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Ettinger Respiratory > 241 Diseases of trachea and small airways > Flashcards

241 Diseases of trachea and small airways Flashcards

1
Q

Noninfectious tracheal diseases (leading to tracheal mucosal inflammation) includes….

A
  • tracheal dorsal membrane
  • flaccidity
  • tracheal collapse
  • tracheal injury/laceration
  • posttraumatic stenosis
  • foreign body
  • intratracheal tumor
  • smoke inhalation
  • prolonged barking (dogs) and - tracheal avulsion (cats)
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2
Q

What are some extratracheal diseases?

A

-extreme cardiac enlargment
- mediastinal enlargment (LN tumor or thymoma, or megaoesopagus) or parenchymal masses, which can cause deviation of trachea, with effect on tracheal shape or lumen size and subsequent obstruction +/- inflammation
allergic lower airway disease can lead to secondary tracheitis

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3
Q

What is tracheal collase

A
  • Characterised by dorsoventral flattening of the tracheal ring with laxity of the dorsal tracheal membrane.
  • malacic airways (bronchial collapse) often associated with tracheal collapse, and would negatively impact therapy and prognosis.
  • Goose-honk sound is characteristic
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4
Q

What causes tracheal collapse?

A
  • multifactorial cause
  • requires weakness of tracheal rings and factors that progress to symptomatic stage.
  • the cartilage rings soften due to reduction of glycosaminoglycan and chondroitan sulfate which leads to decreased ability to maintain rigidity
  • triggers include obesity, cardiomegaly, inhaling irritants, periodontal disease, respiratory infections, and endotracheal intubation.
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5
Q

When does the cervical and thoracic trachea collapse?

A

cervical trachea collapses during inspiration, and thoracic trachea collapses during expiration

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6
Q

What are secondary causes of tracheal collapse?

A
  • WHWT with idiopathic pulmonary fibrosis (IPF), tracheal collapse is encountered frequently in advanced cases
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7
Q

What is the clinical presentation?

A
  • middle aged to older miniature, toy, and small breed dogs.
  • overrepresented breeds include yorkshire terrier, pomeranian, pug, poodle, Maltese, and Chihauhua
  • Signs = chronic cough, mild-severe panting, exercise intolerance, and varying degree of insp/expiratory dyspnea (resp distress), cyanosis in advanced cases.
  • good honk cough +/- terminal retch
  • Thoracic auscultation may show crackles on inspiration/expiration with small airway collapse +/- bronchitis.
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8
Q

what is the differential Dx for tracheal collapse?

A
  • chronic MVD
  • chronic bronchitis +/- tracheitis
  • secondarily tracheal collapse
  • chronic pulmonary parenchymal disorder (IPF)
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9
Q

How is tracheal collapse diagnosed?

A
  • suspected based on signalment, Hx of cough, and physical exam
  • additional radiography, fluoroscopy, echocardiography, bronchoscopy, and pulmonary function testing
  • ## Rads: lateral projection, tangential (rostrocaudal) projection of thoracic inlet (skyline projection, collapsed trachea seen as oval, C, or cresent shape)
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10
Q

What is seen on radiographs in patients with collapsing trachea?

A
  • tracheal membrane invaginates into lumen on dorsal aspect of trachea, and during inspiration it will cause increased tracheal diameter
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11
Q

How is tracheal collapse managed with marked resp difficulty managed?

A

Marked resp difficulty:

  • O2, sedation, antitussive
  • butorphanol 0.05-0.2 mg/kg q 4-6h or ace (0.01-0.1 mg/kg) injected SC, and pred 15-30 mg/kg IV used to decrease acute inflammation.
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12
Q

How is tracheal collapse managed long term?

A
  • weight reduction
  • replacement neck collars with harnesses
  • remove from resp irritants
  • treat other disease such as chronic airway disease, cardiac disease, and hyperadrenocorticism
  • low dose c-roids: prednisolone 0.1 mg/kg PO q 24h x 1-2 weeks at 3 month intervals) or inhalation (fluticasone 120mcg puff q 12h using face mask and spacer)
  • antitussive agents effective in controlling cough include hydrocodone (0.22 mg/kg PO q12h and butorphanol (0.55 mg/kg PO q 12h)
  • bronchodilators can reduce small airway spasm to prevent lowering intrathoracic pressures, improve mucociliary clearance, and reduce diaphragmatic fatigue.
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13
Q

What if dogs cannot be managed with medical management.

A
  • extraluminal tracheal rings for cervical tracheal collapse
  • intrathoracic tracheal collapse is diagnosed and cannot be managed medically treatment involve placement of intraluminal self-expanding stenting devices
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14
Q

What is the prognosis of tracheal collapse?

A

Condition is progressive, and long-term progosis is poor

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15
Q

What are the clinical signs of tracheoesophageal or bronchoesophageal fistula?
- How is it diagnosed?

A
  • chronic cough, recurrent lower resp tract infections, and gas accumulaiton in GIT due to passage of air from trachea into GIT.
  • connection between trachea of esophagus can be evaluated by bronchoscopy, contrast radiography, fluoroscopy, or CT.
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16
Q

What causes obstructive/traumatic tracheal disease?

A
  • collapsed tracheal rings, stenosis due to injuries, foreign bodies, neoplasia, granulomas, external compression, or complication of tracheostomy
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17
Q

How can tracheal injuries occur?

A
  • small lacerations or avulsions and caused by intraluminal or external trauma
  • intraluminal trauma associated with endotracheal intubation,
  • external trauma seen with dog fight or automobile accident
  • cats recieving stenosis after necrosis/rupture following overinflation of ET tube.
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18
Q

What is the type of intratracheal tumors that occur?

A
  • osteochondroma in older dogs or cats

- MCT, CC, adenocarcinoma, osteosarcoma, extramedullary, plasmacytoma, leiomyoma, or fibrosarcoma.

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19
Q

How do tracheal granulomas occur? What can they be treated with?

A
  • can be complication after intraluminal stent placement and cause small lumen
  • treat with C-roids, PO or nebulisation to decrease granuloma size
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20
Q

What can cause a parasitic granuloma? How is it treated?

A

= lungowrm Oslerus osleri; Filaroides osleri; cuterebrosis in cats
- remove granuloma via tracheoscopy or thoracotomy

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21
Q

What is the the clinical presentation of a patient with tracheal injury?

A

subcutaneous emphysema over cervical and thoracic areas, often associated with inspiratory stridor with prolonged inspiratory phase, followed by variable expiratory phase..

  • Cough, exercise intolerance, gag, exertional distress, fever, change in bark, cyanosis/collapse, open mouth breathing cats.
  • pneumomediastinum
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22
Q

What is the typical clinical presentation of infectious tracheitis?

A
  • mild dry cough
  • nasal discharge can be present
  • wide range of signs from mild illness to severe pneumonia leading to death, depending on severity of infection and presence of other viral or bacterial pathogens, as well as immune and vaccination status.
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23
Q

How is infectious tracheitis diagnosed?

A
  • ## Positive bacterial culture, or recently PCR from bronchoalveolar lavage fluid.
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24
Q

How is infectious tracheitis managed?

A
  • vaccination
  • treatment of doxycycline 10mg/kg PO q12h is antimicrobial choice due to efficacy against Bb, its low cost, and ease of use.
  • nebulised antibacterials, such as gentamicin for 3 weeks can be effective in reducing population
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25
Q

What is chronic nonspecific bronchitis in dogs?

A
  • incurable disease in onsidious onset, characterised by chronic or persistent cough, related to inflammed airways. Often syndrome not a that final diagnosis
  • 3 diagnostic criteria:
    1) chronic cough for 2 months
    2) excessive mucus or mucous hypersecretion
    3) exclusion of other chronic cariopulmonary diseases
  • dogs with longstanding bronchitis exhibit bronchiectasis (dilation and destruction of bronchi) or bronchomalacia (airway collapse during expiration and cough)
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26
Q

What is the aetiology of chronic bronchitis?

A
  • poorly understood
  • diagnosed in middle-aged to older, smaller breed dogs, but can occur in larger breeds.
  • overweight dogs and periodontal disease are risk factors
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27
Q

What is the pathophysiology of chronic bronchitis?

A
  • inflammatory changes with bronchial mucosa, including increased mucus production
  • bronchial wall thickening and progressive bronchomalacia contribute to airflow obstruction and worsen inflammation inducing cough a
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28
Q

What is the typical presentation of chronic bronchitis?

A
  • persistent sonorous cough with paroxysms followed by terminal retch
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29
Q

what is the differential diagnosis of chronic bronchitis?

A
  • tracheal collapse
  • lung fibrosis
  • eosinophilic bronchopneumopathy
  • parasitic lung diseases
  • bronchial or lung primary or secondary tumors
  • mitral valve disease
30
Q

What diagnostic tests can be performed to exclude other causes of chronic cough?

A
  • CBC - a peripheral eosinophilia can be pulmonary or parasite
  • HW Ag
  • Fecal analysis for eggs and lungworm larva
  • NT-BNP
  • T-rads show bronchial wall thickening, and can exclude CHF, lung masses, pleural effusion, and interstitial lung disease
  • fluoroscopy
  • US to isolate peripheral lesion or pleural effusion
  • CT with evaluating laryngeal function, bronchoscopy, collecting cytologic airway samples in dogs.
  • bronchoscopic findings are variable, and include irregular mucosal surface with a granular and roughened aspect and sometimes signs o partial bronchial collapse. Thick, sticky mucus in airway.
  • cytological evaluation of BALF -> mucus, hyperplastic epithelial cells, and increased numbers of neutrophils, goblet cells, and macrophages.
31
Q

What is involved in the management and monitoring of chronic bronchitis?

A
  • not reversable, so try to reduce inflammation, limit coughing, and improve exercise capacity
  • no smoking, control body weight, use harness, control oral/periodontal infection
  • glucocorticoids reduce mucous hypersecretion and bronchial mucosal thickening which reduces cough.
  • glucocorticoids administered orally or dosed at 1-2 mg/kg PO q24h and then tapered to lowest effective dose. inhaled fluticasone (AeroDawg) is more expensive but better QOL.
  • Antibiotics with acute exacerbation
32
Q

What cough suppressants can be used in canine chronic bronchitis?

A
  • butorphanol 0.25-1.1 mg/kg PO q8-12h
  • hydrocodone 0.2-0.3 mg/kg PO q 8-12h

Unestablished:

  • gabapentin 2-5 mg/kg PO q 8h
  • Methocarbamol 15-30 mg/kg PO q 12h
33
Q

What is the aetiology of eosinophilic bronchopneumopathy (EBP) in dogs?

A
  • characterised by eosinophilic infiltration of lung and bronchial mucosa, considered to be manifestation of immunological hypersensitivity.
  • aetiology is unknown, the association of eosinophilic infiltration and predominance of CD4+ T cells favors a dominant Th2 immune response in the lower airways.
  • mostly diagnosed in young dogs, Siberian Huskies and malamutes are affected predominantly, but many other breeds can be affected.
34
Q

What is the clinical presentation of EBP?

A
  • usuall good, unless associated with concomitant bacterial bronchopneumonia
  • cough, gagging and retching, which are present in 100% in cases.
  • In acute cases gagging and retching are main complaint
  • sometimes dysnea and nasal discharge
35
Q

What are the diagnostic tests for EBP?

A
  • historical factors, clinical sigs, radiograhic and bronchoscopic findings, blood eosinophilia, rissue eosinophilic infiltration as demonstrated by cytological and histopath
36
Q

What is the common rad finding? What is seen on bronchoscopy?

A
  • x-ray = mixed, moderate-severe, bronchointerstitial pattern.
  • Bronchoscope= abundant yellow-green mucus or mucopurulent material, severe thickening of mucosa with irregular or polypoid surface and is come cases, partial airway closure during expiration.
37
Q

What is the differential diagnosis of EBP?

A
  • strongyloides s., ascaris spp. toxocara canis, and ancylostoma spp. can lead to eosinophilic pneumonia in humans
  • dirofilaria immitis
  • angiostrongylus vasorum
38
Q

How is EBP managed? What is the prognosis?

A
  • Pred at 1mg/kg PO q12h x1week, then 1mg/kg PO q 12h but on alternate days x 1 week, then 1mg/kg PO q 24h on alternate days 1 week, followed by gradual decrease in maintenance dosage.
  • Relapse occurs in weeks to months after discontinuation, but some dogs can remain clinical sign free
39
Q

How can patients with primary ciliary dyskinesia (PCD) present?

A
  • results from heterogenous group of inherited diseases that cause defective ciliary motility.
  • incoordinated ciliary function result in ineffective clearance of mucus from airways leading to chronic mucus plugging and inflammation of nasal cavities and airways
40
Q

What is the aetiology of PCD?

A
  • genetic disease inherited in autosomal recessive mode
  • CCDC39 has been identified in old english sheepdogs and genetic test is available for prebreeding evaluation in this breed
41
Q

What is the clinical presentation of PCD?

A
  • chronic resp abnormalities - rhinosinusitis, bronchitis, bronchopneumonia, and bronchiectasis
    other ciliated epithelia or microtubules can have problems: otitis media, infertility in females, asthenoteratospermia in males, hydrocephalus, and renal fibrosis or dilation of renal tubules
  • hallmark features = recurrent bilateral nasal discharge and repeated episodes of bronchitis or bronchopneumonia
42
Q

How is PCD diagnosed?

A
  • hallmark feature + situs inversus
  • in vitro functional analysis of cilia using scintigrahy to evaluate mucociliary clearance
  • in vivo analysis demonstrates uncoordinated or dyskinetic ciliary beat
43
Q

What are other causes of recurrent bacterial infection of the upper and lower airways?

A
  • immune deficiency, resistant bacteria, or bronchial foreign body
  • Irish Wolfhounds get a rhinitis/bronchopneumonia syndroma, characterised by transient to persistent mucoid or mucopurulent rhinorrhea, cough, and dyspnea since an early age has been described.
44
Q

How is PCD managed?

A
  • not curable disorder
  • key to monitor for infecting microorganisms and judicious use of AB;s
  • systemic and local hydration together with daily coupage and vigorous exercise helps clear mucus from airways
45
Q

What is prognosis of PCD?

A
  • medium to long term prognosis is poor, despite management.
46
Q

What is a bronchoesophageal fistula?

A
  • a communication between esophagus and one or more bronchi.

- most cases are secondary to foreignbody ingestion and penetration in young to middle-aged dogs.

47
Q

What are the clinical signs of bronchoesophageal fistula?

A
  • noisy rales, depression, fever, and loss of appetite.

- pleural effusion in addition to localised pneumonia

48
Q

How is bronchoesophageal fistula diagnosed?

A
  • plain radiographs with evidence of pneumonia, and esophageal FB, gas distension of esophagus, and pleural effusion present.
  • oral administration of barium
  • endoscope gives direct view
  • CBC = increase WBC with left shift
49
Q

How is bronchoesophageal fistula managed?

A
  • thoracic surgery to reduce defect, lavage area, and perform lobectomy to remove infected tissues.
  • if disorder is identified early and treated properly the prognosis is good.
50
Q

What is bronchial mineralisation?

A
  • rare
  • secondary to chronic inflammatory or infectious conditions.
  • peribronchial mucous glands can mineralise in normal cats, apearing as multifocal mineralised opacities
51
Q

What is bronchiectasis?

A
  • abnormal and permanent dilation and distortion of subsegmental airways, which results from chronic airway inflammation that damages elastic components of bronchi and leads to bronchial wall destruction and impaired clearance of respiratory secretions
52
Q

What is the aetiology of bronchiectasis?

A
  • CF causing mutations in the CFTR gene mutations are relatively common in domestic dogs but failed to identify a higher expression rate of CFTR mutations in dogs with bronchiectasis
  • Bronchiectasis is mainly due to non-CF bronchiectasis
53
Q

What can be the cause of diffuse bronchiectasis as a secondary disease?

A
  • aspiration or inhalation injury
  • chronic infectious bronchopneumonia
  • chronic infection with BB or Pneumocystis carinii in dogs with immune deficiency
  • eosinophilic bronchopneumopathy
    chronic bronchitis
  • allergic bronchopulmonary aspergillosis

In cats chronic bronchial inflammation has been suggested as common aetiology associated with bronchiectasis, especially chronic bronchitis, neoplasia, an bronchopneumonia

54
Q

What is the pathophysiology of bronchiectasis?

A

Dysfunction of mucociliary clearance, allows pooling of mucus, exudate, and microbes, and secondary infection stimulates a host inflammatory response, creating vicious circle of further damage to airway wall and predisposition to recurrent bronchopulmonary infections

55
Q

What is the signalment/history/presentation of bronchiectasis?

A
  • American cocker spaniel, miniature poodle, siberian husky, and ESS
  • > 7 yo
  • CS: cough, gag, tachypnea, dyspnea, and fever
  • Bronchiectasis can be seen on t-rad and high-resolution CT or bronchoscopy.
  • bronchiectasis is normal endoscopic finding in older beagles, and does not seem associated with increased neutrophilic content of BALF.
  • C&S of BALF for aerobic and anaerobic bacteria : Pseudomonas aeruginosa, Haemophius influenza, Staphylococcus aureus
  • Cytology: neutrophilia, eosinophilia, squamous metaplasia of epithelial cells. PCR can identify BB, mycoplasma, or aspergillus.
56
Q

How bronchiectasia managed?

A
  • macrolides reduce frequency and mainstay anti-inflammatory therapy in bronchiectasis
  • macrolides have anti-inflammatory and immunomodulatory properties in addition to antibacterial activity.
  • The advantage of using macrolides instead of glucocorticoids to manage inflammation is immunomodulation without immunosuppression
57
Q

What is the prognosis ?

A
  • can survive for years

- focal broncheictasis can be surgically resected.

58
Q

What is bronchomalacia?

A

= weakness of wall of principle or smaller bronchi, leading to collapse of the bronchial wall.

  • unclear aetiology
  • can be static +/- dynamic.
  • static BM is common in brachycephalic dogs, dynamic BM occurs in association with tracheal collapse = tracheobronchomalacea
59
Q

What is the clinical presentation of bronchomalacea?

A
  • poodles and yorkshire terriers especially when overweight or obese
  • brachycephalic dogs show static BM
  • CS= chronic cough, wheezing, intermittent/continuous dyspnea, unable to clear secretions, and recurrent bronchitis and pneumonia.
  • Pulmonary crackles
  • some radiographs are poorly sensitive, documentation of BM requires bronchoscopy.
  • static and dynamic types of BM exist concurrently, particularly larger dogs, with pulmonary hypertension, a bronchial radiograph, and nodularity on endoscope exam.
60
Q

How is BM diagnosed?

A
  • both lungs affected; in half cases the disease appears affect the left lung predominately
  • analysis of BALF and biopsies of bronchial mucosa are warranted and can reveal evidence of infectious bronchitis in half affected dogs.
61
Q

What is treatment and prognosis of BM?

A
  • supportive treatment

- unsure about prognosis.

62
Q

What does feline lower airway disease refer to?

A
  • FLAD refers to all inflammatory and noninflammatory bronchial diseases.
  • Cat cough is fairly specific for tracheobronchial disease as cough of cardiac origin is rare.
63
Q

What is feline inflammatory bronchial disease?

A

= feline asthma or bronchitis & is characterised by inflammation of lower airways without an obvious identifiable cause
- recognised by combinations of cough, wheeze, exercise intolerance, and respiratory distress, attributable to airway obstruction caused by bronchial inflammation.

64
Q

What is the difference in asthma and bronchitis?

A
  • Chronic bronchitis arises secondarily to previous insult that damaged airway permanently leading to clinicopathological features similar to those of asthma, Chronic bronchitis involves a daily cough.
  • Feline asthma is allergic, and includes a cough, wheeze and respiratory distress.
65
Q

What is the signalment for inflammatory bronchial disease diagnosed?

A
  • young- middle afed cats

- middle-aged females and possibly siamese cats

66
Q

What are the clinical signs of inflammatory bronchial disease diagnosed?

A
  • chronic or slowly progressive.
  • mildly affect have brief episodes separated by long time periods
  • mod-severe cases the cough is daily and poor QOL with breathing discomfort.
  • asthmatic crisis= open mouth breathing, dyspnea, and cyanosis.
67
Q

How is inflammatory bronchial disease diagnosed?

A

Imaging: bronchial wall thickening (doughnuts or railroad track), bronchointerstital pattern; air trapping (lucency and flattening diaphragm(, and some cats show evidence of right middle lung lobe atelectasis.

  • CT- bronchial wall thickeninc, patchy alveolar, bronchiectasis
  • stress leukogram and nonspecific hyperglobulinemia in 14-50% of cases
  • 20% have peripheral eosinophilia
68
Q

What is seen on bronchoscopy and BALF analysis? What are some problems with bronchoscopy?

A
  • Cats have small airway size and higher airway responsiveness. When the cat is dyspneic the procedure is hazardous and anaesthesia risks increase
  • bronchoscopic findings are not specific and include large amounts of mucoid or viscous material without airway mucosal hyperemia.
  • BAL = increased eosinophils and neutrophils.
  • mycoplasma can cause lower resp tract infection and might be associated with bronchial disease
  • Aerulostrongylus abstrusus can cause a similar clinical picture.
  • endothelin-1 (ET-1) in Balf might differentiate normal cats from experimentally induced asthma; so BALF-ET1 might be potential diagnostic biomarker for asthma.
69
Q

how is ACUTE inflammatory bronchial disease managed ?

A
  • O2
  • Bronchodilator: beta-2 agonist terbutaline 0.01 mg/kg IV, IM, or SC, or rapidly acting c-steroid 0.25-0.5 mg/kg IV or IM
  • inhaled treatment if minimum amount reach bronchi.
  • if no response then pneumothorax needs to be considered and thoracocentesis must be considered
70
Q

How is CHRONIC inflammatory bronchial disease managed ?

A
  • oral c-steroid: pred 1-2 mg/kg PO q 12h for 1-2 weeks
    +propentofylline a methylxanthine derivative with bronchodilating actions is good adjunct.
  • inhaled fluticasone and bronchodilators (albuterol) palliate an acute exacerbation of signs
  • bronchodilators used in caution due to adverse effects such as tachycardia, CNS stimulation, tremors, and hypokalemia
  • weight loss
  • saline nebulisation and mucolytics or phytotherapeutic agents not proven beneficial and administered with great caution.
  • N-acetylcysteine a drug with mucolytic and antioxidant properties increased airway resistance and is not recommenced
71
Q

What is the prognosis of inflammatory bronchial disease managed?

A
  • substantial morbidity and mortality in cats
  • most cats controlled with oral or nebulised therapy and require lifelong treatment.
  • in chronic cases when remodelling takes place, alleviation can be challenging and lead to euthanasia.

Ettinger Respiratory (8 decks)

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