Exam 5 Flashcards
Lecture 1
Nasal Disease
- Common clinical sigs
- Radiographs and CT interpretation basic abnormal findings
- History and C/S
- Ddx
- Compare and contrast the common biopsy techniques utilized for evaluating nasal disease, nasal swabs, flush, pinch biopsy, and turbinectomy
Clinical signs of nasal disorders
- Nasal discharge
-Sneezing
-Stertor (snoring/snorting-reverse)
-Facial deformity
-Systemic signs of illness
-Central nervous system signs if disease breaches the cribriform plate of calvarium
Nasal Discharge
- Serous: clear, watery, may be normal.
-Associated with viral disease
-May precede mucopurulent discharge - Mucopurulent - what usually causes to be brought to the clinic
-Thick, ropey
-White, yellow, green
-Associated with inflammation
-Viral, bacterial, fungal infections
-Foreign bodies
-Neoplasia
Oral disease - tooth root abscess or oral fistula
Lower airway disease - bronchopneumonia - Hemorrhagic (epistaxis)
-Blood from one of both nostrils
-Can be associated with fungal disease or neoplasia
-Trauma, locally aggressive disease, hypertension, coagulopathies
Diagnostic Approach
- Thorough History
-History of onset
-Duration of disease
-Exposure to travel - Complete PE
-Determine airflow on both sides of nasal cavities with chilled glass slide (or cotton ball test)
-Examine head, oral cavity, eyes, and surrounding soft tissues for symmetry
Fundic exam
FIV
-retinal detachment
-negative menace
-myadrosis
Chronic Nasal discharge - Diagnostic approach
Phase I (noninvasive testing)
-Hx, PE, fundic exam, fecal float, thoracic rads, cytology, tick titers, nasal swab, viral testing (FIV/FELV), MDB, coagulation times, BP, etc.
Phase II (general anesthesia)
-Nasal rads, rhinos copy, dental rads, nasal biopsy with histopath, deep nasal culture, CT
Phase III (referral)
-CT or MRI, frontal sinus exploration
Phase IV (consider referral)
-Repeat phase II in several months using CT or MRI, exploratory rhinotomy with turbinectomy
Diagnostic Tests - Nasal Swab
-Least invasive
-Patient can be awake
-Produces only cytologic sample
-Findings tend to be non-specific
Exeption: cryptococcus in the feline patient
Diagnostic Tests - Nasal Flush
-Minimally invasive
-Patient must be under anesthesia: important to protect airway
-Saline is flushed from internal nares rostrally towards external nares
-Produces only cytologic sample
-findings tend to be non-specific
-Nasal mites occasionally identified
-May flush out foreign body/mites
Diagnostic Tests - Pinch Biopsy
Invasive - coagulation panel and BMBT prior to procedure
-Under general anesthesia
-Small forceps as alligator biopsy cur forces utilized to collect tissue samples
-Produces cytology (touch prep) and histopathology samples
-Minimum 6 samples should be collected
Diagnostic Tests - Turbinectomy
-More invasive
-Under GA
-Performed through a rhinotomy incision (referral)
-Produces cytologic samples (touch prep) and histopathologic samples
Lecture 2
Nasal mycoses in Feline and Canine
Feline Herpes Virus (aka Feline rhinotracheitis)
-Corneal ulceration, dermatitis, abortion, neonatal death
Tx
-Lysine, feline recombinant omega interferon, human alpha 2b interferon
Feline URI (upper respiratory infection)
-Upper respiratory disease complex: highly contagious
-Cats are stressed, immunocompromised or young in age are more susceptible
-Spread through direct contact and fomites
-Mixture of viral and bacterial agents
-Acute and Chronic infections
C/S
-Sneezing, nasal discharge, conjunctivitis, ocular discharge, salivation, anorexia, dehydration
Tx
-Supportive care
-Quickly dehydrate
-Hydration
-Nutrition
No Steroids
-Clear mucus and crusted discharge: vaporizer in bathroom, nasal saline, pediatric nasal decongestants (0.25% phenylephrine or 0.25% oxymetazoline)
-Antibiotics for secondary infection:
First: Doxycycline
Second amoxicillin
Dx
-Based on largely on signalment
-Clinical presentation
-Conjunctival swabs can demonstrate intracytoplasmic inclusion bodies consistent with Chlamydophila felis
-Commercial PCR respiratory panels are useful in some individual cats, and in management of cattery populations
Feline Calici Virus
-Oral ulceration, interstitial pneumonia, polyarthritis
Feline URI - Chlamydophila felis
-Conjunctivitis
Feline URI - Bordetella bronchi septa
-Coughing, pneumonia in young kittens
Feline URI - Mycoplasma spp
-Ubiquitous organism
-Variable relation to disease
Bacterial Rhinitis
-Majority is secondary infection due to inflamed, compromised nasal mucosa
-Very common sequela to nasal disease
-Mycoplasma spp. and Streptococcus equi, subspecies. zooepidemicus may be primary pathogens
-Direct appropriate antibiotic therapy based on cytology, cultures and underlying disease process (e.g., oronasal fistula)
-duration of therapy depends on underlying disease
-typically 7-10 days Tx
-Chronic infections may require 4-6 weeks (should see improvement in 1 week)
Feline Cryptococcus
Cryptococcus neoformans
-Saprophytiuc yeast-like; found in avian excrement
-3-7 micrometer with large polysaccharide capsule
-Occasional systemic signs
-Immunosuppression does NOT predispose
C/S
-Facial swelling/deformity
-Sneezing
-Mucopurulent discharge (=/- hemorrhagic)
-Unilateral or bilateral nasal discharge
-Ulcerative lesion on nasal planum
-Granulomatous lesion from nares
-Submandibular lymphadenopathy
-Ophthalmic lesions (guarded)
-CNS signs (grave)
Dx
-Cytology: FNA of facial lesion, nasal discharge
-Serology: cryptococcal latex agglutination capsular titer. CSF or Serum. Positive titer is diagnostic. Titer may be used to monitor response to therapy
Tx
-Itraconazole: preferred
-Fluconazole
-Ketoconazole
Guidelines
-Tx minimum of two months
-One month beyond resolution or until titer is negative
-Prolonged Tx is some cases (1 year)
Prognosis
-Overall good
-FeLV/FIV positive cats do not respond well
-Magnitude of titer is not prognostic, but can help to monitor response to Tx
-Ocular or CNS lesions = poor prognosis
Feline Cryptococcus
Canine Aspergillosis (common)
Fungal nasal disease in dogs - Aspergillosis
-Aspergillus fumigatus
-Ubiquitous, saprophytic
-Contaminants present in normal animals
-Destruction of nasal turbinates
-Systemic disease rare
C/S
-Mesocephalic to dolichocephalic breeds
-Immunosuppression NOT predisposing factor
-Unilateral mucopurulent discharge with intermittent epistaxis
-May progress to bilateral
-Ulceration/depigmentation
-Nasofacial discomfort common
-Rads: loss of nasal turbinates, unilateral or bilateral, multiple well defined lytic zones within the nasal cavity.
-Increase in soft tissue or fluid density, affects caudal nasal cavity and frontal sinuses. Typically no lysis or deviation of vomer or frontal bones.
Dx
-CT: better at assessing integrity of nasal turbinates and cribriform plate
-Rhinoscopy: turbinate destruction, white or gray mats, plaques or granulomas, Debulk plaques prior to Tx
-Cytology and Histopathology: Branching hyphae
-Fungal culture: usually not necessary. May be normal inhabitant of nasal cavity. Positive culture only supportive
-Serology: Serum antibody titers supportive. False positives occur, can not use to assess response to treatment
Tx
-Topical medications
Clotrimazole 1%
Enilconazole
Procedure:
-Anesthesia, multiple tube placement, infusion for 1 hr,
-C/S resolve within 2 weeks
-Repeat if necessary
-May require sinus trephination
Alternative Tx
-Trephination and placement of tubes into sinuses and nasal cavities . Daily infusion of enilconazole or clotrimazole BID x 7-10d
-Systemic therapy: Indicated if cribriform plate is disrupted or other systemic involvement. Itrazonazole minimum 2-3 mts
CT
Rhinoscopy
Aspergillosis city and history
aspergillosis treatment
Aspergillosis trephination
Aspergillosis Prognosis
-80-90% cure rate with topical Clotrimazole
-60-70% cure rate with systemic therapy
-Debulking plaques improves
Complications
-Meningioencephalitis (often fatal)
-Chronic bacterial rhinitis
Nasal Mites
-Pneumonyssoides caninum
-Sneezing - paroxysmal, violent
-Visualized during rhinos copy and or nasal flushing with saline
Tx
-Milbemycin or Selemectin
Feline Nasopharyngeal polyps
C/S
-Stertor, obstructive breathing pattern, mucopurulent nasal discharge.
-If present in ear canal, can cause head tilt, nystagmus, Horner’s syndrome
-Benign growths that occur in young cats and kittens
-Often attached to base of eustachian tube
- Primary treatment: surgical excision
- short course of antibiotics and prednisone
Nasal Neoplasia
-Older animals >8 years
-Dolicocephalic breeds
-Most tumors malignant (80-90%)
-Locally invasive
-Metastases rare (later stages to LN and lung)
Types
Epithelial (carcinomas)
**Adenocarcinoma (most common in dogs) **
-Squamous cell carcinoma
-Undifferentiated carcinoma
Mesenchymal (sarcomas)
-Chondrosarcoma
-Fibrosarcoma
-Undifferentiated sarcoma
Discrete round cell
-Lymphoma (most common in cats)
-Squamous most common in nasal planum white cats.
-Transmissible general tumor (rare)
-Mast cell tumor (rare)
C/S
-Nasal discharge (unilateral to bilateral)
-Sneezing
-Nasofacial deformities
-Exophthalmia (or exophthalmia)
-Stertor
-Open-mouthed breathing
-Oral deformity
-Dysphagia
-CNS signs
Dx
-Rads: nasal turbinate destruction, soft tissue opacity, bone lysis (frontal vomer), deviation of vomer bone.
-Rhinoscopy with Biopsy
-Blind nasal biopsy
-Rhinotomy, turbinectomy
-Definitive dx requires histopathology
Nasal neoplasia staging and Tx
-Evaluate local lymph nodes
-Thoracic radiographs
Tx
-Radiation therapy = 12-16 months
-Palliative vs. curative = 3-6 mts
Survival factors
-Adenocarcinomas, sarcomas longer
-Undifferentiated and SCC, shorter
-Clinical stage: metastasis to lungs, shorter
-Extensive local invasion, shorter
-Cats tolerate and respond better than dogs
Allergic Rhinitis
-Not well validated in dogs and cats
-hypersensitivity response to airborne allergens
C/S
-Sneezing, serous nasal discharge may progress to mucopurulent
-May worsen with exposure to perfume, smoke, etc
Dx
-History and clinical presentation
-Rads may show increased soft tissue density
Tx
-control allergens
-antihistamines
-corticosteroids
Idiopathic Rhinitis
Feline chronic rhino sinusitis
-Diagnosis of exclusion
-Chronic mucoid or mucopurulent discharge for mts or years
-Sneezing and nasal discharge most consistent signs
-Typically bilateral +/- hemorrhage
-Chronic inflammation leads to turbinate destruction
-Chronic management necessary
-supportive therapy similar to URI
-Nasal/sinus flush may help temporarily
-Antibiotics secondary infections
Canine Lymphoplasmacytic Rhinitis
-Diagnosis of exclusion
-unknown etiology
-No association with CAV-2, parainfluenza, Chlamydophila or Bartonella.
-C/S and cytology similar to feline chronic rhinitis
-Tx: prednisone, antibiotics for secondary infections, higher immunosuppressive doses
-unresponsive in both dogs and cats
Lecture 3
Laryngeal and Pharyngeal disease
Clinical sigs of Laryngeal Disease
-Hallmark signs regardless of etiology are respiratory distress and stridor (high pitch wheezing sound on inspiration due to upper airway obstruction)
Gagging and coughing may be present
-Voice change is indicative of laryngeal disease (dysphonia) but not consistent finding
-Airway obstruction with laryngeal disease causes profound respiratory distress (often acutely)
-Initially patients limit their own physical activity
-Crisis if animal overheats, respiratory effort increases
-Paradoxical motion: soft tissues are pulled into airway during inspiration due to increased negative pressure, which causes the tissue to become more inflamed and edematous
-Respiratory rate is normal to slightly elevated (30-40 bpm) which is abnormal for level of distress
-Inspiration is prolonged and labored
-Expiration is more passive but tissue edema can cause dynamic obstruction during expiration
May be associated with aspiration pneumonia
-Cough
-Lathergy
-Anorexia
-Fever
-Tachypnea
-Abnormal lung sounds
Ddx
-Laryngeal paralysis (large dogs not cats)
-Obstructive neoplasia
-Obstructive laryngitis
-Laryngeal collapse
-Web formation
-Trauma
-Foreign body
-Extraluminal mass
-Acute laryngitis
Pharyngial disease - Clinical signs
Stertor, gagging, coughing, reverse sneezing and dysphagia are more common clinical signs
Ddx
-Brachycephalic airway syndrome
-Elongated soft palate
-Nasopharyngeal polyp
-Foreign body
-Neoplasia
-Abscess
-Granuloma
-Extraluminal mass
-Nasopharyngeal stenosis
Diagnostics
-Rads for identifying radio dense foreign, bony changes, some masses
-Not as useful for dynamic disease: laryngeal paralysis, collapsing airways
-Fluoroscopy: most useful for dynamic disease in which observation of abnormal motion is necessary for diagnosis . Increased exposure to radiation
-Bronchoscope: non-invasive option
-CT/ MRI
-Laryngoscopy/pharungoscopy : useful for direct visual examination of tissues and movement
-Be prepared for more definitive immediate treatment of airway obstruction when scoping
Laryngeal Paralysis Exam
-Ideally performed with flexible laryngoscope, resulting in the least distortion of the laryngeal structures
-Can be performed by direct visualization through oral cavity using a blade laryngoscope
-Short acting injectable agent (e.g., propofol) to produce light plane anesthesia
-Maintain spontaneous deep respirations
-Arytenoid movement is enhanced by administering IV do pram by increasing respiratory rate and effort
-With laryngeal paralysis, one or both sides do not abduct sufficiently with inspiration
-Flow-by-oxygen should be administered during the exam
-Have endotracheal tube available in case your patient has paradoxical motion, laryngeal collapse or recovering
-Don’t do this exam if you are not ready to deal with potential respiratory problems upon recovery
What is a common cause of stertor in the dog and cat?
Dog-brachycephalic syndrome due to elongated soft palate
-Cat-nasopharyngeal polyp
Lecture 4
Laryngeal and pharyngeal disorders
Laryngeal paralysis (LP)
-Failure of the arytenoid cartilages to abduct during inspiration
-Creates an upper airway obstruction
-Abductor muscles are innervated by the right and left Recurrent laryngeal nerves
-Dogs most commonly affected
Causes
-Idiopathic
-Ventral cervical lesions
-Trauma to nerves: direct, inflammation, fibrosis
-Neoplasia
-Anterior thoracic lesion: neoplasia, trauma, port-operative
-Polyneuropathy and Polymyopathy: idiopathic, immune mediated
-Endocrinopathy: hypothyroidism
-Other systemic disorder: toxicity
-Congenital disease
-Myasthenia Gravis
Etiology
-Idiopathic LP is part of generalized neuromuscular or polyneuropathy complex
-Polyneuropathies have been associated with immune-mediated disease, endocrinopathies, other systemic disorders
Congenital LP: Bouvier des Flandres, Siberian Huskies, Bull Terriers
-LP-polyneuropathy complex reported in Dalmations, Rottweilers and Great Pyrenees
Labrador Retrievers
-Damage to the laryngeal nerves of larynx can lead to LP
Laryngeal Paralysis
C/S
-Any age, any breed
-Most common in older, larger-breed dogs
-Hallmark signs of respiratory distress and stridor
-Vocal change may be noted by owner
-Stridorous breathing dog may turn blue
Often acute respiratory crisis requires emergency intervention
-Often present with a history of gagging or coughing, especially when drinking or eating
Diagnosis
-Further workup should be continued to rule out underlying disease
-Evaluate for concurrent pulmonary disease, such as aspiration pneumonia
-Rule out pharyngeal and esophageal dysmotility and megaesophagus
Treatment
-Emergency management of airway obstruction
-Sedation acepromazine, butorphanol or morphine (nothing by mouth because it can get trapped in the trachea)
-Provide cool, oxygen rich environment
-Evaluate for surgical management once stable
**Arytenoid lateralization (“tie-back”) unilateral or bilateral, not if megaesophagus **
-Increase diameter of airflow but not so large to encourage aspiration
Medical management
-When surgery is not an option, it can be attempted
-+/- corticosteroids to reduce inflammation
-Weight management
-Exercise/heat restriction
-Walkin in harness vs. collar
Prognosis
-Fair to good
-Aspiration pneumonia is most common complication
-Guarded prognosis for generalized neuromuscular disease or/and megaesophagus
Brachycephalic Airway Syndrome
C/S
-Vomiting and regurgitation
-Concurrent with GI disease
-Increased intrathoracic pressure created with increased inspiratory effort
Anatomic abnormalities
- Stenotic nares (cats have them too)
- Elongated soft palate
- Hypoplastic trachea (Bulldogs)
- Everted laryngeal saccules: close to the vocal cords, get edematous and affect the airway space
Brachycephalic Airway syndrome
C/S
-Caused by impaired airflow through the upper airways
-Increased intrathoracic pressure
-Loud upper airway noise associated with obstruction: inspiratory phase STERTOR, SNORING
-Cyanosis, syncope
-GI signs of vomiting and regurgitation
Dx
-Based on breed, clinical presentation
-Cervical and thoracic radiographs to evaluate structure, secondary disease
-Visual exam of oropharynx/larynx via scoping
Tx
-Enhance passage or air through limited airways
-Minimize stress factors: limit exercise, cool ambient temperature, weight control
-Surgical correction of abnormalities: excise excessive soft palate and everted laryngeal saccules, correct stenotic nares
-Perform procedures early (particularly stenotic nares) at 3-4 months age before clinical signs develop
Laryngeal Neoplasia
-Uncommon in dogs and cats
-Carcinomas: SCC, undifferentiated, adenocarcinoma
-Lymphoma most common in cats
-Melanoma
-Mast cell tumor
-Benign neoplasia
C/S
-Consistent with upper airway disease: noisy respiration, stridor, increased inspiratory efforts, change in voice
-Mass lesions can cause dysphagia, aspiration pneumonia, palpable mass
Dx
-Diagnostic imaging: rads, CT/MRI, laryngoscopy
-FNA and biopsy for histopath
-Staging disease once diagnosed with malignant neoplasia: local LNs evaluation, thoracic radiographs
Tx
-Depends on tumor type
-Surgical excision, laryngectomy with permanent tracheostomy
-Radiation therapy
-Chemotherapy: e.g., lymphoma
-NSAIDS: Cox-2 inhibition can slow progression
Lecture 5
Lower respiratory tract
Trachea
Bronchi
Bronchioles
Alveoli
Interstitium
Vasculature of lungs
LRT Clinical signs
C/S
Cough
-Productive vs. non-productive
-Intensity: loud, harsh, paroxysmal, soft
-Temporal associations: time of day, activity
Productive Cough
-Moist sound heard during cough
-Mucus, exudate, edema fluid, or blood from airways into oral cavity
-Commonly caused by inflammation, infectious disease, or heart failure
Non-productive cough
-“Dry cough”
-Mostly associated with airway disease such as collapsing trachea
Goose honking = collapsing trachea
Exercise Intolerance
-Restricts itself from too much activity
-Mild tachypnea and subtly decreased activity - exercise intolerance and Dyspnea at rest
-Often present in overt (and “sudden”) distress
-Orthopnic: extended neck
Respiratory Distress
Evaluating
-Resting respiratory rate: upper limit 20-30
-Mucous membrane color: pallor (acute hypoxemia), cyanosis (severe hypoxemia)
-Breathing pattern: rate, depth, inspiratory and expiratory efforts, audible sounds
Inspiratory
-Pulmonary disease primarily but also CHF
-Extrathoracic disease: collapsing trachea, laryngeal paralysis
Expiratory
-Intrathoracic airways
Dyspnea: difficult or labored respiration
Diagnostic approach
Initial evaluation
-PE: complete systemic physical. Thoracic evaluation
-Radiographs
-Blood work: CBC
Auscultation
-Bronchial: most prominent in central area of lungs; tubular sounds over large airways
-Vesicular: most prominent in peripheral lung fields; “breeze blowing through leaves”
Abnormal lung (breath) sounds
-Decreased lungs sounds (pleural effusion, pneumothorax, mass lesions)
-Increased or harsh lung sounds, crackles, wheezes
Radiographs
-Most helpful tool for intrathoracic disease Dx
-Right and left lateral increase sensitivity
-Minimum 2 views: RL and VD
-Dorsoventral views are taken to highlight dorsal pulmonary arteries, and to lessen stress in the dyspneic patient
-Horizontal views to evaluate pleural effusion or cavitary lesions
Peak Inspiration
-Short exposure time
-Cervical radiographs to evaluate trachea and upper airway structures, if clinical signs suggest
-Vascular pattern: characterized by an increased or decreased in size of the artery or vein
-Bronchial pattern: characterized by “donuts and tram lines”
-Alveolar pattern: characterized by air bronchograms and lobar signs
-Interstitial pattern: characterized Structured (nodular) unstructured (diffuse) or a combination in an increase in lung opacity
-Pleural effusion:
Other Findings
-Lung lobe consolidation - entire lobe is soft tissue opacity
-Atelectasis
-Cavitary lesions: abnormal air accumulation in the lung (e.g., bullae)
-Lung torsion
Specialized Diagnostics
-Angiography: used to confirm pulmonary thromboembolism
-Ultrasonography: used to evaluate pulmonary mass lesions and guide collection of FNA samples
-CT/MRI: masses, metastatic disease, PTE, pneumonias, etc
-Nuclear imaging: used to diagnosis ciliary dyskinesia, pulmonary perfusion and ventilation
-Parasitology: direct observation, Blood tests, Cytology analysis of fluid or respiratory samples, Fecal flotation.
-Serology: fungal pulmonary disease: histoplasmosis, blastomycoses, coccidioidomycosis. Toxoplamosis, cryptococcus, heart worm disease.
Tracheal wash
-Transtracheal wash technique, transoral (endotracheal) technique
Broncoalveolar lavage
-Bronchoscopic
-Nonbronchoscopic
Transthoracic lung aspiration
-Ultrasound guided FNA of pulmonary parenchyma
-Potential complications include pneumothorax, hemothorax, and pulmonary hemorrhage
-Can be utilized for masses near body wall and diffuse interstitial lung disease
Bronchoscopy
-Evaluation of major airways
-Bronchio-alveolar lavage (BAL) put sterile fluid in
-Technique of choice for always foreign body removal
What are the three signs of LRD?
- Cough
- Exercise intolerance
- Respiratory distress
Transtracheal wash
Transoral/endotracheal wash
Lecture 6
Common diseases of Trachea and Bronchi
-Canine infectious tracheobronchitis (ITB)
-Canine chronic bronchitis
-Feline bronchitis
-Tracheobronchomalacia or collapsing trachea
-Allergic bronchitis
-Parasitic - Oslerus osleri in young dogs
Canine ITB/CIRDC “Kennel cough”
Pathophysiology
-Viruses, bacteria, and mycoplasma (any or all)
-Most commonly parainfluenza virus, adenovirus with Bordetella bronchiseptica
-Highly contagious from aerosol or direct contact (rarely fomites)
Signalment/history
-Young, unvaccinated dog
-Boarding, parks, etc, exposure
C/S
-Loud, goose-honk cough
-Cough often productive, foamy, clear liquid
-Post-tussive gagging is common
+/- Mucopurulent ocular and nasal discharge, sneezing
Physical examination
-Uncomplicated cases - tracheal sensitivity, normal lung sounds, generally self-limiting
-Complicated cases - fever, crackles or wheezes, anorexia, can progress to bronchopneumonia
-10-14 days resolution usually
Diagnosis
-Uncomplicated cases - empirical (experienced based)
-Complicated cases: CBC, chest radiographs (remember contagious), +/- tracheal wash with cytology and culture
-Highly contagious - coughing dogs should wait in the owner’s vehicle until the exam, avoid exposing other patients
Treatment
-Uncomplicated: typically self limiting, 10-14 days resolution
-Anti-tussives (butorphanol, hydrocodone, tramadol)
+/- anti-inflammatory doses of corticosteroids
+/- antibiotics - empiric choices (doxycycline, amoxicillin: clavulanic acid, trimethoprim sulfa, enrofloxacin)
-Mycoplasma and Bordetella - Doxycycline
-Complicated: antibiotics, culture of tracheal wash fluid is best
-Nebulization of antibiotics (GENTAMICIN) most effective
-Supportive care including maintaining hydration, corticosteroids, courage and nebulization
Prevention
-Vaccine not 100% effective
-Bordetella whiten 5 days
-intranasal Parainfluenza and Bordetella within 5 days
-CAV-2 and Bordetella Parenteral within 14 days
Chronic Bronchitis
-Chronic, persistent cough of 2 or more consecutive months in duration without other disease processes
-Fibrosis, epithelial hyperplasia, glandular hypertrophy and inflammatory infiltrates
-Inflammation initiated by infection, allergy, inhaled irritants or toxins
Signalment
-Middle aged to older
-Small breed
-Terrier, Poodle, Crocker Spaniels
-Cough progresses slowly over months to years
-Complications: bordetella, mycoplasma, pulmonary hypertension, bronchiectasis
Diagnosis
-History, C/S
-Radiographs: bronchial to bronchointerstitial pattern
-BAL: neutrophilic to mixed inflammatory cells, increased mucus
-Bronchoscopy if necessary
Treatment
-Symptomatic management
-Avoid exacerbating factors (e.g., smoke, allergens, perfume)
-Keep secretions moist and moving
-Control weight
-Glucocorticoids decrease inflammation
-Treat secondary infections culture and sensitivity TTW
-Bronchodilators: aminophylline, theophylline, terbutaline, albuterol
Feline Bronchitis
-Feline airways are highly reactive and prone to bronchoconstriction
-Common signs of bronchitis in cats: cough, wheeze, respiratory distress
-Idiopathic bronchitis is a disease of exclusion
-Young and middle aged
Ddx
-Allergic bronchitis
-Heartworm disease
-Pulmonary parasites
-Bacterial bronchitis
-Mycoplasma bronchitis
-Toxoplasmosis
-Carcinoma
-Aspiration pneumonia
C/S
-Coughing
-Intermittent respiratory distress “vomiting hair ball”
- Bronchial asthma: reversible, bronchoconstriction, eosinophils
- Acute bronchitis: reversible airway inflammation <3 mts, increase neutrophils
- Chronic bronchitis: irreversible >3mts
- Emphysema destruction of bronchiolar and alveolar walls similar to COPD
Dx
-History, clinical presentation
-PE, don’t escalate stress in dyspneic cat
-CBC
-Heartworm test and other blood work as indicated
-Fecal testing
-Thoracic radiographs (bronchial pattern)
-Cytology from TTW or BAL
Emergency
-Stabilization with oxygen
-Bronchodilators (terbutaline SC) rapid-acting
-Glucocorticoids (dexmethasone SP, Solu-Medrol, IV, SC or IM)
-Administer albuterol by face mask, multi dose inhaler (MDI), if additional doses needed - Aerokat
-Place in cool, oxygen-rich environment
Chronic
-Glucocorticoids - oral prednisolone
-Inhaled glucocorticoids - Fluticasone delivered MDI
-Bronchodilators may be needed long term
Collapsing Trachea
Pathophy
-Dorsoventral collapse of airway upon inhalation
-Intrathoracic, extra thoracic, and/or mainstream bronchi involvement
-Self-perpetuating
Signalment
-Middle aged to older toy and small breed dogs
C/S
-Dry, non-productive cough
-Worsens with excitement/exercise
-Occasionally associated with post-jussive gagging/retching
-Increased inspiratory effort with extra thoracic
-Increased expiratory effort with intrathoracic
-May present in dyspneic crisis
-Tracheal sensitivity common
Dx
-Radiographs
-Fluoroscopy
-Tracheobronchoscopy - best
-Tracheal wash may be help in ruling out other diseases
Tx
-Combination often needed
-Stable patient: bronchodilators (theophylline, terbutaline, albuterol), anti-inflammatories corticosteroids, antitussives (butorphanol, hydrocodone)
-Weight loss
-Avoid environmental triggers (fragrances)
Dyspneic collapsing trachea patient
-Oxygen
-Anxiolytics (acepromazine, butorphanol, diazepam)
-Nebulization
-Corticosteroids
-Surgical placement of stents
Miscellaneous diseases of the Trachea
-Intraluminal foreign body/mass/neoplasia
-Lymph node
-Thymoma
-Parasites: Oslerus Osleri granulomatous nodule near carina
-Trauma: subcutaneous emphysema, pneumomediastinum HBC, traumatic venipuncture
Lecture 7
Pulmonary parenchyma disease
Viral Pneumonia
Bacterial pneumonia
Aspiration pneumonia
Fungal pneumonia
Pulmonary parasites
Eosinophilic lung disease
Idiopathic interstitial pneumonia
Pulmonary neoplasia
Pulmonary hypertension
Pulmonary thromboembolism
Pulmonary edema
Viral Pneumonia
- Canine Influenza virus (H3N8 - equine, H3N2 - avian)
-Incubation 2-4 days = most contagious NO c/s
-7-10 decreased shedding of virus
C/S
-Coughing, nasal discharge most common
-High fever and pneumonia >serious
-No Tx = >mortality
Dx
-History, exposure
-PCR testing (within 4 days) canine respiratory panels.
-Acute and convalescent serology
Tx
-Primarily supportive
-Vaccination based on risk
-Prevent exposure
- Canine Adenovirus-1 and 2
- Canine Parainfluenza
- Canine Distemper
- Feline Calicivirus (rare)
Bacterial Pneumonia
-Aspiration pneumonia
-Hematogenous route spread
-Immunocompromised animals
-Underlying respiratory disorder (ciliary dyskinesia, chronic bronchitis)
-Not contagious
Bordetella - Puppies
Adults - E. coli, Pasteurella, Bordetella, Streptococcus, Staphylococcus, Klebsiella, Enterococcus, and Pseudomonas
-Anaerobes present in mixed infections where lung lobe consolidation is present
C/S
-Lethargic, pyrexia, anorexia
-Tachypnea to dyspnea
-Increased respiratory phase/effort (inspiration most notable)
-Soft, productive cough
-Nasal discharge
-Crackles or increased bronchovesicular sounds
-Pale or cyanotic mucous membranes
Dx
-Radiographs
-Patchy interstitial and alveolar patterns most common
-Consolidation of lung lobe
-Pleural fissure lines, lobar signs
Cranioventral distribution common with aspiration pneumonia
-Caudal or diffuse distribution common with marked interstitial involvement hematogenous bacterial pneumonia
-CBC - inflammatory leukogram, with left shift
-Blood gas/pulse oximetry <90%
-BAL or TTW culture
-Misc: fecal flotation, serum chem, UA, HWT
Tx
-Oxygen - SpO2 <90% = cage or nasal canula
-Loosen secretions, vaporization, nebulization and or courage
-Antimicrobial therapy
-Antimicrobial: culture of septum, BAL, or TTW. Non-responsice to empirical treatment, chronicity, minimize costs
-Bronchodilators
-Physiotherapy: turn animal every 2 hrs if recumbent
-Mild exercise to promote coughing
Aspiration Pneumonia
-Bacterial pneumonias are primary underlying cause
-Begins as inflammatory process
-CV distribution
-Predisposition: Megaesophagus, GI disease, aggressive force feeding, laryngeal paralysis, anesthesia induced regurgitation/reflux
Fungal Pneumonia
Canine
-Blastomycosis and coccidioidomycosis most common: skin lesions, draining
-Histoplasmosis possible
Feline
-Histoplasmosis and cryptococcosis most common: chronic nasal discharge
-Blastomycosis and coccidioidomycosis possible
C/S
-More chronic
-Weight loss
-Cyclic fever
-Lymphadenopathy
-Blastomycosis: skin lesions, bone, ocular
-Coccidioidomycosis: bone, joint, CNS
-Histoplasmosis: diarrhea in dogs
Dx
-Radiographs: similar to neoplasia pattern
-Diffuse military or nodular pattern
-May occasionally see pleural effusion (chronic) and “mass” lesions
Fungal Pneumonia
Dx
-Serology
-Urine antigen test 94% sensitivity
-CBC, Chem, UA - nonspecific findings: normochromic, normocytic anemia, leukopenia, leukocytosis, hyperglobulinemia, proteinuria
-Cytology: really important
-Skin lesions - Blasto; nasal cavity swabs
-FNA of lungs and/or LNs
-FNA or spleen, liver, affected organs
-TTW or BAL
Tx
-Systemic antifungals
Itraconazole
-Fluconazole
-Ketocanazole
-Prednisone - control inflammation
-Supportive
-60-90 days often 6 mts or longer
-Treat 2 months past resolution of signs
-High change of recurrence
Parasitic Pneumonia
Paragonimus kellicotti
- Small fluke, snail and crayfish
-Geographically limited
-More common in cats vs. dogs
C/S
-Asymptomatic or allergic bronchitis
-Occasional pneumothorax - bullae
-Radiographic lesion - single or multiple solid or cavitary lesions
Tx
-Fenbendazole
Aelustrongylus abstrusus
-Cats only
-Snails/bird intermediate host
-Asymptomatic commonly
-Young cats: bronchitis
Dx
-Larvae in fecal Baermann float or in airway specimens
Tx
-Fenbendazole
Cases
Parasitic Pneumonia
Capillary aerophila
-Dogs and cats
-Small nematode beneath epithelial surfaces of airways
-Usually asymptomatic
-May show allergic bronchitis
Dx
-Radiographs signs of bronchial or bronchointerstitial pattern
Tx
-Fenbendazole
Pulmonary Neoplasia
-Primary pulmonary tumors: carcinoma. Malignant - begin as single mass lesion
-Surgical lobectomy beneficial if caught early
-Metastatic pulmonary tumors: extensive capillary network allows blood-borne neoplastic cells to deposit within lungs
-May present as multi-nodular, single nodule, or mass
Pulmonary Hypertension
> 30 mmHg (normal 25/10 mmHg) pulmonary arterial pressure
-Cardiac disease: CHF, L to R shunts
-Increased pulmonary vascular resistance: pulmonary thromboembolism, heartworm disease
-Chronic pulmonary parenchymal disease
-Pulmonary fibrosis, chronic bronchitis
C/S
-Exercise intolerance
-Weakness
-Syncope
-Respiratory distress
-Physical examination may reveal a loud split S2 heart sound
Dx
-Radiographic signs of right-sided cardiomegaly, prominent main pulmonary artery
Tx
-Aggressively treat underlying disease
-If no underlying disease: Sidenafil citrate (viagra), Pimobendan
Pulmonary Thromboembolism
-Emboli lodge in the low-pressure vascular system of lungs
-First pass for systemic venous thrombi and right ventricle
Acute respiratory distress can be fatal
-Causes hemorrhage, edema, bronchoconstriction, decreased blood flow
-Blood clot formation associated with venous status, turbulent blood flow, endothelial damage, hyper coagulation
-Emboli can also consist of bacteria, parasites, neoplasia or fat
C/S
-Acute respiratory distress
-Cardiovascular shock and sudden death
-Early diagnosis: milder dyspnea and tachypnea (chronic)
Dx
-Easy to overlook
-Based on suspected clinical signs
-Thoracic radiographs (no changes in early stage)
-Arterial blood gas-hypoxemia
-Echocardiography
-Bloodwork
Difenitive = spiral CT angiography, selective angiography (gold standard), nuclear perfusion scan
-Poor response to oxygen supplementation is supportive of PTE
Tx
-Aggressive supportive care, oxygen
-Treat underlying cause
-Eliminate/control predisposing factors
-Fibrinolytic agent use not as well established as in human medicine
-Useful agents may include low molecular weight heparin, aspirin or clopidogrel (Plavix)
Pulmonary Edema
-Mechanisms of edema include decreased plasma oncotic pressure, vascular overload, lymphatic obstruction, and increased vascular permeability
-Edema initially accumulates in the interstitium, moving rapidly to the alveoli
-Respiratory function is compromised by atelectasis, compression of alveoli and decreased surfactant concentration
Dx
-Rads: early changes = interstitial pattern
-Progress to alveolar pattern
Tx
-Activity restriction, minimize stress
-Hypoxemia treated with oxygen supplementation
-Bronchodilators (methylxanthine)
-Furosemide: not if hypovolemic
-Correct underlying cause
-Cardiogenic edema, over hydration, low oncotic pressure - colloids, plasma. Vascular permeability - difficult to treat, look for underlying cause
Lecture 8
Pleural and Mediastinal Disease
General considerations - Pleural abnormalities
-Accumulation of fluid (pleural effusion)
-Accumulation of air (pneumothorax and pneumomediastinum)
-Respiratory dysfunction is associated with interference with normal lung expansion
-Exercise intolerance - overt respiratory distress
-Abdominal effort may be increased
-Increased inspiratory effort
-Paradoxical movement of abdomen inwards during inspiration
-In cats with mediastinal masses, decreased compliance of chest wall in cranial thorax
Radiography
-Pleura is not normally visible on radiographs
-Individual lung lobes are not distinguished
-Abnormalities include pleural thickening, pleural effusion and pneumothorax
-Pleural thickening produces pleural fissure lines ~ 50-100 ml fluid
Pleural Fluid
- Transudates
<2.5-3.0 g/dl protein
<500-100/microL nucleated cells
-Primary macrophages, lymphocytes, mesothelial cells
-Increased hydrostatic pressure: Right CHF, pericardial disease
-Decreased plasma oncotic pressure: hypoalbuminemia <1g/dl
-Lymphatic obstruction: neoplasia, diaphragmatic hernias - Modified transudates
-3.5 g/dL protein content
5000/microL nucleated cell count
-Neutrophils and mononuclear cells
-Chronic diaphragmatic hernias - Exudates
-High protein > 3g/dl
->5000/microL nucleated cells
Nonseptic exudate: neutrophils (non degenerate), macrophages, eosinophils, lymphocytes, no organisms
-Ddx: FIP, neoplasia, chronic diaphragmatic hernia, lung lober torsion, resolving septic exudates
Septic
>50000-100000/microL nucleated cells
-Neutrophils (degenerate), organisms seen
-Ddx: pyothorax, spontaneous, penetrating wound, foreign bodies, extension of bacterial pneumonia.
- Chylous effusions
-Milky white and turbid due to Chylomicrons
-May be blood tinged
-Rarely: clear.colorless
>2.5 g/dl protein
400-10000/microL nucleated cells
-Lymphocytes
-Confirmation: triglycerides in fluid and serum higher than in pleural fluid
-Ddx: leaking from thoracic duct due to idiopathic, congenital, secondary, pericardial disease, lung lobe torsion, heartworm disease, or diaphragmatic hernia - Hemorrhagic effusions
-Grossly red
>3 mg/dl protein
>100/microL nucleated cells
-Erythrophagocytosis, inflammatory response, do not clot, and PCV lower than peripheral blood.
-Associated with trauma, coagulopathies, neoplasia (hemangiosarcoma), lung lobe torsion
-Activated clotting time and platelet count should be initially performed, followed by additional clotting tests as needed - Neoplastic effusion
-Can result in most effusion types
Lymphoma is the only neoplasia reliably identified in neoplastic effusion
-Difficult to establish diagnosis based on cytology
-Inflammation causes metaplastic changes in mesothelial cells, which are hard to distinguish from neoplastic cells
Pneumothorax
-Tension pneumothorax develops if air leaks through functional “one-way valve” lesion in the lungs
-Extrathoracic entry can occur after thoracic well trauma, iatrogenically through a chest tube, or during abdominal surgery if diaphragm is not intact
Of Pulmonary origin
-Blunt chest wall trauma
-Rupture of cavitary lung lesions (cysts, bullae, blebs, necrotic neoplastic tissue, abscesses, etc)
Mediastinal Masses
-Inspiratory distress due to displacement of lung tissue or secondary to pleural fluid accumulation
-Primary differential: Neoplasia (lymphoma common in cats)
-Thymoma, thyroid carcinoma, parathyroid carcinoma, and chemodectoma
-Non-neoplastic masses: abscesses, granulomas, hematomas, and cysts
Ultrasound - TFAST exam
-Rapid
-Minimally invasive assessment of pleural space for fluid or air
CT
-More sensitive than rads for assessing the thorax
-Useful for evaluating extent of masses
-Increases likelihood of finding cavitary lesion in spontaneous pneumothorax
Thoracocentesis
-Indicated for collection of fluid or air from pleural space in the dog or cat
-Possible complications: lung laceration, hemothoraz, iatrogenic pyothorax
7th intercostal space, 2/3rd distance from constochondral junction to spine
-Aseptic technique
-Sternal or lateral recumbency
Chest Tube
-Indicated for tx of pyothorax and accumulating pneumothorax
-Burrowed SQ from 10th intercostal space to 7th intercostal space
Lec 9
Disorders of Pleural Cavity - Feline
Pyothorax
-Septic: most idiopathic origin in cats
-Can result from penetrating wounds, foreign bodies, migrating plant material, intrathoracic esophageal tears (usually foreign body)
C/S
-Tachypnea
-Decreased lung sounds
-Increased abdominal effort with inhalation
-Fever, lethargy
-Acute or chronic
-Asynchronous lung sounds
-Systemic inflammatory response syndrome, septic shock
Dx
-Thoracic rads
-Cytology of pleural fluid, aerobic and anaerobic cultures, Gram staining (filamentous gram +)
-Most bilateral in cats
-Possible mass lesions, pleural fibrosis, or lung lobe torsion
-Pre and post thoracocentesis rads
Tx
-Antibiotic
-Drainage of pleural space and supportive care
-Empirical choice of antibiotics initially
-Anaerobes and Pasteurella: amoxicillin/clavulonic acid PO, or ampicillin/sublactam IV
-Anaerobes: Clindamycin, metronidazole
-Add gram negative coverage: Fluoroquinolone or amino glycoside
-4-6 weeks antibiotics
Lavage pleural space
-Daily with 10ml/kg warm saline, slowly infuse, patient rolled on side to side gently
-Heparin to fluid can decrease fibrin formation
-Obtain thoracic radiographs every 24-48 hours
-Discontinue when volume decreases to <2ml/kg/day
-Cytology resolution of infection
Thoracotomy
-Indicated in animals not responding to medical therapy
-Suspected nidus of infection or foreign bodies
Pneumomediastinum secondary to a tracheal tear after rough intubation during a dental
Lung Lobe torsion
Chylothorax
-Congenital
-Traumatic (surgical or HBC)
-HF in cats, diaphragmatic hernia
-Non-traumatic - neoplasia, cardiomyopathy, pericardial disease, heartworm disease, lung lobe torsion, diaphragmatic hernia, systemic lymphagectasia
-Idiopathic
Originates from thoracic duct, gets dumped into jugular vein. Chyle contains triglycerides, lymphocytes, protein and fast-soluble vitamins
Breeds
-Afghan hounds, Shiba Inu, Siamese, Himalayan cats
C/S
-Lethargy
-Anorexia
-Weight loss
-Exercise intolerance
Dx
-Thoracic radiographs
-Evaluation of effusion (cells and triglycerides)
-Peripheral lymphopenia and panhypoproteinemia may be present
-Evaluate for underlying disease
Tx
-Resolve underlying disease
-Medical management: intermittent thoracocentesis (every 2 weeks)
-Low fat diet
-Administer RUTIN - Benzopyrone drug that decreases protein content of the effusion (promoting resorption of the fluid)
-Surgical ligation of the thoracic duct if not resolved within 3-4 months
-Peuroperitoneal or pleurovenous shunts may be utilized if all else fails
-50-80% response to surgical therapy
Spontaneous pneumothorax
GOLDEN RETRIEVER
-Rupture of cavitary lesions leads to spontaneous pneumothorax
-Occurs more often in dogs than cats
-Leads to rapid, profound respiratory distress following rupture if tension pneumothorax develops
Pulmonary Blebs < 1 cm
Pulmonary Bullae >1cm
Cavitary lesions
-Paragonimus infection
-Necrotic neoplasia
-PTE
-Abscesses and granulomas
-Congenital
-Idiopathic
-Traumatic
-Chronic always disease
-Bullae
Tx
-Thoracocentesis
-Medical treatment successful for Paragonimus (Fenbendazole)
-Most others surgical excision required
Tests to differentiate a chylous vs. purulent pleural effusion and Cervical mass
Compare triglyceride concentration
Evaluate cytology with Diff-Quick stain and a gram stain
Cervical mass
TFAST and check out chest tube and pericardial sites
Lecture 10
Emergency Management of Respiratory Distress and Oxygen Supplementation
Respiratory Distress
C/S
-Orthopnea (shortness of breath)
-Exaggerated abdominal movement
-Cats with notable chest movement or open mouth breathing are seriously compromised
-Cyanosis = severe hypoxemia
-Pallor = acute hypoxemia
-Extended neck breathing, open mouth, adduction of elbows: orthopnea secondary to CHF
Dx
-Perform a rapid PE
-Breathing pattern, auscultation, mm color, pulses, perfusion
-Localize where the problem is
Upper airway: stridor, storting
Lower airway: expiratory difficulty, crackles, wheezes
Pulmonary parenchyma
Pulmonary interstitial or pleural disease
Emergency Management
-Treat for shock: circulatory support, appropriate fluid therapy, balance electrolytes, etc.
-Triad of emergency
1. Decrease stress (sedation, anxiolytic)
2. Place in cool environment
3. Supplement with oxygen to maintain PaO2 > 60 mmHg
Oxygen
PaO2: 85-100 mmHg
PaCo2 : 35-45 mmHg
HCO3: 21-27 mmol/l
pH: 7.35-7.45
-Pulse oximetry: estimates arterial oxygen by measuring hemoglobin saturation
-Arterial blood gas measures both oxygen and CO2: dorsal pedal artery (medium to large dogs). Pre-heparinized syringes and process according to laboratory instructions –Cage-side point of care machines (e.g., IStat with blood gas cartridges)
Acid base status ROME
Respiratory Opposite
Metabolic Equal
Metabolic Acidosis
-pH: decreased
-PCO2: decreased
-HCO3: decreased
-Hyperventilation - compensatory
Metabolic Alkalosis
-pH: Increased
-PCO2: Increased
-HCO3: increased
-Hypoventilation - compensatory
Respiratory Acidosis
-pH: decreased
-PCO2: increased
-HCO3: increased
-Compensatory renal increased HCO3 resorption
Respiratory Alkalosis
-pH: Increased
-PCO2: Decreased
-HCO3: decreased
-Compensatory decreased renal HCO3 resorption
Acid-base status
Primary Hypoventilation
-Increased PCO2, respiratory acidosis
Primary hyperventilation
-Decreased PCO2, respiratory alkalosis
Metabolic acidosis
-Decreased HCO3, drives respiratory hyperventilation (secondary) and decreased PaCO2.
Metabolic alkalosis
-Increased HCO3, drives respiratory hypoventilation (secondary) and increases PCO2
Oxyhemoglobin Dissociation
PaO2: pressure of oxygen dissolved in arterial blood
SaO2: Oxygen saturation of hemoglobin is dependent on PaO2. Clinically measured by pulse oximetry
When PaO2 > 80 mmHg = SaO2 ~100%
Hypoxemia/Oxygen
-Hypoventilation
-V/Q (ventilation/perfusion) mismatch in the lung
-Diffusion abnormality
-Hypercapnia occurs with hypoxemia
-V and Q must be matched for blood to be fully oxygenated upon leaving the lung
-Poor ventilation occurs in most pulmonary diseases, ex edema, alveolar collapse, small airway obstruction (bronchitis)
-Poor ventilated lungs with normal blood flow have low V/Q
-A high V/Q ration is associated with pulmonary thromboembolism
Pulse Oximetry
-Monitors saturation of blood
-Estimation of arterial oxyhemoglobin saturation by transmitting light through tissues
-SpO2 is the difference between light absorption during pulsation (arterial) and background absorption (venous blood, tissue, bone)
-Continuous, immediate, noninvasive estimation of oxygen
Inaccurate SpO2
Artifact
-Probe falls off or poorly positioned
-Dry tongue
-Fluorescent lighting
-Tissue thickness too great
-Pigmented tissue
-Electrical interference (electrocautery)
-Must record a pulse that matches animal’s
Oxygen supplementation
-Indicated if needed to maintain PaO2 >60 mmHg
-Indicated in every patient with respiratory distress or labored breathing
-Cyanosis
-If not responsive to supplemental 100% oxygen, ventilation is the next step
-Oxygen masks - useful for short term supplementation
-Oxygen hoods
-Nasal catheters - long term supplementation
-Endotracheal tubes - requires anesthesia
-Oxygen cages
-Patients requiring supplemental O2 need to be monitored closely
Every 2 hrs get RR, HR, respiratory effort, MM color, and SpO2
Make sure that a bubble humidifier is connected to the oxygen for long term supplementation
Ventilation
-Decrease the retention of CO2 and increase oxygenation
-Referral - labor intensive
-Recommended if patient PaCO2 >60 mmHg
-Positive pressure ventilation recommended for ARDS patients
-Potential detrimental effects of PPV - decreased venous return to the heart, systemic hypertension, decreased lung compliance
