENTION

138
Q

How can facial nerve paralysis present in terms of the nares?

A

-lack of tone of nostril may lead to flutter or collapse

139
Q

What does the middle nasal meatus look like on endoscopy?

A

Mercedes bens sign

140
Q

Where are the ethmoid turbinates and the sinus drainage angle located?

A

In the nasal cavity before reaching the pharynx

141
Q

Describe nasal mucosal hemorrhage

A

Rare- rule out other causes of epistaxis first
-collection of blood vessels “nasal varicosities” may bleed during turbulent airflow or randomly
-treat via laser ablation or just wait it out
-inflammation may cause prominent vasculature that randomly bleeds (rule out other sources of inflammation eg lower airway), trial environmental changes

142
Q

Describe the wry nose abnormality

A

-a congenital malformation of the maxilla
-perform DV radiography to determine degree of deviation (maxillary incisors fail to occlude with mandibular incisors)
-mild cases are common and if there is no dyspnea or problems nursing no treatment is needed but reduce owners expectations for athleticism
-in severe cases can try permanent or temporary tracheostomy, or correction via osteotomy of premaxilla/maxilla and external/internal fixation

143
Q

What is choanal atresia/stenosis?

A

Atresia is failure of the buconasal membrane rupture in early gestation
-bilateral more common than unilateral and bilateral is fatal at birth without tracheotomy
-unilateral may present as exercise intolerance or reduced airflow in older foals, and can be relieved by fenestration with laser or long instruments

Stenosis is when the nasal passages are much narrower than normal leading to exercise intolerance. Treat with palliative care

144
Q

What are nasal polyps?

A

-they are soft painless and benign growths attached in the caudal nasopharynx/sinus
-usually unilateral and a result of chronic inflammation
-amputate by snaring with OB wire through protective tube
-rule out extension of sinus cyst or involvement of dorsal or ventral nasal conchae first (radiography, endoscopy)

145
Q

Describe fungal rhinitis

A

-primary infections caused by cryptococcus, rhinosporidiosis, phycomycosis, coccidiomycosis
-causes bloody and/or mucopurulent discharge
-must rule out other problems extending from sinus
-diagnose through histology/culture of biopsy or cytology
-treat through surgical debulking and systemic antifungals (fluconazole, success variable and need to treat for a while)

ZOONOTIC

146
Q

Which fungus is most commonly indicated after sinus surgery?

A

Aspergillosis

147
Q

T/F: nasal septal defects/deviations are often benign

A

True
-must rule out mass effect from conchal mass

148
Q

What does the frontal chonchal sinus communicate with?

A

The caudal maxillary sinus through the frontomaxillary opening

149
Q

What does the caudal maxillary sinus communicate with?

A

The sphenopalatine sinus

150
Q

Where do the frontochonchal sinus, sphenopalatine sinus, and caudal maxillary sinus drain out of?

A

The sinus drainage angle

151
Q

Why does there tend to be more problems with pus accumulation in the rostral maxillary sinus and ventral conchal sinus than the others?

A
  • the pus sits ventral to the drainage angle
    -gravity works against its drainage
152
Q

Where do the rostral maxillary sinus and the ventral conchal sinus drain out of?

A

Nasomaxillary aperture

153
Q

What should your next diagnostic step be if you see pus coming from the sinus drainage angle on endoscopy?

A

Perform radiographs to highlight the paranasal sinuses

154
Q

T/F: some structures are only seen clearly when enlarged or fluid filled due to summation

A

True
- a good example of this is the ventral conchal sinus

155
Q

Describe the features of head CT in horses

A

-3D imaging modality of choice for sinus diseases and for complex disorders of the paranasal sinuses
-allows for excellent assessment of delicate boney structures in the sinus, can assist with surgical planning for removal of sinus masses, and can be performed standing with short acquisition time
-does not allow for definitive diagnosis of tumor type, it may be difficult to distinguish tissue types so often need to follow up with sinoscopy and biopsy

*should always do radiographs prior

156
Q

Where should you drill holes for sinus trephination?

A

Depends on what sites are effected
- the conchofrontal sinus is the most versatile as it allows you to access the frontal, dorsal conchal, caudal maxillary and sphenopalatine
-the caudal maxillary site communicates with the conchofrontal site for through and through lavage
-the rostral maxillary site can be used to access both it and the ventral conchal sinus

157
Q

T/F: fenestration of the maxillary septal bulla is needed to make all sinus compartments comunicate together

A

True

158
Q

Describe the process of sinus trephination

A

-standing sedation and local analgesia is provided
- a small diameter hole is created through a small stab incision, larger holes through semicircular incisions

159
Q

When would a bone flap be indicated?

A

When you need to remove a large lesion
-allows you to readdress the issue easier if not entirely solved by first surgery

160
Q

What does sinoscopy allow for?

A

Detailed visualization, biopsy, and treatment
-used to be used a lot before we had access to CT

161
Q

What is the most common sinus disease?

A

Sinusitis- half of which is caused by dental disease

162
Q

Compare and contrast primary and secondary sinusitis

A

Primary: diagnosed when you cant find any underlying cause
Secondary: most common. Due to dental related sinusitis or sinus mass resulting in obstruction of the sinus drainage angle (cyst, neoplasia, ethmoid hematoma) or secondary infection of blood after tear in mucosal barrier of sinus

163
Q

Describe some features of primary sinusitis

A

-inflammation of the sinus mucosa causing blockage of the normal sinus drainage angle
-allows mucous to accumulate with bacterial growth
-treat acute cases with broad spectrum antibiotics for 1 week
-perform sinus lavage if no response or chronic (may need to repeat) plus antibiotics

164
Q

What is one of the main causes of treatment failure in sinusitis cases?

A

Inspissated pus
-warrants more extensive exploration

165
Q

What is a sinus cyst?

A

-a circular lesion on oblique radiograph, fluid filled (usually yellow fluid)
-can cause deformation of facial bones and loss of bone architecture as it expands
-can lead to respiratory obstruction and sinusitis
-surgical removal is curative

166
Q

What is the prognosis for sinus neoplasia?

A

Poor
-need biopsy for definitive diagnosis (through trephine) but could be SCC, adenocarcinoma, fibroma, chondroma, hemangiosarcoma, osteosarcoma
-often causes facial deformities, often causes loss of bone architecture

167
Q

What is suture periostitis?

A

-commonly occurs in young horses
-causes gap and periosteal proliferation at facial sutures
-can be secondary to trauma
-treat with topical anti-inflammatory agents and TIME (remodeling doesn’t happen overnight)
-consider a course of antibiotics if its an older horse and is associated with trauma (to prevent secondary sinusitis)

168
Q

Describe the clinical progression of sinus fractures?

A

-often can cause acute epistaxis due to disruption of the respiratory mucosal lining
-can progress to secondary sinusitis
-emphysema may occur if there is a break in the respiratory epithelium
-for evaluation, need to evaluate eye, perform endoscopy and complete full neuro exam, as well as CT and/or radiographs

169
Q

How do you treat sinus fractures?

A

-reduce initial soft tissue swelling using broad spectrum antimicrobials and antiinflammatories
-surgical repair of fractures can improve cosmetics and function depending on location (elevation of bone and wire sutures), but small fractures with minimal indentation may be treated conservatively
-orbital fractures usually need surgical repair to relieve impingement on the globe

170
Q

What is the best way to distinguish between suture periostitis and post fracture callus?

A

Perform multiple oblique radiographs to determine the anatomic location of the bony swelling

171
Q

How do you diagnose a progressive ethmoid hematoma?

A

Clinical signs: intermittent unilateral epistaxis (usually unilateral), abnormal respiratory noise rarely if it extends into nasal passage
-endoscopy: dark red to tan-brown encapsulated mass
-radiographs to check sinus involvement
-CT if long standing or recurrent
-sinoscopy
-histology-fibrous tissue, hemosiderin, calcareous deposits

172
Q

Why do you need both radiology and endoscopy for ethmoid hematoma diagnosis?

A

Radiographs can assess the sinus portion of the ethmoids while endoscopy can assess the nasal portion of the turbinates

173
Q

How can you treat progressive ethmoid hematomas?

A

-formalin injection (most common, 4-10% formalin via trans-endoscopic needle) with 25-50 mL
-repeat every 3-4 weeks
-average 5 repeat injections
-can refer for laser ablation if extremely severe (beware of risk of hitting the brain)
-be sure there is no sinus involvement through performing CT
-recheck every 6-12 months

174
Q

What are the guttural pouches?

A

A pair of ventral diverticula of the eustachian tubes with a volume of 300-500 mL
-divided into lateral and medial compartments by the stylohyoid bone
-lined by ciliated epithelium that contains many lymphocytic follicles
-lining is closely associated with CN 9, 10, 11 and 12

175
Q

How does the gutteral pouch connect to the pharynx?

A

The nasopharyngeal ostia
- pathology of the gutteral pouch can cause narrowing of the pharynx

176
Q

What important artery is in the medial compartment vs lateral compartment of the guttural pouch? What are some other important structures?

A

Medial: internal carotid artery (supplies the brain). Also contains CN 9,10,11,12
Lateral: external carotid, longus capitus

177
Q

What are some of the main clinical signs associated with disease of the gutteral pouch?

A

-nasal discharge (mucopurulent or blood)- often bilateral
-parotid or dorsal pharyngeal wall swelling (leading to dyspnea)
-cranial nerve dysfunction
-facial nerve paralysis, dysphagia, laryngeal dysfunction, horners syndrome (due to dysfunction of cranial sympathetic trunk)

178
Q

What is third eyelid prolapse associated with related to gutteral pouch disease?

A

Horners syndrome

179
Q

What are the different approaches for removing chondroids from the gutteral pouches?

A

-non-surgical best through flushing or endosocpy
-transendoscopic laser to break down large chondroids into smaller pieces
-open surgical as last resort

180
Q

Describe guttural pouch tympany

A

-occurs in first year of life
-can cause dyspnea, dysphagia, secondary empyema
-salpingopharyngeal ostia becomes a one way valve which can cause air to get trapped in one (more common) or both guttural pouches
-diagnose via PE, radiographs or endoscopy

181
Q

How do you treat guttural pouch tympany?

A

-create a fenestration to prevent the valve as acting one wat
-relieve air temporarily with indwelling catheter
-if recurs provide permanent relief with laser surgery (median septum fenestration if unilateral, or transendoscopic laser creation of the salpingopharyngeal fistula, or fenestration into the dorsal pharyngeal recess
-good prognosis

182
Q

What is guttural pouch empyema?

A

-can occur due to extension of URT infection or through burst of retropharyngeal lymph node in the case of strangles
-leads to intermittent nasal discharge (usually unilateral), lymph node enlargement, parotid swelling/pain, respiratory noise, dysphagia
-screen for strangles
-provide daily irrigation for 7-10 days (balanced electrolyte solution)
-quarantine until you get culture/PCR result
-good prognosis

183
Q

What are chondroids exactly?

A

solidified purulent material
-remove via endoscope or surgical

184
Q

What is the main clinical sign associated with gutteral pouch mycosis?

A

-impressive arterial hemorrhage (often stops spontaneously the first time)
-leads to an unpredictable number of bleeds- dont wait for the next!
-nasal discharge in some early cases with low volume
-mycotic plaques may be found incidentally
-treatment is urgent- keep horse quiet and allow clot, then transport to referral center (consider ace to reduce blood pressure and keep calm)
-can use aminocaproic acid or plasma as clotting factors

185
Q

How can you distinguish ethmoid hematoma from guttural pouch mycosis?

A

Ethmoid hematoma would produce a little blood vs guttural pouch mycosis produces a LOT of blood

186
Q

How do you treat GP mycosis?

A

Endoscopy with sedation
- if you see a blood clot at the entry of the pharyngeal ostia, do not go into the pouch unless at a surgical facility (risk of clot destabilization)
- carefully enter pouch and be prepared for bleed

REFERRAL IS RECCOMENDED

187
Q

What are the common areas that mycotic plaques can lie?

A

Internal carotid, external carotid (most common), maxillary artery- can cause arterial wall disease or cranial nerve dysfunction

188
Q

What is the recommendation for treatment of mycotic plaques?

A

Surgical coils or plugs, laser fenestration of the dorsal pharyngeal recess (alters environment and can cause fungal regression). Topical antifungals on own are not effective

-use fluoroscopy to map blood vessels when placing coils or plugs

-prognosis good unless neurological signs are present

189
Q

What is temporohyoid osteoarthropathy?

A

Fusion of the temporohyoid joint unilaterally or bilaterally
-limits motion of the hyoid and can cause head shaking, ear rubbing and abnormal head position
-advanced: see vestibular signs

Diagnose with endoscopy, radiographs or CT

190
Q

How can you treat temporohyoid osteoarthropathy?

A

-can try medical management with antibiotics and antiinflammatories
-or surgical: ceratohyoidectomy (removal of a portion of the hyoid apparatus to cease the movement of the temporal-hyoid articulation)

191
Q

Describe the anatomy of the pharynx

A

Soft tube that is supported by muscle
-to swallow there are constrictors and elevators of the soft palate, and to hold open during inspiration there are dilators and tensors of the soft palate
-muscles are innervated by cranial nerves 5, 10 and 11

192
Q

What forces do negative pressure put on the tissues of the upper airway? What tissue type does this affect the most? what do they need to do to keep the airway open?

A

Tissues will want to collapse. Nares, pharynx and larynx most affected. Muscles need to work hard to prevent this

193
Q

Describe lymphoid hyperplasia

A

-occurs in young horses incidentally due to active lymphoid tissue
-may occur secondary to inflammation in older horses
-graded 1-4 depending on severity

194
Q

What are the different types of palatal dysfunction?

A

-palatable instability (soft palate billows dorsally but does not come dorsal to epiglottis- can progress to DDSP though)
-dorsal displacement of soft palate (most common cause of upper airway obstruction)

195
Q

Describe the pathophysiology behind DDSP?

A

Poorly understood, but may be due to some sort of neuromuscular dysfunction of the intrinsic soft palate muscles, reduced elevation of the larynx by the thyrohyoideus and dysfunction of the hypoglossal nerve

196
Q

How do you diagnose DDSP?

A

-obstruction during expiration (causes gurgling or flutter noise)
-may not see on resting endoscopy
-dynamic endoscopy is the best diagnostic tool

197
Q

What is the effect of swallowing on DDSP cases?

A

Can cause the soft palate to return to normal position

198
Q

How do you manage DDSP?

A

-medical treatment: address all underlying causes of upper or lower airway inflammation
-tack changes: to bring tongue forward or alter position of basihyoid bone or larynx (tongue tie, Cornell collar)
-rest and improved fitness
-surgery: laryngeal tie forward, sternothyroid tenectomy, laser palatoplasty (aim to stiffen soft palate or move position of larynx)

199
Q

What is nasopharyngeal cicatrix?

A

Occurs in hot climates with horses on pasture (maybe environmental allergy)
-healing causes nasopharyngeal fibrosis which can cause deformation of epiglottis, arytenoids, or guttural pouches
-often no clinical signs unless pharyngeal constriction occurs
-can try treatment with antiinflamatories or removal of inciting cause

200
Q

What masses may be found in the nasopharynx?

A

Fungal mycosis, neoplasia, extension of sinus pathology

201
Q

Describe nasopharyngeal dysfunction

A

-occurs in foals in first month of life
-causes respiratory distress and dysphagia due to collapse of pharynx
-diagnose with physical exam, bloodwork, endoscopy, radiographs
-treat through providing patent airway through tracheostomy and provide nutrition with nasogastric tube. Resolves in 30 days

202
Q

How does cleft palate occur?

A

Due to interruption of the embryonic closure of the midline palate
-occurs in rostral to caudal direction
-leads to milk draining from nose, coughing, aspiration pneumonia
-diagnose on oral exam or endoscopy

203
Q

How can you treat cleft palate?

A

-split mandibular symphysis and repair palate directly
-usually a salvage procedure

204
Q

What is the only cartilage of the larynx that is paired?

A

Arytenoids!
-the epiglottis, cricoid and thyroid are all unpaired

205
Q

What is the opening of the larynx called?

A

Rima glottis

206
Q

T/F: the larynx should be maximally abducted during exercise.

A

True-via abduction of arytenoids. However the same degree of abduction also occurs during swallowing on endoscopy
-during exercise all the tissues of larynx are tense and the epiglottis is firmly positioned dorsal to the soft palate

207
Q

If there is an inability for a horse to actively abduct an arytenoid cartilage during maximal exercise, what is the result?

A

The cartilage would be pulled in towards the airway lumen during the negative pressures of inspiration

208
Q

Describe the clinical features of laryngeal hemiplegia

A

-neurogenic atrophy of cricoarytenoid dorsalis muscle (loss of adductor and abductor function)
-leads to inspiratory obstruction as arytenoid cartilage cannot be abducted
-causes inspiratory roaring noise and/or exercise intolerance (occurs more in tall young horses)

209
Q

Why does laryngeal hemiplegia usually occur on the left?

A

The recurrent laryngeal nerve on the left runs a long path-many opportunities for the nerve to be affected

210
Q

What is grade 4 laryngeal neuropathy?

A

Complete immobility of the arytenoid cartilage and vocal fold

211
Q

When should conservative treatment vs surgical treatment be pursued in cases of recurrent laryngeal neuropathy?

A

In non athletic horses
-surgical should be performed in working horses to improve exercise intolerance and reduce noise through prosthetic laryngoplasty (tie-back for function), ventriculocordectomy (to reduce noise), or reinnervation of the muscle

212
Q

How is the tie back method performed?

A

Suture running from the caudal aspect of the cricoid cartilage to the muscular process of the arytenoid cartilage to mimic the function of the cricoarytenoid dorsalis muscle

213
Q

Describe arytenoid chondropathy

A

-similar clinical signs as laryngeal hemiplegia (usually thickened endoscopic appearance)
-arytenoid cartilage deformity due to infection within the cartilage (can be unilateral or bilateral and can cause severe URT obstruction at rest)
-etiology: usually begins with mucosal disruption leading to infection, possibly hematogenous

214
Q

How can you distinguish between arytenoid chondropathy and left laryngeal hemiplegia on ultrasound?

A

With arytenoid chondropathy will see abnormal shape of cartilage, normal muscle

With laryngeal hemiplegia muscle will appear fibrotic and hyperechoic

215
Q

How do you treat arytenoid chondropathy?

A

-emergency tracheotomy if airway is occluded
-medical management with anti-inflammatories and antimicrobials in minor cases
-resection of granulomas (transendoscopic laser or sharp dissection via laryngotomy) paired with medical therapy
-arytenoidectomy: thickened cartilage with no purposeful movement so you can remove the corniculate process and body of the cartilage to open up the airway (remove everything but the muscular process)

216
Q

What is an entrapped epiglottis?

A

-epiglottis covered by aryepiglottic fold and subepiglottal mucosa
-can cause partial airway obstruction and inspiratory noise
-apex of redundant mucosa can be ulcerated
-do not confuse with DDSP
-rarely intermittent (need dynamic endoscopy to recognize)
-check size and shape of the epiglottis (may be small)

217
Q

What is the treatment for epiglottic entrapment?

A

Axial midline division with transoral hooked bistoury under GA, transnasal guarded hooked bistoury, or transendoscopic laser ablation
-excellent prognosis in acute cases with normal epiglottis, worse in chronic cases (better if treating with anti-inflammatories preop)

218
Q

How do subepiglottic cysts, abscesses and granulomas present?

A

-can cause epiglottic entrapment
-may also have DDSP
-treat by snaring off via the mouth and topical/systemic anti-inflammatories

219
Q

What does dynamic endoscopy allow for?

A

Assessment of the larynx and pharynx during horses normal activity or at maximal intensity- either over ground or treadmill
-must assess without endoscope in place first (may alter some pathology such as DDSP)

220
Q

What are the main indications for dynamic endoscopy?

A
  1. Horse presents for upper respiratory tract noise or poor performance, or a horse that you have previously treated has recurrence of noise or poor performance
  2. Resting endoscopy is performed and is normal or resting endoscopy shows an abnormality that you would like more information about during exercise to better develop treatment plan
221
Q

T/F: some conditions are only present on dynamic endoscopy

A

True- sometimes the high negative pressures that occur during exercise are what allow for pathology to be visualized
-often a domino effect can occur during exercise due to worsening negative pressures

222
Q

T/F: it is important to rule out concurrent inflammatory diseases that may alter airway dynamics and predispose to dynamic conditions

A

True

223
Q

How do you place the leads for base-apex ECG?

A

Lead 1
- white is positive and is placed at the right point of the shoulder
-black is negative and is placed at the left axilla
-red can go on the left anywhere else (grounding lead)

224
Q

What are the main 4 things you should look at when interpreting an ECG to determine if there is an arrythmia?

A

-heart rate
-heart rhythm (RR interval-regular or irregular)
-relationship between P waves and QRS
-morphology of complexes

225
Q

T/F: biphasic P waves can be normal in horses

A

True- but they all should appear the same

226
Q

What is the definition of sinus tachycardia in horses?

A

A heart rate above 50 bpm

227
Q

Why are bradyarrythmias so common in horses? What are the most common ones?

A

Due to high normal parasympathetic tone
-AV block most common followed by sinus arrythmia

These should dissapear with an increase in sympathetic tone (such as with exercise) if non-pathologic

228
Q

Describe a sinus arrythmia

A

-rhythmically irregular
-each QRS is normal and proceeded by a P wave and pauses are </= 2 normal PP intervals in length

229
Q
A

Equine BCM (13 decks)

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