Diseases of the lung in dogs and cats

Question 1

Diseases of the small airways

Answer 1

• Canine chronic bronchitis
• Bronchiectasis
• Feline lower airway disease/feline asthma vs. chronic bronchitis
• Airway foreign bodies
• Bronchial neoplasia

Question 2

Types of Bronchitis

Answer 2

• different causes and anatommical localisations (tracheobronchitis, bronchitis, bronchopneumonia)
• Infectious:
• Canine infectious respiratory disease complex (CIRDC):
  
  • CDV, CaHV-1, CRCoV, CIV
  • Kennel cough: CAdV-2, CPIV, Bordetella br., Mycoplasma spp.
• FHV in cats
• Parasites
• fungal
• Non-infectious:
• Aspiration
• Canine chronic bronchitis
• Feline asthma

Question 3

Canine chronic bronchitis (CCB)

• clinical signs and history

Answer 3

–> idiopathic form of bronchitis

• Middle-aged to older dogs; small breeds > large breeds
• Daily cough for more than 2 months (productive/non productive), exercise intolerance
• doog condition/overweight, tracheal sensitivity, inspiratory crackles, expiratory wheezes
• prolonged expiration and expiratory push (expiratory type dyspnea)
• increased vagal tone –> sinus arrytmia

Question 4

Canine chronic bronchitis (CCB)

• Diagnosis

Answer 4

• Blood examination: uslually negative
• Radiography: we can recognize the alveolar pattern
• doughnut sign
• right-sided cariomegaly
• cor pulmonale or negative
• Bronchoscopy: we can recognize the inflammation, the sickened bronchial mucosa
• Hyperemic mucosa
• mucoid or purulent secretions
• fibrous nodules on the mucosa
• BAL, TTL: for microbiology and cytology
• bacteria +/-
• nondegenerate neutrophils
• eosinophils
• mucous

Question 5

Differential diagnosis of CCB

Answer 5

• Infection: kennel cough, parasites, fungi, D.immits
• Aspiration: Accidental, pharyngeal dysphagia, esophageal disease, gastrooesophageal reflux, laryngeal dysfunction
• Eosinophilic bronchopneumopathy
• endocardosis (congestive heart failure)
• pulmonary fibrosis

Question 6

Treatment of CCB

Answer 6

• Can be controlled but never cured. Goals: control inflammation, prevent worsening of airway disease

- Short acting glucocorticoids:

• 0.5-1.0 mg/kg prednisolone BID, decreased by half every 5-10 days

- Bronchodilators:

• Theophylline (GI, tachycardia, excitability)
• terbutaline (1-2-4 mg/dog PO BID)
• Albuterol (50ug/kg PO TID)

- Antitussives:

• if inflammation has beed effectively treated!
• otherwise mucos can trap in the bronchi and worsen clinical signs
• Antibiotics: if BAL cytology and microbiology is postive
• Ancillary therapy:
• weight reduction,
• harness instead of collar
• cool, clean area (smoke, dust, heat)
• nebulization
• Inadequately treated: pulmonary hypertension, bronchiectasis, vasular remodelling

Question 7

What is Bronchiectasis?

Answer 7

• Irreversible dilatation of large airways (bronchi), with accumulation of pulmonary secretions.
• common in Cocker spaniels
• Histopathologic response due to long-standing inflammation/irritation (CCB, primary dyskinesia, foreign body, smoke, dust)

Question 8

Bronchiectasis

• history, symptoms and diagnosis

Answer 8

• History:
• chronic productive cough, frequent bouts of pneumonia (initially respond to antibiotics/relapse)
• Symptoms:
• loud bronchial sounds,
• nasal discharge +/- (pneumonia),
• hemoptysis
• Diagnosis: Radiography, broncoscopy, CT

Question 9

Bronchiectasis

• Treatment

Answer 9

• drugs can not cure the damaged bronchi, only prevent the problem with corect treatment of the underlying disease
• Lobar bronchiectasis –> lobectomy, antibiotics (based on culture), bronchodilators
• Cough suppresents must be avoided!
• Limitation of therapy:
• if the bronchiectasis affects several lung lobes then the only chance is repeated AB-therapy –> multiresistance
• if only one lung lobe is affected, then surgical removal of he affected lung lobe can solve the problem

Question 10

Bronchiectasis

• Prognosis and prevention

Answer 10

• Prognosis:
• chronic recurrent infection
• resistance to AB treatment
• pulmonary hypertension, cor pulmonale
• Prevention:
• appropriate AB therapy in infectious disease
• promp removal of foreign bodies
• appropriate managment of CCB

Question 11

Feline lower airway disease / feline bronchitis

asthma vs chronic bronchitis

• history and symptoms

Answer 11

• main key of feline asthma –> bronchoconstriction!
• increased airway resistance (smooth muscle hypertrophy, bronchial wall edema, glandular hyperplasia) -> cough and respiratory distress
• Symptoms:
• paroxysmal-, dry- “hacking” cough, open mouth (loud) brething, prolonged exhalation. expiratory type dyspnea
• auscultation: harsh lung sounds, crackles, expiratory wheezes or normal
• percussion: increased resonance

Question 12

Diagnostic evaluation of feline asthma

Answer 12

• blood test: eosinophilia in 30%, negative heartworm antibody test
• fecal examination: exclusion of Aelurostrongylus, paragonimus spp, capillaria infection
• Radiopgraphy:
• interstitial-, bronchial-, alveolar pattern or normal, hallmark: peribronchial cuffing
• infiltrated medial lung lobe
• pulmonary emphysema
• Bronchoscopy:
• BAL cytology: sthma eosinophilia vs. neutrophilia in chronic bronchitis, culture
• Specific test for asthma:
• whole body plethysmography (increased airway reactivity to nonspecific aerosol stimulant)

Question 13

Diff diagnosis of feline asthma

Answer 13

• infection:
• pulmonary parasites, toxoplasmosis, D. immitis, mycoplasmosis, bacterial, fungal, viral infection)
• Aspiration: accidental, esophageal disease -> reflux
• idiopathic pulmonary fibrosis
• neoplasia (carcinoma)

Question 14

Treatment of feline asthma

Answer 14

-Acute therapy: emergency situation

• cyanosis, open mouth breathing
• oxygen cage; terbutaline, glucocorticoids + bronchodilatoros
• chronic managment
• glucocorticcosteroids
• prednisolone
• inhaled fluticasone
• methyl-perdisolone acetate
• bronchodilators (terbutaline)
• anitbiotics

Question 15

Prevention and prognosis of Feline asthma

Answer 15

• Prevention:
• Beta-blockers should be avoided! (propranolol, atenolol)
• cigarette smoke, aerosol spray, upper respiratory viruses
• Prognosis:
• anti-inflammatories and bronchodilators alleviates acute clinical signs
• recurrance of signs

Question 16

Brochial neoplasia

• clinical signs, diagnosis, treatment

Answer 16

• Cough, obstructive breathing pattern (loud respirations), hemoptysis
• Ausculatation: harsh wheezing noises
• Radiography: soliter mass lesion
• Treatment: same as pulmonary neoplasia

Question 17

Pulmonary parenchymal diseases

Answer 17

• Pneumonia
• infectious diseases
• aspiration pneumonia
• eosinophil bronchopneumopathy
• pulmonary edema
• pulmonary contusions
• smoke inhalation
• ARDS
• Pulmonary fibrosis
• Lung lobe torsion
• pulmonary thromboembolism
• pulmonary neoplasia

Question 18

Pneumonia classification

Answer 18

• Anatomy:
• Bronchopneumonia: can be parenchyma and bronchi affected together. e.g in viral infections like Distemper
• pneumonia
• interstitial pneumonia: if only the interalveolar space in the level of alveoli is inflammed
• Lobular or diffuse
• Origin:
• Infectious: bacterial, viral, fungal, parasitic
• Non- infectious: aspiration, idiopathic
• Duration:
• acute, subacute, chronic

Question 19

Bacterial pneumonia

• common complications and protection mechanisms

Answer 19

• Common complications:
• laryngeal dysfunction, viral pneumoni, aspiration, GI disease, encephalopathy
• protection mechanism of lower airways:
• laryngeal function, coughing reflex, mucociliary clearance, epithelial barrier, IgA, alveolar macrophages, IgG

Question 20

Bacterial pneumonia

• symptoms

Answer 20

• lethargy, fever, dyspnea, coughing (dog >> cat) acute/chronic, exercise intolerance, nasal discharge, hemoptysis and severe dyspnea
• underlying disease (dysphagia, regurgitation, vomiting, muscular weakness)
• increased lung sounds and crackles or wheezes + inflammatory fluid

Question 21

Bacterial pneumonia

• diagnosis and treatment

Answer 21

• Diagnostic evaluation:
• hematology: WBC increased
• Radiography:
  
  • focal or diffuse alveolar pattern (aspiration: cranioventral lung regions)
  • brochiectasis, megaesophagus, mass
• TTL, Bronchoscopy:
  
  • BAL (culture, cytology), mass, foreign body, bronchooesophageal fistule, lobular pneumonia (aspiration)
• Treatment:
• AB, bronchodilator, lobectomy (focal pneumonia, abscess),
• saline nebulization, underlying disease (foreign body, neopplasia, GI disease)
• Organisms: E.coli, Bordetella, Klebsiella, Pasterurella, Pseudomonas, Mycoplasma spp.

Question 22

Viral bronchipneumonia

Answer 22

• Distemper, Morbillivirus (paramyxoviridae family)
• Exposure (inhalation, po infected secretions) –> replication in macrophages, tonsils –> viremia (2-4 daus: initial fever) –> several tissues (lung, bowel, skin, CNS) –> bronchopneumonia, enteritis, encephalitis
• Mucopurulent oculonasal discharge, fever, PCR (blood, urine), lethargy, neurologic symptoms (50%), radiography (interstitial, alveolar pattern)
• treatment: largely supportive (AB, bronchodilators, fluid), seizure control (diaxepam, KBr, phenobarbital), antobody

Question 23

Fungal pneumonia

Answer 23

• Histoplasma capsulatum, Blastomyces dermatitidis, coccidioides immitis, cryptococcus neoformans, aspergillus fumigatus, pneumocystis carinii
• Diagnosis:
• BAL/fine needle aspiration of lung; cytology, microbiology, PCR; blood: serology
• Therapy:
• itraconazole
• pneumocystis: trimethoprim + sulfamethoxazole

Question 24

Aspiration pneumonia

• findings

Answer 24

• aspiration of fluid, food, gastric contents results in pulmonary inflammation
• megaesophagus
• laryngeal and pharyngeal dysfunction
• neuromuscular disease
• anesthesia, encephalopathy
• brachycephalic airway conformation
• forced feeding (contrast radiography)
• severity of lung injury:
• volume, pH, toxicity –> obstruction, pulmonary hemorrhage, edema, inflammation, necrosis, bronchoconstriction, infection

Question 25

Aspiration pneumonia

• clincal signs, diagnosis

Answer 25

• clinical signs:
• cough, tachypnea, acute onset of rspiratory distress, fever, lethargy, shock
• cats: wheezes (bronchospasm)
• diagnostic evaulation:
• history of vomiting, regurgitation
• radiography: quite different (interstitial/alveolar, focal/diffuse), but interstitio-alveolar pattern in cranioventral and middle lung lobes
• megaesophagus
• complete blood count: leukocytosis
• bronchoscopy: BAL for culture, cytology

Question 26

Treatment of aspiration pneumonia

Answer 26

• respiratory distress:
• oxygen
• fluid therapy (but increased capillary permeability can lead to oedema)
• Bronchoscopy: removal of the content
• Antibiotics:
• culture or empirical; after fever/X-ray lesions + 2-3 weeks
• Saline inhalation, coupage; +/- bronchodilators
• corticosteroids: NOT allowed!!
• prognisis: severity of lung injury/underlying cause

Question 27

Eosinophilic bronchopneumopathy

• history, clinical signs

Answer 27

• inflammatory disease, unknown etiology
• hypersensitivity to an environmental or endogenous antigen
• all breeds, huskies
• history:
• coughing, gagging, difficulty breathing, nasal discharge (mucopurulent or serous), ethargy and anorexia
• physical examination:
• nasal dicharge, crackles, increased lung sounds (or normal auscultation)

Question 28

Eosinophilic bronchopneumopathy

• diagnosis and treatment

Answer 28

• Radiography:
• diffuse interstitial, alveolar, bronchial or combination
• nodules or mass-like lesions (eosinophilic granulomatosis)
• Blood test:
• peripheral eosinophilia
• Bronchoscopy:
• green, green-yellow mucos, mucosal thickening
• BAL, mucosal brushing (large number of eosinophils)
• Diagnosis:
• rule out other causes!
  
  • migrating parasites, bacterial or fungal infections, heartwor or neoplasia, allergy testing
• Treatment:
• glucocorticoids at immunosuppresove dosages lasting weeks to months; hyposensitization?
• prognosis: generally good

Question 29

Pulmonary oedema

• physiological processes

Answer 29

• Fluid accumulation in the interstitium and alveoli

1. vascular hydrostatic pressure increases: left-sided congestive hearth failure (CHF), excessive fluid administration (anuric renal failure)
2. plasma oncotic pressure decreases: hypoalbuminemia
3. vascular permability increases: vasculitis, ARDS
   
   • Protein rich fluid will enter the interstitium, and this protein will bind water. fureosemide will not be so effective in this case.
4. impared lymphatic drainage: left-sided CHF, neoplastic process
5. decreased transpulmonary pressure: upper airway obstruction

• Noncardiogenic oedema: ARDS, acute upper airway obstruction, neurogenic oedema (seizures, head trauma)
• Cardiogenic pulmonary oedema: CHF

Question 30

Pulmonary oedema

• symptoms, diagnosis and treatment

Answer 30

• Symptoms
• restricted type dyspnea. It is superficial, rapid respiration without coughing.
• panting + cyanosis
• Coughing: in severe cases bloody expectoration of blood-tinged fluid
• Auscultation:
• Lung: crackles hear on inspiration and end-expiration (in dorso-caudal lung fields). In severe edeme quiet lung sounds in cats!
• Heart: murmur +/- (but mitral endocardiosis, cardiomyopathy), arrhytmia, tachycardia
  
  • Heart murur without sinus tachycardia: pulmonary disease > cardiogenic edema
• Radiography:
• Cardiogenic edema: interstitial pattern in the hilar and caudo-dorsal lung regions, cardiomegaly, pulmonary veous enlargement
• Noncardiogenic: absence of cardiac and pulmonary venous changes
• Treatment:
• Furosemide (2-4 mg/kg IV every 4-12 hr)
• oxygen therapy (intubation, positive pressure ventilation)
• sedatives: acepromazine in dog and cat. Morphine sulfate in dog
• prognosis: variable
• severity of edema, treatment and underlying disease

Question 31

Smoke inhalation

• history and etiology

Answer 31

• direct injury: heat, particulate matter, toxic gases
• etiology:
• acute phase (0-36 hr) tissue injury –> capillary permability increases –> oedema, tissue hypoxia
  
  • shock, pain
  • CO gas inhibits oxygen binding to Hb –> tissue hypoxia
• Later phase (2-4 days): edema decrease, mucosal secretion increase, decreased mucociliary clearance, secondary bacterial colonization –> tracheobronchtis, pneumonia

Question 32

Smoke inhalation

• clinica signs, diagnosis

Answer 32

• Clinical signs:
• skin injury, smell of smoke, loss of consciousness, upper airway stridor (laryngeal edema), ocular and nasal discharge, cyanosis
• some patients have minima signs but 24-36 hr later then can occur! (ARDS, infection, laryngeal edema).
• Diagnostic evaluation:
• history, clinical signs, radiography (oedema, pneumonia), BAL, culture
• Carboxyhemoglobin is not distinguished from oxyhemoglobi with blood gas analysis or pulse oxymetry!

Question 33

Smoke inhalation

• treatment

Answer 33

• observation for at least 24-48hr
• tracheostomy: severe laryngeal oedema, obstruction
• oxygen cage: half-life of CO in room air is 4hr, in 100% O2 30 min
• bronchodilators, antibiotics (culture)
• fluid therapy (but edema!)
• analgesic
• Corticosteroids: laryngeal edema/acute cardiovascular shock!
• prognosis: wrong if severe respiratory distress, infectious pneumonia, neurological signs and cutaneous burns

Question 34

ARDS

• history, pathogenesis

Answer 34

= Acute Respiratory Distress Syndrome

• acute hypoxemic respiratory failure caused by lung injury and pulmonary capillary permeability increase
• Sepcial form of pulmonary edema caused by damaged capillary network, caued by cytochrome storm
• the cytochrome storm will increase capillary permability. protein rich fluid can enter the pulmonary interstitium, leading to intersitial pattern o X-ray and interstitial hypoxia
• Secondary to: sepsis, pancreatitis, aspiration, shock, microbal pneumonia, SIRS, babesiosis
• Pathogenesis: pporly understood
• early phase: proteinaceous fluid (capillary perm increase)
• Later: inflammtory cells increase, hyaline membrane formation, fibrosis –> pulmonary hypertension
• irreversible

Question 35

ARDS

• clinical signs, diagnosis, treatment

Answer 35

• Clinical signs:
• extreme anxiety, tachycardia, cyanosis, crackles (end-inspiration, expiration), wheezes, underlying disease
• Diagnosis:
• noncardiogenic lung oedema: auscultation, radiography, echocardiography
• protein (edema)/protein(plasma): 80-90%, in cardiogenic edema 50%
• Treatment:
• oxygen therapy (intubation, PEEP)
• fluid therapy (low-normal circulatory volume)
• furosemide (early phase)
• glucocorticoids?
• blood gas analysis (control)
• prognosis: generally poor

Question 36

Pulmonary fibrosis

Answer 36

• Idiopathic interstitial lung disease (pneumonia): WHW, staffordshire bill terriers, (cats)
• pathologically: alveolar septic fibrosis, interstitial fibrosis, epithelial hyperplasia, focal calcification
• dyspnea, exercise intolerance, cough +/-, cyanosis, crackles
• • Ca: chronic and progressive pulmonary signs
• • Fe: rare, faster course of the disease. Acute!
• radiography: diffuse interstitial pattern
• echocardiography: moderate to severe pulmonary hypertension
• biopsy, poor prognosis: die of hypoxaemia
• dog: 1-3 years
• cat: few weeks
• there is no effective treatment!
• cough suppressants, PHT: syldenafil, glucocorticoids?, bronchodilators?

Question 37

Lung lobe torsion

Answer 37

• Large, deep-chested dogs (greyhounds)
• idiopathic, pleural effusion, surgery, trauma= acute disease
• lung lobe torsion –> venous congestion –> exudation (bloody pleural effusion), necrosis, anemia
• clinical signs:
• respiratory distress, tachypnea, cough, hypotension, dyspnea, fever, lethargy
• diagnosis:
• deep chested dogs, pleural effusion,
• radiography: rounding of the lung lobe edges
• bronschospy, CT
• surgical exploration
• treatment:
• removal of pleural flud, oxygen, fluid/shock therapy, surgery

Question 38

Pulmonary thromboembolism (PTE)

Answer 38

• secondary to:
• heartworm disease, IMHA, neoplasia, DIC, hyperadrenocorticism, PLE, PL-nephropathy etc.
• PTE: abnormal gas exchange, pulmonary infarction
• Clinical signs:
• middle-aged to older, acute respiratory distress, tachypnea, cyanosis
• acute, lethat disease
• Diagnosis:
• difficult to diagnose
• D-dimer, antitrombin III, blood gas, radiography, echocardiography (logated in the pulmonary artery)
• pulmonary agniogram is the gold standard
• treatment:
• Thrombolytic therapy (surgical, catheter, drugs: tissue plasminogen activator etc.)
• • underlying disease

Question 39

Pulmonary edema

• clinical sigs, diagnois

Answer 39

• Metastatic > primary (carcinoma, osteosarcoma)
• chronic cough, exercise intolerance, respiratory distress, dyspnea, weight loss, anorexia
• physcal examination:
• origin of metastasis: abdominal mass, effusion, lameness
• auscultation, percussion
• radiography:
• is the key tool in the diagnostic approach!
• LL x2, VD/DV
• false negative: size, obscured by the heart or liver; periosteal proliferation (hypertrophic osteopathy)
• false positive: eosinophlic bronchopneumopaty
• CT: more sensitive to tumors
• Definitive diagnosis: biopsy ,(thoracoscopy) or FNA
• Treatment:
• primary pulmonary neoplasia: lobectomy