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368 Cards in this Set
- Front
- Back
Causes of Pulmonary Parenchymal Disease
|
-Pneumonia
-Pulmonary edema: cardiogenic and non-cardiogenic -Hemorrhage -Pulmonary thromboembolism -Neoplasia -Pulmonary inflammatory disease -Acute Respiratory Distress Syndrome (ARDS) |
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Clinical signs of Pulmonary Parenchymal Disease
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-Increased respiratory rate and effort
-Restrictive respiratory pattern -Harsh Broncho-vesicular sounds or crackles -Nasal discharge -Productive cough -Hypoxemia signs |
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Diagnosis of Pulmonary Parenchymal Disease
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-PE and Hx
--especially history of travel -CBC/chem screen --look for inflammatory response -Thoracic radiographs -CT scan -Tracheal wash to identify bacteria or neoplasia -Bronchoscopy -Lung aspirate -Lung biopsy |
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Normal defense mechanisms in the Respiratory System
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-Nasopharynx
-Mucociliary escalator -Cough reflex -Brounchus-associated lymphoid tissue (BALT) -IgA -Alveolar macrophages -Pulmonary lymphatics and lymph nodes |
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Causes of Pneumonia
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-Aspiration (most common)
--subdivision of bacterial pneumonia -Bacterial -Viral --can lead to secondary bacterial infection -Protozoal -Fungal -Pneumonia is more common in dogs than in cats |
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Causes of Bacterial Pneumonia
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-Immunosuppression
--cushing's disease, increased cortisol levels -Anatomical abnormalities --cleft palate -Chronic airway disease --asthma -Aspiration -Viral, fungal, or parasitic disease -Trauma or hemorrhage -Inhalation of irritant gasses |
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Aspiration Pneumonia
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-Inhalation of foreign material
--most often GI contents, oral secretions, foreign material -Underlying conditions can predispose patient --pharyngeal/laryngeal dysfunction --megaesophagus --cleft palate --abnormal mentation --recumbency, debilitation --sedation or anesthesia -Recovering from surgery greatly increases predisposition |
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Phases of Aspiration Pneumonia
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1. low pH of GI contents cause injury and bronchoconstriction
2. Inflammation occurs and results in edema 3. Bacteria in aspirated material causes secondary bacterial pneumonia -Clinical signs, diagnosis, and treatment are the same as for other bacterial pneumonias |
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Bacterial Pneumonia Clinical Signs
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-Signs range in severity from intermittent coughing and mild exercise intolerance to dyspnea, cyanosis, and septic shock
-"Walking pneumonia" -Can also have nasal discharge, productive cough, fever, and leukocytosis |
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bacterial Pneumonia route of infection
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1. Inhalation is most common
--Will see cranioventral alveolar pattern and air bronchograms on radiographs --Due to primary pathogens or aspiration of foreign material 2. Hematogenous spread --uncommon in cats and dogs --occurs with bacteremia, bacteria can end up anywhere --will see nodular infiltrates on radiographs |
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Primary pathogens in Bacterial Pneumonia in Dogs
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-Bordetella bronchiseptica
-Streptococcus zooepidemicus -Mycobacterium |
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Opportunistic pathogens in Bacterial Pneumonia in Dogs
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-E. coli
-Pseudomonas -Klebsiella -Enterobacter -Pasteurella -Streotococcus -Staphylococcus -Mycoplasma -Acinetobacter |
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Bordetella bronchiseptica
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-Gram- rod bacteria
-Transmitted by aerosolization -Attaches to columnar epithelial cells in respiratory tract --causes ciliary stasis, paralyzes muco-ciliary elevator --Allows organism to persist in the airway for prolonged periods of time -Adult dogs will show upper airway signs -Puppies can present with bronchopneumonia -Often present in pet stores |
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Primary pathogens in Bacterial Pneumonia in Cats
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-Bordetella bronchiseptica
-Streptococcus sooepidemicus -Mycobacterium -Mycoplasma Mix of gram+ and gram- |
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Opportunist bacteria in Bacterial Pneumonia in Cats
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-Pasteurella
-Pseudomonas -Staphylococcus -Streptococcus -E.coli -Nocardia -Actinomyces -Bacteroides |
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Mycoplasma
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-Smallest free-living microorganisms
-Lack cell walls -Need special culture media to grow -Can be normal flora in the lungs of dogs --NOT normal flora in lungs of cats -Sensitive to fluroquinolones, macrolides, tetracyclines, and chloramphenicol |
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Diagnosis of Bacterial Pneumonia
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-Thoracic radiographs are main diagnostic tool
--air bronchograms --lobar sign -Evaluate patient to find any underlying cause -CBC/Chemistry screen/Urinalysis -Take samples for cytology, culture and sensitivity --trans-tracheal wash --endotracheal wash --broncho-alveolar lavage -Obtain test results before starting antibiotic therapy |
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Trans-tracheal wash
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-Use to diagnose pneumonia
-Don't want animal too sedate, they have to cough to get stuff -Put needle into trachea between cartilage rings |
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Endo-tracheal wash
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-Can do in anesthetized animals
--big aggressive dogs --squirrely cats --any animal that is going to be anesthetized anyway for a procedure |
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Treatment of Bacterial Pneumonia
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-Broad-spectrum antibiotics, start as early as possible
--give IV if patient is critical -Supplemental O2 -IV fluid therapy --very important! keep patient well-hydrated without over-hydrating! |
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Oral antibiotic therapy for Bacterial Pneumonia
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-Clavamox (broad spectrum)
-Azythromycin (bordatella) -Enrofloxacin (good penetration into lungs) |
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IV antibiotic therapy for bacterial Pneumonia
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-Ampicillin/Enrofloxacin
-Clindamycin/Enrofloxacin -Ampicillin/Amikacin -Timentin -Clindamycin/2nd or 3rd generation cephalosporin |
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Treatment for Bacterial Pneumonia
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-Nebulization and coupage
--fine mist to get meds as deep as possible -Bronchodilators can be used for acute aspiration --you SAW it happen --not great for long-term -Mucolytics to break up mucus |
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Monitoring Patient with Pneumonia
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-Pneumonia causes Hypoxemia
--V/Q mismatch, intrapulmonary shunt -Pulse Oximetry, should be more than 94% -Arterial blood gasses, should be more than 80mmHg -PaO2:FiO2 ratio --normal is over 400 -Repeat thoracic radiographs |
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Viral Pneumonia
Distemper |
-Viral pneumonia in Dogs
-Infects epithelial cells throughout the body -1st sign is conjunctivitis with a dry cough -Progresses to productive cough and GI signs -Predisposes animal to secondary bacterial infection --disruption and inflammation of immune system |
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Distemper on Thoracic Radiographs
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-Diffuse interstitial pattern
-Progresses to alveolar pattern with secondary bacterial pneumonia |
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Diagnostic testing of Distemper
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-Thoracic radiographs
--diffuse interstitial pattern that progresses to alveolar pattern -CBC: leukopenia -Fluorescent antibody testing on conjunctival epithelial cells |
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Distemper treatment
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-Supportive care
-Treat for secondary bacterial pneumonia |
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Canine Influenza
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-Viral pneumonia in dogs
-Highly contagious respiratory disease (new in 2004) -Similar to equine influenza virus, mutated to dogs -Mild clinical form: soft or dry cough --may have nasal discharge -Severe clinical form: High fever, clinical signs of pneumonia --affects 5-8% --5% mortality rate Dx: serology, acute and convalescent titers -Tx: Supportive care, antibiotics for secondary bacterial infection -Prevention: vaccinate! |
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Dogs with increased risk to Canine Influenza
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-Show dogs
-Dogs at a boarding facility -Shelter dogs -Racing dogs |
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Protozoal Pneumonia
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-Toxoplasma Gondii is main concern
-Worldwide distribution, exists everywhere! -Common in cats, look for FeLV/FIV immunosuppression -Rare in dogs -Radiographs will show fluffy interstitial to nodular alveolar pattern -Dx: tachyzoites in tracheal wash or bronchio-alveolar fluids --can also do serology -Tx: clindamycin or sulfa drugs |
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Fungal Pneumonia
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-Secondary to histoplasmosis, blastomycosis, and coccidiomycosis
-History of slowly progressive respiratory signs --weight loss --lymphadenopathy --fever -Geographical location and travel history are important for diagnosis |
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Geographical Distribution of Fungal Pneumonia
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1. Histoplasmosis:
--Mississippi --Missouri --Ohio river valley 2. Blastomycosis: --Mississippi, Missouri, Ohio river valleys --Mid-atlantic states along waterways 3. Coccidiomycosis: --SW us and Mexico |
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Diagnosis of Fungal Pneumonia
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-Thoracic Radiographs
--diffuse interstitial pattern to nodular pattern --hilar lymphadenopathy -Tracheal wash, broncho-alveolar lavage, lung aspirates --identify organism -Lung biopsy -Fungal Cultures -Serology -Can look like metastatic neoplasia |
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Treatment of Fungal Pneumonia
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-Do not treat unless you see the organism!!
-Antifungals --Itraconazole, Fluconizole, Amphotericin B --watch out for toxic side effects -Long treatment, 4-6 months or longer -Patient may get worse initially due to inflammation from death of organisms |
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Pneumocystis carnii
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-Causes pulmonary disease in immuno-compromised patients
-Rare in dogs, esp. young dogs -Not reported in cats -Chronic signs --weight loss, exercise intolerance, respiratory distress, non-productive cough -Initially classified as a protozoal |
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Pneumocystis carnii Diagnosis and Treatment
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-Radiographs: mixed alveolar or diffuse interstitial pattern
--cor pulmonale (right sided heart enlargement) -Dx: organisms in tracheal wash or lung aspirates -Tx: trimethoprim sulfa or pentamidine -Poor prognosis, but some reports of success |
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Key points of Pneumonia
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-Common cause of respiratory disease in the dog and cat
-Bacterial pneumonia is the most common --aspiration --infectious --hematogenous -Diagnostics should include physical exam, history, thoracic radiographs, and tracheal wash -Other less common infectious causes of pulmonary parenchymal disease: --viral --fungal --protozoal |
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Anatomy of the Pleura
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-Pleura is a single layer of cells
-Visceral pleura covers the lungs -parietal Pleura lines the thoracic cavity -Mediastinum is anatomically pleura but not functionally -Pleural fluid is formed by starling forces |
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Pleural Space
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-Potential space between visceral and parietal pleura
-Filled with a small amount of fluid |
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Act of Breathing
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-Increases volume due to contraction of the diaphragm
-Increase in volume causes decrease in pressure -Anything in the pleural space that takes up space and volume allows for less of a decrease in pressure --less inflation of the lung |
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Pathophysiology of the Pleura
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-Air or fluid in the pleural space causes parietal and visceral pleura to separate
-Lungs collapse due to changes in pressure -Chest wall expands |
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Hypoventilation
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-Not enough CO2 is blown off
-Results in ventilation/perfusion mismatch -CO2 is most soluble, will be affected the least by disease -O2 is much less soluble, is affected easily by disease |
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Clinical Findings of Lung Issues
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-Great variability
-Insidious onset or acute decompensation with chronic disease -Rapid shallow breathing due to decreased tidal volume, decreased functional reserve capacity, or decreased compliance |
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Signs of Lung issues
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-Elbows abducted
-Head extended -Working hard to breathe -Animal is sternal or sitting -Cough -Muffled heart sounds -Breath sounds are absent ventrally with effusions |
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Reasons an animal might have to work hard to breathe
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-Upper airway obstruction
-Issue in pleural space -Diaphragm -Issue with lungs |
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Reasons for Muffled Heart sounds
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-Fluid
-Air -intestines -Just fat |
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Diagnosis of Lung issues
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-Thoracic radiographs (orthogonal views)
-Thoracocentesis -Pleural fluid analysis |
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Chest tap Rules
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1. Tap where the heart is not
2. Do not tap the liver or into the abdomen --tap cranial to the 8th or 9th rib 3. Tap on the cranial side of the rib --avoid intercostal vessels that run on caudal side of the rib 4. Tap until you get negative pressure --do not pull too hard! Will dislodge clots Chest tap normally makes the animal feel much better -some free air remaining in the pleural space is OK if animal looks fine otherwise |
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Chest Tube
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-Use with repeated or continuous aspiration of chest cavity
--more than 3 chest taps, time for a chest tube -Ideally place with anesthesia and control of airway --intubate! -Tunnel technique, open technique, or trochar technique |
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Open technique for Chest Tube placement
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-Have to close 2 incisions
-Have controlled placement of the tube -Pull skin forward, make incision --releasing skin moves cutaneous incision away from location of pleural incision |
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Chest tube/3-way stopcock interface
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-Not a very good system
-Increased potential for leakage with more components -Need to make sure connections are secure -Test by clamping chest tube and trying to pull off air --if you can get air with tube clamped, there is a leak somewhere |
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3 bottle technique for chest tap
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-Pre-determines suction on the system
-Prevents air from going back into the chest |
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Pneumothorax on Radiograph
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-heart will be elevated
--decreased cardiosternal contact -Will see free air in the pleural space |
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Causes of Pneumothorax
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-Penetrating wounds
-Pulmonary trauma --Most often blunt trauma -Esophageal rupture -Rupture of pulmonary blebs or bullae --can cause spontaneous pneumothorax |
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Hypoxic Pulmonary Vasoconstriction
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-Decreased oxygen in alveolus results in Ventilation Perfusion mismatch
-Alveolus collapses, blood is shunted through tissue -Arteries constrict, constriction slows blood flow --attempts to rectify mismatch -Arteries redirect blood to alveoli with air |
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Tension Pneumothorax
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-Leak in the lung
-Each time animal breathes in air gets into pleural space and does not come out -Blood is pulled out of the chest due to change in pressure -DO NOT VENTILATE this animal! --Intubate and tap at the same time |
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Signs of Tension Pneumothorax
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-Difficulty breathing
-Circulatory collapse -If using chest tap, will be pulling off way too much air with 3-way stopcock -On radiographs will see pleura pulling away from chest wall |
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Spontaneous Pneumothorax
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-Caused by blebs/bullae
-hard to image |
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Pleural Effusion treatment
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-Treat underlying cause
-Get sample |
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Pleural Effusion Diagnosis
|
-Analysis of pleural fluid (get a sample!!)
-Evaluation of cardiac function --ascultation, radiographs, echocardiography -Bloodwork -Investigation of lungs, mediastinum, and diaphragm -Investigation of other diseases --pancreatitis --protein losing nephropathy, enteropathy |
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Pleural Fluid Analysis
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-Total cell count
-Total protein and specific gravity -Aerobic and anaerobic culture -Direct smears stained for cytology -With chylothorax, get triglyceride and cholesterol levels |
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Pleural Effusion Treatment
|
-Drain all fluids
--unless hemorrhagic and coagulopathy is suspected (rodenticide) -Do not drain all fluids if need ultrasonographic window --cannot ultrasound through gas, can through fluid |
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Trasudates
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-Fluid with low protein count, low cell count
-Less than 1500 cells per uL -Low total protein, less than 3g/dL -Usually the result of hypoalbuminemia -Decreased production of proteins in liver or increased loss of proteins in kidney and GI |
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Modified Transudates
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-1500-5000 cells per uL
-Total protein is 3g/dL -Almost any disease causing long-standing effusion will have modified transudates --chronic effusion leads to modified transudates |
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Differential Diagnoses for Modified Transudates
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-Myocardial failure
-Pericardial effusions -Neoplasia -Diaphragmatic hernia -Lung lobe torsion -Pancreatitis |
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Exudates
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-More than 5,000 cells per uL
-More than 3g/dL of protein -High nuclear cell counts -Non-septic causes: --FIP, chylothorax, neoplasia, fungal infection, foreign body -Septic causes: --Wound, esophageal perforation, necrotic tumor, pulmonary abscess |
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Chylothorax
|
-Accumulation of Chyle in pleural space
-Milky white fluid -Trauma was originally suspected as cause, but unlikely --thoracic duct repairs itself quickly -Dilation and leakage from thoracic duct --Lymphangectasia --Leak in duct AND increased pressure |
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Lymphangectasia
|
-Physical obstruction of lymph flow into cranial vena cava
-Causes: --neoplasia --heartworm --thormbosis --lung lobe torsion -Increased cranial vena caval pressure due to heart failure, pericardial disease, or throboembolism -Very often idiopathic |
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Chylothorax Fluid
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-Pleural fluid to serum triglyceride ratio should be more than 1
--pleural fluid should be higher -Pleural fluid triglyceride levels should be more than 100mg/dL -Compare triglyceride in serum to pleural fluid -Interpret with caution in animals that have not eaten for several days |
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Chylothorax Treatment
|
1. Medical:
--drain pleura --put animal on low-fat diet (does not reduce volume of chyle) 2. Surgical: --thoracic duct ligation as close to the diaphragm as possible --pericardectomy |
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Pyothorax
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-Usually occur secondary to something else
-Penetrating wounds -Esophageal perforations -Migrating foreign bodies -Extension from Pneumonia -Pulmonary abscessation -Neoplasia -Hematogenous Spread |
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Pyothorax in Cats
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-Anaerobes:
--peptostreptococcus --Bacteroides --fusobacterium --prevotella -Aerobes --pasturella --actinomyces |
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Pyothorax in Dogs
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-Anaerobes:
--peptostreptococcus --bacteroides --Fusobacterium --porphyromonas -Aerobes: --actinomyces --pasturella --E. coli --Streptococcus |
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Treatment for Pyothorax
|
-Chest tube drainage
-IV fluids -Colloids -Appropriate antimicrobial therapy |
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Pyothorax Indications for Surgery
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-Failure to respond to medical therapy
--inability to aspirate effusion through properly placed and functional thoracostomy tubes --Failure of effusion to resolve over reasonable period of time, usually a week -Obvious surgical lesion found --abscessed lung lobe --foreign body |
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Pulmonary Contusions
|
-Interstitial and Alveolar hemorrhage following blunt thoracic trauma
-May have other concurrent thoracic injuries also --rib fractures --pneumothorax --pleural effusion |
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Clinical Signs of Pulmonary Contusions
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-Acute or delayed onset, may not see signs right away
-Can worsen over several hours -Dyspnea -Increased breath sounds or crackles -Shock -Concurrent injuries -Hemoptysis (coughing up blood) is uncommon |
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Treatment for Pulmonary Contusions
|
-Mostly supportive care
-Oxygen -Careful IV fluids --do not want to blow off clots -Analgesia -May or may not intubate for positive pressure ventilation -Be aware of coagulopathies |
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Allergic Airway Disease
|
-Broad spectrum of diseases
-Parasitic -Allergic Bronchitis -Feline Asthma --be sure to ask about hairballs, hairballs look like asthma to owners -Pulmonary infiltrates with eosinophils |
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Pathology of Allergic Airway Disease
|
-Bronchial and alveolar inflammation
--Edema --mucous secretion --smooth muscle hypertrophy --bronchi and bronchiolar constriction -Eosinophils often predominate -Dyspnea due to closure of bronchioles |
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Clinical Signs of Allergic Airway Disease
|
-Can be acute or chronic
-Rapid, shallow breathing -Expiratory dyspnea, difficulty exhaling -Cough -Loud breath sounds on ascultation --crackles and wheezes can also be heard --wheezes typically on expiration -Radiographs will show bronchiolar or interstitial pattern |
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DDx for Allergic Airway Disease
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-Hypersensitivity reaction
--Lung parasites --heartworm --drugs --inhaled allergens --bacterial, fungal, or neoplastic issues |
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Bronchus with Allergic Airway Disease
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-Will be hyerpemic
-Narrow lumen -Mucus present in lumen |
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Diagnostics for Allergic Airway Disease
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-CBC/Chem/Urinalysis
-Radiographs -Endotracheal wash or BAL -Possible tests: --lung aspirate or biopsy --heartworm testing --fecal float --fungal testing depending on geography |
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Treatment for Allergic Airway Disease
|
-Treat any underlying infections
-Discontinue any medications -Minimize exposure to allergens -Glucocorticoids to treat inflammation -Bronchodilators to treat bronchoconstriction -Consider inhaled medications |
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Pulmonary Edema
|
-Fluid in the interstitium or alveoli
--fluid in the airspace itself -Cardiogenic: high-pressure edema --congestive heart failure -Non-cardiogenic: leaky-vessel edema --neurogenic edema --acute lung injury or ARDS |
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Neurogenic Edema in Lungs
|
-Non-cardiogenic
-"Leaky-vessel" edema -Most often seen after an event --upper airway obstruction, choking --seizure, head trauma, electrocution --non-fatal drowning -Unknown pathogenesis --vasoconstriction in periphery and blood goes to the brain? -Clinical signs vary with severity -Alveolar pattern in caudodorsal lung fields on radiographs -Good prognosis with Supportive care |
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Neurogenic Edema on radiographs
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-Alveolar pattern in caudo-dorsal lung fields
|
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ALI/ARDS causes
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-Continuum of pulmonary injury, inflammation, and vasculitis
-Often the result of systemic inflammation that originates outside of the lung --SIRS --Sepsis --Heat stroke --Trauma --Pancreatitis |
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ALI/ARDS
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-High protein fluid and inflammatory infiltrate in air spaces
-Acute to sub-acute onset of tachypnea and dyspnea -Moderate to severe hypoxemia -Coughing, crackles or wheezes audible on auscultation |
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ARDS lung
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-Inflamed tissue
-Oozes on cut surface -Lots of fluid in the lung -Can develop quickly -No longer light pink, clean structure -Closed airways with lots of inflammatory cels and proteinaceous fluid |
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ARDS on radiograph
|
-Alveolar pattern without evidence of congestive heart failure
-Will see air bronchograms -Alveolar infiltrates |
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Treatment for ALI/ARDS
|
-Supportive care
-Treat underlying diseases --there is always a trigger, need to find underlying cause -Give cautious fluid therapy --can flood the lungs if too much is given -Intubate for positive-pressure ventilation |
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Pulmonary Thromboemobilsm
|
-Acute or Chronic pulmonary vascular occlusion
-Emboli can be secondary to fat or clotting -Interferes with normal pulmonary blood flow and gas exchange --alveoli get fresh O2 but no blood flow --pulmonary dead space |
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Predisposing Causes for Pulmonary Thromboembolism
|
-SIRS/Sepsis
-Pancreatitis -Protein-losing enteropathy or nephropathy -IMHA -Endocrine Disease -Steroid therapy -Many other diseases can predispose -Catheter can be nidus for clot formation |
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Clinical Signs of Pulmonary Thromboembolsim
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-Labored breathing
-Tachypnea -Lethargy -Altered mentation -Collapse -Signs are related to comorbidities -Many are clinically silent --incidental finding |
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Diagnostic workup for Pulmonary Thromboembolism
|
-Chemistry/CBC/Urinalysis
-Arterial Blood gas -Endocrine testing -Coagulation testing +/- thromboelastography --D-Dimers indicate breakdown product of a clot -Radiographs or advanced imaging |
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Pulmonary Thromboembolism Treatment
|
-Supportive Care
-Anticoagulation therapy short-term or long-term -Thrombolytic therapy? --Meds that break down clot that is already present -Treat underlying diseases! Underlying hypercoagulability |
|
Pulmonary Fibrosis
|
-Pathologic inflammation of the lung with scarring
--excessive remodeling of tissue -Unknown cause, likely mediated by inflammatory cytokines (IL, TNF-a) |
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Possible Predisposing Causes for Pulmonary Fibrosis
|
-Primary pulmonary disease with deranged remodeling
-Connective tissue disorder, disorder of formation -Environmental pollutants -Drug reactions --systemic drugs affecting the lungs -Neoplasia -Idiopathic in west-highland terriers |
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Clinical Signs of Pulmonary Fibrosis
|
-Often slow or subtle in onset
--chronic disease -Exercise intolerance -Cough -Dyspnea -Collapse -Increased blood pressure in pulmonary circuit --pulmonary hypertension |
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Pulmonary Fibrosis on Radiograph
|
-Diffuse multi-lobar interstitial pattern
-Pulmonary hypertension -Right ventricular hypertrophy |
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Fibrotic Lungs with Pulmonary Fibrosis
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-Abnormal, gross-looking lungs
|
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Pulmonary Fibrosis Diagnostic Testing
|
-Radiographs with or without CT scan
-Arterial blood gas -Endotracheal wash or BAL --need to rule out pneumonia or neoplastic cause -Lung biopsy |
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Pulmonary Fibrosis Treatment
|
-Supportive Care
-Glucocorticoids -Bronchodilators -Guarded prognosis, depends on how severe the patient is -Slow onset and gradual progression |
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3 Components of Bovine Respiratory Disease
|
1. Management
--environment, feeding, herd density 2. Viral Disease --viral diseases can lead to bacterial infections --suppress immune system and allow bacteria to invade 3. Bacterial disease |
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Respiratory Disease in Young Calves
|
-HUGE problem in young animals
-A calf getting sick dramatically reduces productive life of the calf -Keeping animals individualized when young prevents spread of disease --stress allows for vulnerability |
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Young Stock Respiratory Disease in Beef
|
-Disease generally comes during weaning
-Calves are a little older than in dairy -Disease caused by stressful movements and changes |
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Adult Bovine Respiratory Disease
|
-Sporadic issue, not common
-Animal density and confinement will increase the respiratory disease process |
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Ventilation and Bovine Respiratory Issues
|
-Animal density is critical for ventialtion
-Need a minimum of 4 air changes every hour to ensure clean, safe air --needs to occur year-round |
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Functions of Ventilation of a Barn
|
1. Remove CO2 and ammonia
--damages upper respiratory tract 2. Remove heat and moisture --decreases amount of airborne bacteria --Large animals produce a lot of heat, need to get rid of it |
|
Natural Ventilation Systems in Barns
|
-Open roof systems
-Allows hot air to rise and exit -Old bars are not designed for optimal air flow -Natural air flow is not very consistent or reliable -best when combined with big mechanical fans or +pressure tubes |
|
Mechanical Ventilation Systems in barns
|
-Fans in closed barn
-Air has to go in AND out -Positive pressure tubes --holes placed at regular intervals provide airflow --gives consistent airflow throughout the entire barn --easy to adapt to older barns -Do not want to create drafts! |
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Pulmonary Defense Mechanisms
|
1. Mucociliary defense system
2. Pulmonary Alveolar macrophages 3. Secretory System |
|
Mucociliary Defense System
|
-Warms and filters incoming air
-Cilia remove dust and organisms --give escalator effect, brings mucus back up and out -Very efficient, most efficient method for defending against pathogens -Mucus captures and traps pathogens going from upper respiratory tract to lower respiratory tract --prevents bacteria from getting into lower respiratory tract -90% effective |
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Factors Affecting Mucociliary Defense System
|
-Dehydration decreases mucus production
-Starvation -Toxic gasses, Ammonia --death of mucociliary cells and ciliostasis -Viral infections -Stress -Rectify by keeping animals warm and dry, well fed, and decrease stress |
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Pulmonary Alveolar Macrophages
|
-Lower Respiratory Tract
-Macropahges -NOT neutrophils -Less efficient system, 50% efficiency --takes a few days to respond and remove particles -Neutrophils only enter lung to respond to infection --infection has to be present |
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Secretory System
|
-Cell-mediated immunity
-Local immunity --most important, IgA and Interferon, natural antiviral properties -Serum antibody is less important -Secretory and local antibodies are both produced and important |
|
Anatomy of the Bovine Lung
|
-Unique lung system
-Right accessory lung lobe -Right lung has more lung tissue than left lung, more capacity --55-60% of total capacity -Right cranial bronchus comes off before tracheal bifurcation --Enters right cranial lung lobe --first opportunity for pathogens to get into the lungs --will see disease in right cranial lung lobe 1st -Infections are easily walled off to prevent collateral exchange |
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Basal Lung Metabolism
|
-Uses 45% of bovine lung capacity
--cows use more of lung capacity for lung metabolism -Horses and humans use 20% of basal metabolism |
|
Lung sounds in the Bovine
|
-Duller on left side due to rumen
-Vesicular sounds can be heard throughout the entire lung field -Bronchovesicular sounds are heard best in bronchi |
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Signs of Bovine Respiratory Disease
|
-Animal looks sick
-Dehydrates easily, dry nose -Do not cough regularly, cough is not very efficient -Sunken eyes -Droopy ears |
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Bovine Viral Respiratory Diseases
|
-Infectious Bovine Rhinotracheitis
-Parainfluenza Type 3 -Bovine Respiratory Syncytial Virus -Bovine Viral Diarrhea Virus -Animal does not usually just have a virus, usually has virus AND bacterial infection |
|
Infectious Bovine Rhinotracheitis
IBR |
-Affects mucosa of nasal and upper respiratory passages
-herpes type I virus --latency period, goes dormant after initial infection -More than 80% of cattle are seropositive -Latent infections are common |
|
IBR Syndromes/forms of Disease/Sequelae
|
-Respiratory
-Conjunctival --not always corneal, no corneal lesions -Infectious Pustular vulvovaginitis -Abortion -Low conception rates -Follicular Disease |
|
Infectious Pustular Vulvovaginitis
|
-Ulcerated lesions on vulva and vagina
-Syndrome of Infectious Bovine Rhinotracheitis (IBR) |
|
IBR clinical Signs
|
-High fever, over 105F
-Mild dyspnea --not huffing and puffing, but not normal either -White nasal plaques (Pathognomonic for herpes viral infections) -WBC profile is normal -Mild/rapid recovery without secondary bacterial infection --should recover in a few days |
|
Herpes Infections in cattle
|
-Serous nasal discharge
-Bacterial infection causes cloudy, dense nasal secretions -White plaques with red and inflamed nasal tissue --"red nose" disease -Lungs should sound normal --upper respiratory infection -Trachea should sound abnormal |
|
IBR Rare Presentations
|
-Encephalitis
--with meningitis --non-purulent -Fatal septicemia --in calves less than 1 week old --necrosis in GI tract with peritonitis -Balanopostitis: localized infection of white plaques --plaques on penis and prepuce |
|
IBR Diagnosis
|
-Serology
--not best method, 80% of animals are seropositive --virus neutralization -Can compare acute and convalescent paired titers --4x increase from acute to convalescent indicates infection -Virus isolation -Fluorescent Antibody -PCR |
|
IBR Treatment
|
-Palliative treatment
-Analgesic.antipyretic -Banamine (Flunixin meglumine) |
|
IBR Prevention
|
-Vaccination!
-Do not rely on natural exposure for treatment -ALL Cattle should be vaccinated against herpesvirus 1 -Can give as modified live intranasally or as killed virus |
|
IBR Intranasal Vaccine
|
-Best production of interferons
-Rapid onset of immunity --will have local antibodies in 48 hours --secretory antibodies in 1 week -Does not cause abortions -Difficult to give, have to put it up the nose -Very useful in outbreaks |
|
IBR Modified Live Virus vaccine
|
-Injectable vaccine
-Abortogenic, can cause abortions --can be avoided with routine vaccination schedule --if unknown vaccination history, do not give to pregnant animal -Longest lasting immunity, do not need to booster -Strongly recommended for all young stock |
|
IBR Killed Vaccine
|
-Safest vaccine
-few reactions -no replication of the virus in the body -2 doses are needed for initial immunity -Need an annual booster (VERY important!) |
|
IBR Summary
|
-Herpes virus
-high sero-prevalence, 80% of cattle have seen virus -Not very pathogenic alone --sets stage for bacterial infection -WBC profile is normal -White plaques on mucosa, esp. nasal passages -Predisposes animal to bacterial pneumonia --IMPORTANT with shipping! --Shipping fever, weaning and shipping stress -Has may syndromes -Can cause abortions |
|
Parainfluenza Virus in Bovine
PI-3 |
-Paramyxovirus
-90% seroprevalence in cattle -Not pathogenic alone, will not cause a problem by itself in animals -Very important in combination with pasteurella or Mannheimia bacteria --Can lead to bacterial Pneumonia |
|
Clinical Signs of PI-3
|
-Mild increase in respiratory effort
-No real definitive signs, all are non-specific |
|
PI-3 Vaccine
|
-Included in all IBR vaccines
--easy to incorporate and animals react to vaccine well --ALWAYS as a combo vaccine -Provides short-term immunity --3 months -Don't need to booster, just give with IBR vaccine -Can be useful before shipping |
|
Bovine Respiratory Syncytial Virus
BRSV |
-Paramyxovirus
-High sero-prevalence --50-80% of cattle are seropositive -NOT Bovine syncytial virus -Latent infection is common and important --can become latent even though it is a paramyxovirus -Infection comes via aerosol from dam at birth --calving is stressful for the cow, will shed virus and spread the virus to the calf -Stress causes recurrence of the virus and emergence of disease later |
|
Diagnosis of BRSV
|
-Serology is not useful
-Passive immunity is not protective --colostrum is not helpful for calves -Short incubation period, 3-5 days -Highest incidence occurs between 2 and 5 months of age --2 months= weaning in dairy --5 months= weaning in beef |
|
Clinical Picture of BRSV
|
1. Atypical Interstitial Pneumonia
--emphysema in interstitium of the lungs, air bubbles where there should not be any 2. ARDS --animal is having problems exchanging air -Subcutaneous Emphysema, air under the skin -High fever -No membrane changes, animal does not look toxic -Big increase in salivation and saliva production -May not have an increase in nasal or ocular discharge -Slight increase in RR |
|
Treatment for BRSV
|
-Animal can recover on own
-Also can go into respiratory distress a week or so later --Mostly an issue with animals that are worked or stressed --mortality rate increases with work/stress -Can give antibiotic and NSAID or steroid |
|
BRSV Lungs
|
-Whole lung mass is involved
-Lungs are over-inflated and push the ribs out -Syncitial cells join membranes --form one giant cell with multiple nuclei |
|
BRSV diagnosis
|
-Difficult to make, hard to definitively culture organisms
-Virus is very fragile -Virus is only present early in the clinical course of disease -Can use fluorescent antibodies and immunohistochemisry to identify parts and pieces of a virus -Virus isolation is not useful due to fragile virus -Serology is not useful and difficult to interpret |
|
BRSV vaccination
|
-Not clear if it actually works!
-Passive immunity is not protective -Serum antibodies are not protective -Killed and modified live vaccines are available -Requires a booster --need to challenge system again to get response -Initially can give as combo vaccine -Booster with specific BRSV vaccine |
|
Bovine Viral Diarrhea Virus
BVDV |
-Flaviviridae, pestivirus genus
-Major bovine pathogen -Causes diarrhea, fever, mucosal erosions, abortions -Predisposes animal to bacterial infection -Immunosuppressive -Causes oral ulcerations and erosions -Persistent Infection, an infected animal is ALWAYS infected |
|
BVDV Persistently Infected Animals
|
-Calf is exposed to virus in-utero at a very specific timeframe
-Fetus recognizes virus as "self" -Animal can look normal and act normal, but spreads virus EVERYWHERE -Any calves delivered will be PI calves -Animal is persistently infected, will always be infected, and will never not be affected |
|
BVDV vaccination
|
-Vaccination is effective
-Can be given as a combo vaccine |
|
Progression of Bovine Respiratory Infections
|
-Poor management leads to viral infections that lead to bacterial infections
|
|
Bovine Bacterial Bronchopneumonia
|
-5 pathogens cause 95% of disease
1. Mannheimia haemolytica (#1 cause of bronchopneumonia) 2. Pasturella multocida 3. Histophilus somni 4. Mycoplasma bovis 5. Truperella pyrogenes (only gram+) --most common abscess forming bacteria in all food animals -Mostly gram- bacteria -Cause issues in lower respiratory tract --take out mucociliary escalator, allows bacteria to get into lower respiratory tract |
|
Gram- vs. Gram+ bacteria
|
S.S. BECCLR DAMNT
-Staph -Strep -Bacillus -Erisypilothrix -Clostridium -Corynebacter -Listeria -Rhodococcus -Dermatophilus -Arcanobacterium -Mycobacterium -Nocardia -Truperella |
|
Bovine Bacterial Bronchopneumonia Pathogenesis
|
-Endotoxin: all gram- bacteria have endotoxin as cause of disease
--kills bacteria and tissue around the bacteria -Exotoxin -Chemotactic factors and hemolysins --stimulates complement system that destroys tissue -Macrophage activity is decreased, leads to terrible infection |
|
Crackles in lung
|
-Collapse of air sacs and bronchioles
-Need to open airways |
|
Wheezes in lung
|
-Narrowing of airspace
--Stenosis -Can be via collapse OR filling of lumen with mucus |
|
Bovine Respiratory Disease
BRD |
-Stress reduces host defense
-Virus damages upper respiratory tract -Bacteria is able to invade lower respiratory tract -Final outcome is bronchopneumonia -Can be acute or chronic |
|
BRD Acute Bronchopneumonia
|
-Mannheimia is primary pathogen
--high morbidity and high mortality -pasturella multocida --high morbidity, not as high mortality -Histophilus somni -Happens all of a sudden -Bacterial infections are toxic, mucus membranes will change color (brick red) -Endotoxins affect the entire body -Will see weak animal with ocular and nasal discharge -LOTS of damage to tissues in the lungs |
|
Factors leading to BRD Acute bronchopneumonia
|
-Shipping fever
-Herd outbreak -Sudden death -Toxic animals --purple or red mucus membranes -Painful respiration due to pleuritis -treat with antimicrobial! -Common in shipped beef or weaned dairy, times of stress |
|
BRD Acute bronchopneumonia Necropsy Results
|
-Fibrinous bronchopneumonia
-Antero-ventral lung consolidation -May or may not have bulbous emphysema of the lung -Fibrin tags cause friction rubs on the pleura --fibrin turns into fibrous accumulations over time |
|
BRD Chronic Bronchopneumonia
|
-Pasteurella multocida is most common
-Truperella pyrogenes, causes abscesses -Histophilus somni -Mycoplasma bovis |
|
Clinical Signs of BRD Chronic Bronchopneumonia
|
-Small, stunted animal
-60% of lung tissue is compromised -Milk production is down if animal makes it to parturition -Often seen in younger animals -Will have moist, productive cough -Abnormal lung sounds -Endemic or epidemic |
|
BRD Histophilus somni
|
-Normal inhabitant of the upper respiratory tract
-Culture requires special media -Serology is useful -Difficult to diagnose in chronic situations |
|
BRD Mycoplasma
|
-Can be Mycoplasma bovis or Mycoplasma dyspar
--Bovis causes most of the issues -Mycoplasma mycoides in other countries -No good treatment -Mycoplasma is an intracellular organism --hides from antimicrobials and immune system -No vaccine available -Looks like BSE or FMD |
|
Treatment of Chronic BRD
|
-Long-term antibiotic therapy
--10 days or more -Must start treatment early! -Look for abscess |
|
BRD vaccination
|
-Mannheimia and pasteurella are bacterins
--vaccination will not work -useful against endotoxin -Active endotoxin in vaccine can cause endotoxemia in cattle, have to be careful! |
|
BRD Best treatment
|
-Prevention!
-Pre-condition animals with vaccines and immunostimulants |
|
Enzootic Calf Pneumonia
|
-"Syndrome"
-Multiple pathogens present -Chronic disease -Due to poor ventilation and ammonia buildup --ammonia leads to pneumonia -Most common in heifers 2-6 months -Recurrent -Get better with treatment, but will continue to relapse of conditions are not changed |
|
BRD and antimicrobials
|
-Treatment is all about antimicrobials
-Label use is best -Can use some drugs off-label --limited by feds -Do not want any residues -With-holds only apply if used on-label |
|
BRD Antibiotic treatment
|
-Most commonly used:
--cephalosporin --macrolide --florfenicol --oxytetracycline -Least commonly used: --beta-lactam (not very effective) --Sulfas --Rifampin (helps other microbials penetrate the bacterial cell wall |
|
Cephalosporin in Large Animals
|
-Prohibited off-label or off-indication
-Naxcel -Excenel -Excede -3rd generation -Very effective against pasteurella multocida |
|
Naxcel
|
-No milk with-hold
-4 day meat with-hold -Pneumonia and foot rot |
|
Excenel
|
-No milk with-hold
-3 day meat with-hold -Pneumonia, foot rot, metritis -Very effective against pasteurella multocida |
|
Excede
|
-No milk with hold
-13 day meat with-hold |
|
Macrolide
|
-Tilmicosin (micotil)
-Tulathromycin (Draxxin) -Gamithromycin (Zactran) -42 day meat with-hold, LONG with-hold -NOT to be used in lactating dairy cows --other better drugs are available -Very toxic to humans an other animals --do not use in swine or equine --cardiac toxicity, kills myocardial cells |
|
Florfenicol
|
-Nuflor
-Synthetic derivative -Not for lactating cows -28 day meat with hold -Good activity against mannheimia haemolytica, Pasteurella multocida, Histiophilus somni |
|
Florfenicol and Flunixin meglumine
|
-Resflor Gold
-Not for lactating cows -38 day meat with-hold -Basically NSAID and antimicrobial -Good activity against Mannheimia haemolytica, pasteurella multocida, and histiophilus somni |
|
Fluoroquinolones
|
-Endofloxacin (Baytril)
-Not for lactating cows -28-day meat with-hold -Good activity against Mannheimia haemolytica, pasteurella multocida, histophilus somni |
|
Oxytetracycline
|
-Can be put into feed
-Many routes of administration -Long-acting forms are available -Often used in combination with other anti-microbials -Long meat with-hold, 30 days -Can be used in lactating cattle |
|
Beta Lactam
|
-Procaine Penicillin G (PPG)
--Test for meat and milk with-hold -Polyflex --48 hour milk with hold, 6 day meat with hold |
|
Sulfas
|
-Albon Bolus
-60 hour milk with-hold -7 day meat with-hold |
|
BRD Non-infectious
|
-Interstitial or Atypical Pneumonia
1. Acute Respiratory Distress Syndrome (ARDS) 2. Hypersensitivity 3. Chronic Interstitial Pneumonia 4. Parasitic Pneumonia |
|
ARDS anatomical changes
|
-Pulmonary congestion or edema
-Hyaline membrane in alveoli -Hyperplasia of alveolar epithelium -Interstitial emphysema -May find on necropsy -need to find at least 1 in order to confirm ARDS |
|
ARDS syndromes
|
1. Acute bovine Pulmonary Emphysema
--fog fever 2. Moldy Sweet Potato 3. Misc. toxicities --Perilla mint toxicity --NO Quick changes in diet to lush grass from hay -Microbes work on tryptophan, convert into 3-methyl indole -3-methyl indole ends up in lung and destroys pneumocytes |
|
Acute Bovine Pulmonary Emphysema
ABPE |
-Fog Fever
-Occurs in Adult cattle -Need a very specific history --switch from dry to lush pasture -Lush pasture has more tryptophan, increased tryptophan in diet -Tryptophan is converted into 3-methyl-indole in rumen -During eructation and rumination 3-methyl-indole gas ends up in the lungs --causes vasoconstriction in the lungs |
|
ABPE Disease Progression
|
-Acute onset
--occurs within 2 days of the switch -Animal in respiratory distress --head held out --open mouth breathing -Morbidity is high, all animals with the same diet change will be affected -Normal temperature -increased major airway sounds -Diagnose by history and clinical signs |
|
ABPE Clinical Signs
|
-No toxemia
-No increased temperature -ON necropsy will see severe emphysema -Lungs do not collapse -Alveolar epithelial hyperplasia |
|
ABPE Treatment
|
-Take cows off lush green pasture
-Give NSAIDs -Give microbials to decrease bacterial infections |
|
Hypersensitivity Pneumonia
|
-AKA
--proliferative pneumonia --bronchiolitis obliterans --chronic non-infectious interstitial pneumonia -Same progress as "farmer's lung" -Slowly progressive -Due to chronic exposure to micropolysore molds -Lung has immune-mediated response to mold or spores in hay --Type III hypersensitivity -Destruction of bronchioles -Alveolar hyperplasia and fibrosis --loss of alveolar sac |
|
Misc. Pneumonia
|
-Necrotic laryngitis
-Metastatic Pneumonia -Caudal Vena cava thrombosis -Lung abscesses -Inhalation/aspiration pneumonia -Lungworm (Dictyocaulus viviparous) -Iatrogenic pharyngeal abscesses -Allergic rhinitis |
|
Necrotic Laryngitis
|
-"Calf Diptheria"
-Fusobacterium necrophorum -Occurs in 2-6 month old calves -Need break in mucosa --coarse feed or stemmy hay --hay damages larynx -Bacteria sets up shop in the damaged mucosa -only seen in damp dark barns |
|
Necrotic laryngitis Clinical Signs
|
-Upper respiratory obstruction
-Fetid breath due to necrosis and tissue death -Respiratory stridor -Can see lesions in the back of the mouth |
|
Metastatic Pneumonia
|
-Low incidence
-Sporadic individual cases only -No prior pneumonia history -Most often seen in neonatal calves --can occur secondary to E. coli septicemia |
|
Caudal Vena Cava Thrombosis Syndrome Pathology
|
1. Rumen acidosis causes ulcerative damage to rumen wall
2. Bacteria invades lesions 3. Bacteria gets into the blood stream and spreads hematogenously to liver and causes abscesses in liver 4.Thrombi form and are released 5. Thrombi travel from hepatic vein to caudal vena cava to heart and lung 6. "Embolic shower" in the lungs, causes necrotic tissue |
|
Caudal Vena Cava Syndrome
|
-Usually seen in cattle more than 1 year old
-Can be seen as increased RR -Epistaxis (nose bleeds) --once nose-bleed is seen, damage is done -Very poor prognosis |
|
Allergic Rhinitis
|
-"summer sniffles"
-Pastured mature cattle -Localized immediate type I hypersensitivity -Causes sneezing nasal pruritus -Becomes granulomatous when chronic |
|
Diaphragm Function
|
-Active Respiratory bellows
-Contracts, moves caudally and creates negative pressure in the chest cavity -Chest moves cranially and dorsally -Sub-atmospheric pressure overcomes airway resistance and elastic recoil of lung -Diaphragm relaxes for expiration --Allows for elastic recoil of the lung and chest wall |
|
Deviated Sternum
|
-Can cause significant difficulty breathing for animal
-Fix by putting sutures around the ribs and sternum --If placing suture around the sternum, start on the side with the heart |
|
Sternal Osteomyelitis
|
-Looks like lytic sternebrae
-Could be neoplasia or infection --Have to biopsy to know for sure |
|
Infective Pleuritis
|
-Antibiotics do not work long-term
-Have to remove infected bone |
|
Bite wounds to the chest
|
-Painful!
-Poor ventilation -Substantial hemorrhage in the lungs can lead to bruising --leads to poor ventilation and ventilation perfusion mismatch |
|
Hypoxia in Thoracic trauma
|
-Secondary to pulmonary parenchymal disease, interpleural disease, and pain
-Pain causes hypoxia |
|
Flail Chest
|
-Ribs broken in 2 places
-Segment moves paradoxically to inhalation/exhalation -Treat animal for pain -Can wire rib ends back together -Can also sp |
|
Rib Neoplasia
|
-Determine if chondrosarcoma cs. osteosarcoma
--Do not remove osteosarcoma --chondrosarcoma removal has good prognosis -Look for metastatic disease -Will see displaced ribs with periosteal reaction on radiographs --trachea may also be deviated |
|
Removing Rib Chondrosarcoma
|
-Remove entire section of ribs
-Hard to close, have to use mesh and stitch mesh to body wall -Put omentum over the mesh |
|
Septum transversarium
|
-Forms central tendinous region of diaphragm
-Failure of fusion or incomplete formation results in peritoneo-pericardial hernia |
|
Holes in the Diaphragm
|
1. Caval foramen: caudal vena cava
2. Esophageal Hiatus: esophagus 3. Aortic Hiatus: aorta, azygous vein, hemiazygous vein, lumbar cistern of the thoracic duct |
|
Anatomy of the Diaphragm
|
-Musculotendinous partition
-Central tendinous section and 3 separate muscles --costal --sternal --lumbar |
|
Embryology of the Diaphragm
|
-Diaphragm originates from cervical region in the embryo
--C5-C7 -Origin of phrenic nerve roots is C5-C7 -Transverse septum eventually forms central tendon -Dorsal mesentery of the esophagus forms crura of diaphragm -Failure of fusion or no complete formation of transverse septum results in peritoneo-pericardial hernia |
|
Peritoneopericardial Hernias
|
-Failure of the transverse septum to form properly or fuse medially
-Herniation of abdominal viscera into pericardial sac -Sternal abnormalities -Cranial abdominal wall defects -Umbillical hernia -Cardiac defects -Usually have other mid-line defects --VSD |
|
Surgical Repair of Peritoneopericardial Hernia
|
-Clip all the way to the neck
--want to have option of entering thoracic cavity if necessary -Usually will just be in the pericardial space, not pleural space |
|
Diaphragmatic hernia Causes
|
-Mostly traumatic (77-85%)
--kicked, hit by car -5-10% are congenital -Few are unknown cause -Sudden increase in intra-abdominal pressure with glottis open will cause herniation --Normal pressure is 7-20cm --greater than 100cm will cause herniation |
|
Diaphragmatic Hernia Types
|
-Male dogs 1-3 years old are greatest risk
-Costal muscles are most frequently ruptured -Circumferential rupture 40% -Radial rupture 40% -Combination 20% |
|
Diaphragmatic Hernia Sequelae
|
-Interferes with cardiorespiratory function
--things in thorax that should not be there prevent lung from inflating fully -Incarceration, strangulation, or obstruction of bowel -Hepatic venous stasis due to pressure change -Necrosis -Bile stasis |
|
Downward spiral of Diaphragmatic Hernia
|
-Dyspnea causes swallowing of air
-Air in stomach inflates stomach, stomach takes up more space in thoracic cavity -Less space for lungs to expand, more dyspnea -More dyspnea, more air is swallowed |
|
Clinical Signs of Diaphragmatic hernia
|
-No clinical signs are pathognomonic
-Dyspnea and exercise intolerance present in 40% of cases -GI signs including vomiting and weight loss are common -ON Auscultation heart sounds are muffled or louder on one side compared to the other |
|
Radiographic Signs of Diaphragmatic hernia or issues
|
-Cannot see the line of the diaphragm where it should be
-Can see gas or intestines in the thoracic cavity -Can do sterile water-soluble iodine contrast study --inject iodine into the abdomen, and if it ends up in the thoracic cavity something is wrong --Abdominal cavity should not communicate with the thoracic cavity -Barium swallow with fluroscopy |
|
Diaphragmatic hernia Surgery
|
-Higher mortality of surgery is performed within 24 hours of injury?
-Only an emergency procedure if severe cardio-respiratory compromise occurs -If you can't get something to go where you want it to, make a bigger hole --do not pull harder, may be fused to a delicate structure |
|
Anesthesia for Diaphragmatic hernia cases
|
-Do not forcibly reinflate lungs that have been chronically collapsed due to changes in pressure!
-Will result in reperfusion pulmonary edema -Keep at 10-15cm H2O -Need someone who is good at anesthesia, need to be prepared for collapsed lungs with diaphragmatic hernia surgery |
|
Post-operative Management of patient with Diaphragmatic hernia
|
-Respiratory Function: monitor and treat
-Chest tube management -Pain --epidural catheter --intrapleural bi |
|
Hiatal hernia
|
-Stomach slides up into the chest cavity
-Usually occurs because esophageal hiatus is too big --should be small enough to prevent stomach from moving into the thorax -Zone of high pressure at distal end of esophagus (caudal esophageal sphincter) also prevents movement -Diaphragmatic crus, angle of the esophagus at the cardia, gastric mucosal folds, and phreno-esophageal membrane also prevent movement -Can be congenital, post-traumatic, or due to respiratory onstruction |
|
Clinical signs of Hiatal hernia
|
-GI signs: vomiting and regurgitation
-Abnormal/decreased esophageal motility --Occurs secondary to GE reflux and esophagitis? -Aspiration pneumonia |
|
Upper airway Obstruction and Diaphragmatic hernia
|
-Severe upper airway obstruction can cause a change in pressure
-Decreased pressure at caudal esophageal sphincter will allow stomach to be pulled into chest cavity |
|
Diaphragmatic hernia Important factors
|
-Underlying disease?
-Is animal showing clinical signs? -Loss of functinon of caudal esophageal sphincter? -Reflux esophagitis? -Esophageal ulceration? -Is medical treatment working? |
|
Thoracic Surgery in the Small Animal
|
-Often done in clinical veterinary practice
-Indications: --repair congenital and acquired cardiac defects --esophageal conditions --diseases of the conducting airways --Pulmonary and pleural disease --Conditions of the thoracic wall |
|
Special considerations for Thoracic Surgery
|
-Surgeon needs intimate knowledge of anatomy and physiology of the thorax and associated structures
-Need special attention with anesthesia -Procedures are technically challenging, but can be very rewarding |
|
Bite wound with Normal thoracic Radiographs
|
-Mild dyspnea
-No evidence of pneumothorax -No evidence of pulmonary contusions -Can stabilize and re-check -Normal thoracic radiographs do not rule out substantial thoracic pathology in bite wound cases --bite wounds do not show up on radiographs! |
|
History of the patient with thoracic disease
|
-Change in respiratory effort
-Change in attitude (more lethargic) -Change in appetite -Vomiting or regurgitation -Weight loss -Need to check out heart and respiratory systems both |
|
Physical Examination of a Patient with thoracic disease
|
-CRT, compare crainal and caudal aspects of the body
-Arterial pulse rate and quality -Jugular venous distention or pulsation -Auscultation of the thoracic cavity -Tracheal irritation |
|
Cyanosis and Hb curve
|
-Cyanosis occurs when 33% of Hb is unsaturated
-Pulse Ox will be 66! -BAD news! very poor perfusion! |
|
Diagnostic tests for patient with thoracic disease
|
-CBC/Chem
-Thoracic radiography |
|
Pre-operative considerations for a patient with Thoracic Disease
|
-Stabilize cardiac disease prior to surgery
-Tap pneumothorax and pleural effusion before surgery -Restrain animal with caution, struggling increases O2 consumption -Take pre-operative arterial blood gas to rule out pneumonia or pulmonary metastatic disease in hypoxic animals |
|
Pre-operative considerations for patient with Thoracic Disease
|
-Perioperative antimicrobial drugs
-Availability of blood products -Owners give informed consent -Well-prepared and capable anesthesiologists -Well-prepared and capable OR staff -Appropriate instruments and skill level of surgeon |
|
Anesthesia of a patient with Thoracic Disease
|
-Give supplemental O2
-Rapid induction and intubation -Monitor closely with pressure gauge, BP monitor, and venous access -Epidural with straight morphine can give good pain relief |
|
Effects of Thoracotomy
|
-Loss of negative intrapleural pressure prevents normal lung expansion and decreases venous return to the heart
--need sub-atmospheric pressure for venous return to the heart -Positive-pressure ventilation restores ventilation --further decreases cardiac return -Will have atelectasis of dependent lung |
|
Thoracic Wall Anatomy
|
-13 pairs of ribs
--Ribs 1-9 articulate with sternum --ribs 10-12 form costal arch --13th rib is "floating" -Intercostal muscles -Latissimus dorsi -Serratus ventralis, serratus dorsalis -External abdominal oblique muscle -Scalenus |
|
Common surgical approaches to the thoracic cavity
|
-Lateral intercostal thoracotomy
-Lateral thoracotomy with rib resection -Median sternotomy -Trans-diaphragmatic -Trans-sternal -Rib pivot |
|
Lateral Intercostal approach to Thoracic Cavity
|
1. Skin incision
2. Latissimus dorsi incision 3. Scalenus incision and elevation --attached to the 5th rib 4. Serratus incision and elevation 5. Intercostal incision 6. Pleural incision |
|
Lateral Intercostal Closure
|
1. Place thoracostomy tube
--secure properly with careful connections 2. Pre-place 4-6 circumcostal sutures 3. Use rib approxmator or tension on sutures 4. Repair muscles cut during approach 5. Aspirate thoracostomy tube once a seal is formed 6. Light bandage after skin closure |
|
Lateral Rib Resection
|
-Remove a rib for more room
-Enter as for a lateral intercostal thoracostomy -Elevate periosteum and cut rib -Incise periosteum and parietal pleura -Close periosteum and pleura with simple interrupted sutures |
|
Median Sternotomy
|
-Useful when need to get to both sides of the chest
-Ventral midline skin incision -Divide pectoral muscles along the midline -Incise the sternebrae exactly down the midle -Leave either caudal or cranial 2 sternebrae intact when possible -Close sternum securely with 18 gauge surgical wire |
|
Post-operative care and monitoring of a Thoracotomy patient
|
-Balanced electrolyte solution at 4-8 ml/kg/hour
--fluid replacement therapy -PCV/TS/Azo/Dextrose every 4-6 hours -Arterial blood pressure -Mucous membranes and CRT -Aspirate chest tube every 2-4 hours or put on continuous pleural drainage --5-10 ml/kg/day --if getting blood out, check PCV, low PVC no big deal -Check respiration rate and effort -Urine production -Continuous or intermittent ECG -Arterial blood gas to check ventilation, pulmonary function, and acid/base -Pulse oximetry and O2 saturation -Auscultation of the chest -Continue analgesic protocol, manage pain -Nutritional support of needed (feeding tube) -Encourage ambulation or turn patient regularly to improve ventilation -Gradually reduce intensity of care and animal improves |
|
Observing Equine Respirations
|
-Eyes and ears are key
-Check respiratory effort --depth --inspiration vs expiration --paradoxical breathing --Asymmetrical breathing -Stridor and Stertor -Check mucous membranes --should be pale pink |
|
Stethscope as a tool for Equine Respiratory Assessment
|
-Sensitivity is poor in the adult, animal is too big
-Foal auscultation is fair to good -Can use re-breathing exam to induce respiratory sounds --Hypercapnia (NOT hypoxia) --Increases respiratory depth and rate |
|
Normal Equine Respiratory Auscultation
|
-Should hear bronchovesicular sounds
-Should not hear crackles, wheezes, radiating heart sounds -Inspiration should be bigger than expiration -Dorsally sounds should be suiet -Increased RR will increase level of respiratory noise |
|
Radiating heart sounds
|
-Indicates pleural fluid is present
-Fluid allows radiating heart sound |
|
Ultrasound for Equine Respiratory Evaluation
|
-Very good at evaluating the pleura
--pleural effusion --Superficial abscesses --Consolidation of alveoli --Pneumothorax -Easy to do! -Poor for aerated parenchyma -If lung is filled with gas, cannot see anything on ultrasound |
|
Ultrasound Specifics
|
-2 White lines: pleural surfaces
--slide against each other when the animal breathes -As lungs become less aerated and more consolidated, will see more details on ultrasound --comet-tails --abscesses --consolidated lung --Pleural effusion and fluid |
|
"Triangle of Death"
|
-Caudodorsal aspect of equine lung
-If animal is sick, will just see a small triangle between vena cava, diaphragm, and heart silhouete -Bad news! Indicates disease! |
|
Trans-Tracheal Wash
|
-Test for bacterial Pneumonia
-Good test if disease is in specific part of the lung, will get effluent from entire lung --focal lung disease --gets a pooled sample from the entire lung -Best sample for culture -Use needle or endoscope, put sterile saline into lungs at carina and aspirate |
|
Bronchoalveolar Lavage
BAL |
-Use for Heaves, EIPH, fungal pneumonia, silicosis
-Put scope or Bivona tube into distal bronchus --add large aliquot of saline and aspirate -Only samples a random, small portion of the lung -Great for GLOBAL lung disease --ideally the whole lung is affected in the same way, so any focal sample will have the same bugs -NOT a sterile procedure |
|
Pulmonary Function Testing
|
-Tests for Recurrent Airway Obstruction or inflammatory Airway Disease
-Shows how "twitchy" airways are |
|
Lower Airway Disease
|
1. Infectious
--viral, bacterial, fungal --Most common lung disease 2. Inflammatory --recurrent airway obstruction/Heaves --Inflammatory Airway Disease 3. Toxic --perilla mint, silicosis 4. Neoplastic --primary or metastatic neoplastic disease |
|
Equine Influenza
|
-Influenza A virus, H3N8 strain
-Lots of genetic divergence, makes vaccination difficult --be sure to use most current vaccine when vaccinating -Generally affects young animals -48 hour incubation period -Rarely fatal -Treatment: rest! --one week for every day of fever --virus will resolve on its own with rest --DO NOT give antibiotics unless concurrent bacterial infection is present |
|
Equine Influenza Clinical Signs
|
-Thin nasal discharge
-Cough -Temperature, febrile patient -Crackles in lung -Increased RR |
|
Things Contributing to a Problem List
|
-History
-Physical Exam -Bloodwork |
|
Equine Influenza Diagnostics
|
-Ultrasound: should see comet-tails indicating pleural roughening
--fibrin tags, thick pleura -Radiographs -Nasal Swab |
|
Equine Influenza Control
|
-Vaccines are generally poor, not very useful
--short duration, high genetic variation -intranasal and IM vaccines exist -Start foal vaccination at 6 months -Be sure to give most recent version of the vaccine for most effective protection! |
|
Equine Herpes Virus 1 and 4
|
-Looks a lot like equine influenza on clinical presentation
-EHV 4 is less severe, respiratory signs only -EHV 1 can cause abortion storms, neonatal death, myeloencephalopathy -Reportable disease! REPORT!! |
|
Equine herpes Virus Clinical Presentation
|
-Looks a lot like Equine Influenza
-Biphasic fever -Cough, nasal discharge -EHV4 can also have abortion storms, neonatal death, myeloenceophalopathy |
|
Equine herpes Virus Pathogenesis
|
-Infects Respiratory epithelium
-Causes lymphocyte viremia -Latency in lymph nodes -Most horses are seropositive -Young adults are very contagious |
|
Equine Herpes Virus Treatment
|
-Rest, rest rest!
--one week for every day with fever -Do not give antibiotics, will not do anything -Vaccine for control, give every 6 months --inactivated IM injection is generally poor with short protection -EHV1 vaccine cross-protects with EHV4 vaccine |
|
Equine Herpes Virus 2 and 5
|
-VERY common, mild signs
-Are present on diagnostic panels -EHV5 is very common and really not a big deal -Will show up on nasal swabs regularly |
|
Equine Rhinitis Virus A and B
|
-Very common
-Most horses are seropositive by early adulthood -Mild clinical signs, mild transient outbreaks -New vaccine exists |
|
Equine Respiratory Viruses
|
-Equine Influenza Virus
-Equine Herpes Virus 1 and 4 -Equine Rhinitis Virus A and B -Viruses kill mucociliary escalator --no primary defense system for the lungs anymore --Have to take time to grow back ciliated epithelial cells -Does not normally result in pleural effusion |
|
Equine Pleuropneumonia
|
-Pleural tissues AND lung parenchyma is affected
|
|
Equine Pleuropneumonia Clinical Signs
|
-Anorexia
-Nasal discharge -Cough can be present sometimes, not consistent -Fever -Tachypnea, increased RR -slightly Increased HR -Pleural pain that can look like colic (fake colic) -Pleural effusion is often present -Crackles can be heard |
|
Equine Pleuropneumonia Diagnostic tests
|
-CBC, should see increased fibrinogen and neutrophils
-Ultrasound -Radiographs -TTW: should see severe suppurative inflammation --degenerate neutrophils --intra and extra-cellular bacteria -Culture TTW |
|
Klebsiella pneumoniae in Horse TTW
|
-Scope contaminant
-Can cause disease, but will probably be present on culture anyway |
|
Pleuropneumonia Pleural Fluid
|
-Often will have different organisms present compared to TTW
-Glucose should be low, bacteria eat glucose -pH will be low, bacteria make environment more acidic |
|
Equine Pleuropneumonia Treatment
|
-Antibiotics
--broad spectrum until culture results are available -NSAIDS in 1st 48 hours --careful of stomach, kidneys --careful to mask fever, need to know if antibiotics are working -Thoracic drains can be used if necessary --also provide nidus for infection and prevents proper ventilation -Supportive care, esp. calories! -Antibiotics, NSAIDS, Hydration, Calories |
|
Equine Pleuropneumonia Antibiotic Choice
|
-Start with broad-spectrum antibiotic
-4 quadrant coverate --gram+/gram- --anaerobic/aerobic -No need for enrofloxacin, no strep zoo effect |
|
Equine Pleuropneumonia and Thoracic Drains
|
-May be necessary with lots o pleural effusion
-Heimlich valve allows one-way drainage -Fibrin can clog tubes, have to put in new tube if clogged -Sometimes fibrin gets to bad lung is glued to chest wall |
|
Pleuropneumonia end of treatment
|
-Can be treated for months
-Re-check with radiographs and ultrasound -Normal fibrinogen or WBC count -Mild cases usually take 1-3 weeks of treatment -Absecesses or necrotic lungs can take 1-6 months to treat --can cost more than $5,000 --must be committed! |
|
Equine Pleuropneumonia Epidemiology
|
-82% of cases occur in young patients
-Often occur after shipping (main risk factor) -Esophageal obstruction is also possible -Anesthesia -Recent viral infections |
|
Strangles
Strep equi equi |
-Occurs in 1-3 year old horses most often, but can occur in any age
-Highly contagious! -Lymphadenopathy, fever, nasal discharge are main signs |
|
Strangles/Strep equi equi Clinical Signs
|
-Fever, nasal discharge
-lethargic -Purulent nasal discharge -Sumbandibular/retropharyngeal lymphadenopathy --swollen lymph nodes --pathognomonic for strangles -Blood work: --high neutrophil count --high fibrinogen, more than 1,000 indicates ABSCESS |
|
High Fever in horses
|
-Virus
-Rikketsial disease -Primary bacterial disease |
|
Nasal Discharge in Horses
|
-Pneumonia
-Viral upper respiratory tract infection -Heaves -Strangles/strep equi equi |
|
Diagnostic plan for Strangles/Strep equi equi
|
-Aspirate lymph nodes
--gram+ cocci in singles, pairs, and chains -PCR/culture is main diagnostic tool` |
|
Strangles/Strep equi equi pathophysiology
|
-Gram+ cocci
-VERY contagious! -Spread by inhalation or ingestion -Fomites can also spread --buckets, water troughs, humans, vets -Not very persistent in the environment -Some horses can become persistent shedders --reservoir in gurrural pouch --can rule out persistent shedder with 3 negative flushes |
|
Strangles/Strep equi equi treatment
|
Mild: let disease run its course
-Fever, mild anorexia, no respiratory distress -Symptomatic therapy -Drain amscesses -Cautious NSAID use Severe: antibiotics -Animal is in respiratory distress, can to tracheostomy -drain abscesses -Give penicillin (kryptonite for strangles!) |
|
Prevention of Strangles/Strep equi equi
Environmental |
-Isolate affected horses until negative
-Use excellent hygiene -Identify persistent shedders/carriers -75% of animals are immune after being infected |
|
Prevention of Strangles/Strep equi equi
Vaccine |
-IM injection is not very effective
-Intranasal modified live vaccine is more effective --give as last vaccine if giving multiple vaccines -Do not give during an outbreak --give a year later --animal has good post-infection immunity --increases risk of purpura |
|
Strangles/Strep equi equi Complications
|
-Metastatic Streptococcus Equi
--bastard strangles --10% of strangles cases --Can cause Abscesses in the abdomen, brain, liver, spleen, kidneys, etc. -Guttural Pouch empyema or chondroids |
|
Bastard Strangles
|
-Dx:
--strep M protein titer --inflammatory blood work --history --ultrasound, CSF tap -Tx: --long-term antibiotics, 1-6 months --Penicillin |
|
Immune Mediated complications of Strangles/Strep equi equi
|
1. Purpura hemorrhagica
--vasculitis and severe edema --Treat with steroids and penicillin 2. Streptococcal myositis --infarcts --rhabdomyolysis with atrophy in quarter horses |
|
Equine Interstitial Pneumonia
|
-Totally hazy chest radiographs
-Can't see vessels at all -Infiltrate or fluid in lung parenchyma -May see dense milliary pattern -DDx: --fungal pneumonia --Neoplasia |
|
Fungal Hyphae in Lungs
|
-Can't really see on tracheal wash
-VERY important when seen on BAL |
|
Fungal Pneumonia
|
1. Primary: specific fungal pathogens present
--Caused by specific fungal pathogens --based on discrete geographical locations --Animal must live or have traveled to these areas 2. Opportunistic/secondary fungal infection: --immunocompromised animals --Aspergillus and other environmental species |
|
Primary Fungal Pneumonia
|
-Blastomyces dermatiditis
-Coccidoides immitis -Cryptococcus neoformans -Histoplasma capsulatum -Non-specific clinical signs --weight loss, exercise intolerance, cough -History of travel to endemic area is key |
|
Primary Fungal Pneumonia Dx and Tx
|
-Dx: must get travel history!
--radiographs, BAL, biopsy --Serum titers only show exposure, not infection -Tx: systemic anti-fungals --very expensive! -Generally poor prognosis |
|
Fungal Hyphae in Tracheal Wash TTW
|
-Do not over-interpret!
-Up to 70% of animals have evidence of fungal elements -Normal finding! -Do not treat with antifungal medication unless good evidence for real fungal pneumonia -Good evidence: --large numbers of intra and extra cellular fungal elements --consistent radiographic changes |
|
Opportunistic Fungal Pneumonia Organisms
|
-Aspergillus
-Candida -Fusarium -Pneumocystis carinii (immunocompromised animals) |
|
Opportunistic Fungal Pneumonia
|
-Usually occurs in immuno-compromised individuals
--cancer --recent GI disease -generally rare occurrence -Clinical signs include cough, tachypnea, fever, adventitial lung sounds, nasal discharge |
|
Opportunistic Fungal Pneumonia Dx, Tx
|
-Dx with radiographs, BAL, biopsy
-Can test immune function of the animal -Tx: systemic anti-fungals --SMZ-TMS for pneumocystis in foals -Prognosis is generally poor |
|
Interstitial Pneumonia
|
-Rare!
-NOT COMMON! -Clinical signs are severe -Can be secondary to sepsis -Usually idiopathic -Inflammation in the lung interstitium |
|
Clinical signs of Interstitial pneumonia
|
-Severe clinical signs!
-Tachypnea -Cyanosis -Fever -Cough -Weight loss |
|
Diagnosis of Interstitial Pneumonia
|
-Radiographs: Diffuse pattern
--looks like ground glass --miliary, little grains everywhere --Nodular pattern possible -BAL, look for DDx of fungal or neoplastic cells -Lung biopsy |
|
Etiology of Interstitial Pneumonia
|
1. Infectious
--acute is viral or bacterial --Systemic inflammation, ARDS --EHV5 --Equine Multi-nodular pulmonary fibrosis 2. Silicosis 3. Toxins: perilla mint from hay 4. Idiopathic |
|
Interstitial Pneumonia Treatment
|
-Corticosteroids
-Anti-virals Prognosis is guarded to poor, 25% success |
|
Rhodococcus equi
|
-Occurs mostly in foals 1-6 months
-Will have respiratory signs AND extra-pulmonary disease -Main clinical sign is chronic suppurative pneumonia with abscessation |
|
Pulmonary Signs of Rhodococcus equi
|
-Fever
-Tachypnea -Adventitial lung sounds, crackles and wheezes -Death! --On necropsy, will see big abscess nodules in lung parenchyma |
|
Extrapulmonary clinical signs of Rhodococcus equi
|
-Diarrhea
-Colic --Typhlitis, inflammation of the cecum --Enterocolitis -Lymph node abscesses -Uveitis -Polysynovitis --not lame, just swollen joints -Septic arthritis or osteomyelitis --rhodococcus seeds into the joints |
|
Rhodococcus Diagnosis
|
-Cytology: look for gram+ pleomorphic rods
-Culture --growth in a dish indicates it is a live organism -PCR: VapA specific --may be too sensitive, VapA is present in dirt -No serology, no correlation between a positive titer and clinical disease |
|
Rhodococus Pathology
|
-Gram+ cocobacillus
-Ubiquitous soil organism, present everywhere -Inhaled into the lung early in life? -Intracellular organism -Shed in feces -Virulent strain is VapA positive --2-23% of all environmental isolates -Not very contagious |
|
Rhodococcus treatment
|
-Long-term antibiotics, gram+
-Macrolides with or without rifampin --azithromycin --Clarithromycin --Tulathromycin -Some resistance is appearing! -May have co-infection and need to add gram- coverage |
|
Venner and Rhodocoddus pulmonary absecesses
|
-Abscess lesions less than 1-10cm do not recover faster with antimicrobials
--do not treat if abscesses are smaller than 10cm! --Contributes to resistance |
|
Rhodococcus Prevention
|
-Screening
-Environmental management (not proven to be effective) -Chemoprophylaxis -Passive immunization (very expensive!) --hyper-immunized serum on days 1 and 30 -Vaccination has not been proven to be effective |
|
Foal Pneumonia
|
-Neonatal pneumonia
-1-6 year old foals --strep equi zooepidemicus, gram+ coccus (normal commensual bacteria in upper airway) --Rhodococcus equi, gram+ coccobacilli -Sporadic presentation -Clinical signs: fever, tachypnea, adventitial lung sounds, hypoxemia, nasal discharge, depression |
|
Foal Pneumonia Dx
|
-Radiographs, ultrasound
-TTW, culture -Inflammatory leukogram -Increased fibrinogen |
|
Foal Pneumonia Tx
|
-Broad spectrum antibiotics
-Ensure Strep coverage --Penicillin --Cephalosporins --SMZ-TMS --Macrolides |
|
Foal Pneumonia Radiographs
|
-Air bronchograms will be present
-Cranioventral lung disease |
|
Recurrent Airway Obstruction
RAO |
-AKA Heaves
-Occurs in older horses, 6+ -Asthma of horses -Horse will NOT die of heaves! --human CAN die from asthma attack -Controllable, not curable disease |
|
Recurrent Airway Obstruction Clinical Signs
|
-Severe, episodic occurrences of difficulty breathing
-Expiratory effort due to stiff lungs -Cough -"Heave line" -May or may not have nasal discharge |
|
Inflammatory Airway Disease
|
-Airway disease second to musculoskeletal injury
-Occurs in 11-50% of thoroughbred and standardbred race horses -Huge issue in young to middle-aged horses -Controllable but not curable disease |
|
Inflammatory Airway Disease Clinical Signs
|
-Cough
-Tracheal mucus -Exercise intolerance -No episodic dyspnea |
|
Inflammatory Airway Disease Diagnosis
|
-Normal physical exam
-No consistent signs on radiographs -Exercise intolerant on treadmill -Tracheal mucous on endoscopy -May have low blood oxygen after exercise |
|
Pathophysiology of Recurrent Airway Obstruction and Inflammatory Airway Disease
|
-Environmental toxins
--dust, mold, endotoxins from manure -Allergies --summer pasture associated heaves -Genetics: warmbloods |
|
Allergies and Recurrent Airway Obstruction and Inflammatory Airway Disease
|
-Skin test: variable results, controversial
-Serum allergy test --RAST, IgE based ELISAs --Not useful for screening for allergen hypersensitivity in horses -Measuring air quality may be helpful, horse may be in a toxic environment -DO NOT LET HEAVEY HORSES NEAR STRAW |
|
Heavey horse exposed to trigger
|
1. Sensitivity of the horse triggers episode
2. Airways are hyper-reactive "twitchy" --triggers cause more bronchospasms, make it hard to breathe 3. Airways become inflamed --neutrophils and pus accumualte in the small airways --airways can become scarred and unable to open 4. Airways become blocked --mucus becomes sticker and stays in airways --bronchospasm makes it hard to breathe |
|
BAL and Inflammatory Airway Disease vs. Recurrent Airway Obstruction
|
1. Normal BAL:
--neutrophils are less than 5% --Eosinophils are less than 0.5% --Mast cells are less than 2% --rest are lymphoctes and macrophages 2. IAD: --more than 5% neutrophils --more than 0.5% eosinophils --more than 2% mast cells 3. RAO: --usually more than 25% neutrophils |
|
Treatment of Inflammatory Airway Disease and Recurrent Airway Obstruction
Management |
-Decrease dust, hay, and allergens present
--get horse away from the triggers -Turnout all day -Leave horse out of stall for more than 2 hours after cleaning, let dust settle -Ensure good ventillation --put horse in stall b door, no hay stored overhead -Soak hay before feeding -Put horse on shavings, not straw -Avoid summer pasture? |
|
Treatment of Inflammatory Airway Disease and Recurrent Airway Obstruction
Corticosteroids |
-Great treatment for inflammatory disease
-Oral steroids induce remission, are most effective --Prednisolone or dexamethasone -Can also go inhaled steroid route --maintain remission --very expensive but with fewer side effects --Not best for a crisis |
|
Treatment of inflammatory Airway Disease and Recurrent Airway Obstruction
Bronchodilators |
-Not to be used as sole treatment
-Albuterol, slameterol, ipratroprium --cannot give albuterol orally, not bioavailable -Use 30 min before exercise or before steroid puffer -Do not give clenbuterol for more than 14 days unless combined with steroids --B2 agonist -Atropine can be used as rescue therapy --can cause severe colic, only give 1 dose |
|
Equine Epistaxis
|
-Unilateral vs. bilateral?
-Chronic, acute, or recurrent? -Recent speed work? -Amount of blood is important |
|
Exercise-induced Pulmonary Hemorrhage
EIPH |
-Huge problem in equine industry
-Occurs in horses that run fast -More common in older horses vs. younger horses -80-87% of horses have some EIPH --pretty common after exercise -Severe bleeding can lead to secondary bacterial infection -Multi-factorial condition --involved airway, vascular, cardiac, locomotory componentds --Contribution of different factors varies between individuals and even in same horse over time |
|
EIPH clinical Signs
|
-Tracheal blood after exercise
-Epistaxis in severe cases -Rarely results in death -May cause poor performance |
|
EIPH Pathophysiology
|
-Alveolar capillaries in caudodorsal lung burst
--capillaries from pulmonary circulation 1. Due to increased transmural pressure --increased pulmonary artery pressure during exercise combined with very negative pleural pressure during exercise --pressure differential between pulmonary arteries and pleural pressure causes rupture 2. Locomotory Pressures --Forelimbs have no bony attachment to axial skeleton --Forces transmitted while galloping creates shear stress and capillary disruption --maximum pressure over caudodorsal lung field Still pretty unknown pathogenesis |
|
EIPH Diagnosis
|
-Blood in the trachea 30-120 minutes post-exercise for 1-3 days
-BAL will show RBCs for up to 7 days --Hemosiderophages for more than 21 days, macrophages are removing RBCs -Radiographs are not sensitive --may see opacity in caudodorsal lung field (indicates hemorrhage in alveoli) |
|
EIPH and Performance
|
-More speed leads to more bleeding?
-Newer studies suggest that EIPH limits performance in thoroughbreds -EIPH associated with better performance in standardbreds |
|
EIPH Treatment
|
-Lots of treatments available
-Furosemide/lasix --give before a race -Dehydration --reduces blood volume, decreases pulmonary alveolar pressure --reduces weight so horses run faster --Also increases blood viscosity, may lead to more shear force? |
|
Furosemide and EIPH
|
-Furosemide decreases incidence and severity of EIPH in thoroughbred horses
-No indication as to how it affects speed! |
|
Equine Pulmonary neoplasia
|
-Rare in horses
-Usually occurs in old horses -Non-specific clinical signs -Diagnose with radiographs, ultrasound, or biopsy -Primary neoplasia is rare, secondary neoplasia is more common --melanoma --gastric squamous cell carcinoma --hemangiosarcoma |
|
Equine Pulmonary Neoplasia Treatment
|
-Palliative care
-Corticosteroids for lymphoma -Get oncology consult |
|
Cough
|
-Sign, not a diagnosis
-Sign of airway disease -Can be a diagnostic and therapeutic challenge -Acute cough vs Chronic cough --chronic cough lasts more than 2 months |
|
Pathophysiology of Coughing
|
-Non-specific response to airway inflammation or stretch
-has lots of triggers -Viral, bacterial, parasite infections -Allergic hypersensitivity reactions -Foreign material -External compression, something pressing on the airway -Structural abnormalities, collapsed trachea -Cough reflex backs up other airway protective mechanisms --reflex removes exudates or foreign material from lungs |
|
Cough Reflex
|
-Triggered locally in airways
-Controlled by cough centers in the brainstem -Can treat locally in airway or in brainstem -Occurs at maximal inspiration -Initial forced exhalation against a closed glottis -Sudden opening of the glottis produces rapid expulsion of air under pressure -Simultaneous contraction of bronchial smooth muscle narrows airways, increases force of expulsion of material -moves stuff crainially to mouth to be swallowed |
|
Types of Coughing
|
-Have to hear cough so it can be categorized
-Productive cough: --soft, moist --often followed by swallowing --helpful cough! Getting stuff to move up and out -Non-productive cough --harsh, high-pitched, honking cough --loud and rough --Paroxysmal --not helpful to the animal, want to suppress |
|
Initial Evaluation of the Coughing Dog
|
-Hx:
--exposure to infection (kennel cough, travel) --Exposure to noxious substances (smoke inhalation) -Signalment: --Age --previous infections --degenerative disease --breed predispositions |
|
Obesity and Airway Disease
|
-Obesity exacerbates airway disease
-Dogs accumulate fat in neck area, puts additional pressure on the trachea |
|
Observation of the Coughing Patient at Rest
|
-Airway disease: patient may be normal at rest
-Pulmonary disease, excluding edema: patient may be abnormal at rest --increased RR and effort at rest |
|
Physical Exam of the Coughing Dog
|
1. Inside mouth:
--pharynx, tonsils, gag reflex 2. Palpation: --airway, including cervical vertebrae --Look for compressibility and masses --Evaluate for cardiac thrill 3. induce cough via tracheal compression --characterize cough as productive, non-productive, or honking 4. Check for jugular venous distention |
|
Coughing Dog Auscultation
|
-Heart: Evidence of cardiac disease?
--murmur or arrhythmia -Lung fields --increased bronchovesicular sound --Crackles --Wheezes ("squeaks", indicate stenosis and primary bronchiole disease) -Cervical airway: --increased upper airway noise at the site of compression Are noises coming from within the lungs or from the airway and neck? |
|
DDx of coughing in dogs
|
-Infectious tracheobronchitis
-Collapsing trachea -Chronic bronchitis -Compression of the left mainstream bronchus -Left-sided congestive heart failure -Bronchiectasis -Bronchopneumonia -Inhaled Foreign Body -Tracheal or bronchial neoplasia -Parasites -Heartworms -Laryngeal paralysis -Brachycephalic airway syndrome -Fungal infections -Pulmonary inflammatory disorders |
|
DDx of coughing in Cats
|
-Feline Asthma (top Ddx)
-Chronic bronchitis -Bronchiectasis -Emphysema -Parasites -Aspirated foreign bodies -Bronchopneumonia -Pulmonary fungal infections -Pulmonary toxoplasmosis -Cranial mediastinal masses -heartworms |
|
Cardiogenic causes of Coughing
|
-Congestive heart failure
-Left mainstem bronchus compression by L atrium |
|
Airway causes of coughing
|
-Collapsing trachea
-Chronic bronchitis -Foreign body -Neoplasia |
|
Pulmonary causes of Coughing
|
-Pneumonia
-Pulmonary thromboembolism -Fibrosis -Neoplasia -Other |
|
Airway causes of coughing in a Cat
|
-Feline asthma
-Chronic bronchitis foriegn body and neoplasia are less common |
|
Congestive Heart Failure and Coughing
|
-Pulmonary venous congestion
--mitral valve disease --cardiomyopathy --arrhythmia -increased hydrostatic pressure in lungs and lung vessels due to backup from the heart -Increased hydrostatic pressure leads to increased vascular fluid flux -Edema occurs when the pulmonary lymphatic system is overwhelmed |
|
Dx of left sided congestive Heart Failure
|
-Pulmonary Edema
-Acuscult a murmur and arrhythmia -Auscultation of moist crackles -Presence of hypoxia or cyanosis -Radiographs show cardiomegaly, alveolar disease, and pulmonary venous congestion --enlarged, tortuous pulmonary vein -Can do echocardiography |
|
Left mainstem Bronchus Compression
|
-Left atrial enlargement causes direct compression of the left mainstem bronchus
-Leads to harsh, dry cough without pulmonary edema |
|
Treatment of Coughing due to heart Disease
|
1. Pulmonary edema:
--diuretics --vasodilators --inotropes --anti-arrhythmics 2. Airway compression: --manage like a collapsing trachea or chronic bronchitis |
|
Tracheal collapse
|
-Progressive degenerative disorder of the trachea
-Predominantly in small breed dogs --mini poodles, yorkies, pomeranians |
|
tracheal Collapse Pathology
|
-Cartilage of the tracheal rings is misshapen and softer than normal
-Abnormal cartilage matrix in trachea -Deficient GAGs --Decreased number of chondrocytes -Tracheal dorsal membrane is floppy and stretched -Variable mucosal inflammation results in edema and mucus accumulation -more coughing leads to worse inflammation |
|
Tracheal Collapse Categorization
|
-Categorized based on location and severity
-Grade 1: 25% obstruction -Grade 2: 50% obstruction -Grade 3: 75% obstruction -Grade 4: 100% obstruction -Extrathoracic -Thoracic inlet -Intrathoracic -Mainstem bronchus -Location affects treatment |
|
Tracheal Collapse Diagnosis
|
-Clinical signs
-Thoracic and cervical radiographs -Fluoroscopy -trachealbronchoscopy |
|
Chronic bronchitis
|
-Chronic inflammation of the airways caused by allergy or idiopathic cause
--allergy: eosinophils --idiopathic: neutrophils, most common -Inflammation is focused on the Bronchi -Common problem and difficult to diagnose -Inflammation causes: --increased mucus and cellular infiltrates --abnormal mucociliary escalator function --Mucosal edema and hyperemia |
|
Diagnostic testing for Chronic bronchitis
|
-Take radiographs to exclude other causes of chronic cough
-Do non-invasive tests first -Test for heartworm and lungworm parasites -Bronchoscopy to evaluate for collapse -Can sample from airway for cytology or culture |
|
Bronchiectasis
|
-Dilated airways
-Cylindrical is bad news, decreases mucociliary escalator function --get accumulation of mucus -Can be acquired or congenital -Acquired from sequela of chronic airway inflammation -Delayed clearance due to poor mucociliary function -Affected animals are predispised to recurrent infections --may require intermittent or continuous antibiotic therapy |
|
Cor Pulmonale
|
-Right heart enlargement that results in lung pathology
-Chronic long-standing lung disease and inflammation |
|
Anti-tussives
|
-Centrally acting opiate derivatives
-Suppress coughing and allow patient to exercise and sleep -Mild sedation can also be helpful -Dosing frequency is adjusted to effect -Do not use anti-tussives with a productive cough, want animal to get stuff up and out! -Anti-tussive agents: --hydrocodone --butorphanol --dextromethorphan |
|
Bronchodilators
|
-Have variable efficacy
-Good idea in general, improves oxygenation --may not change frequency of the cough or life expectancy -Give it a try, and if ti does not work discontinue -Methylxanthines (aminophylline) -B2 agonists cause bronchodilation (terbutaline, albuterol) |
|
Corticosteroids in treatment of coughing
|
-Anti-inflammatory doses can be beneficial during acute crisis
-decrease airway inflammation and mucus accumulation -Doses should be minimized and used to effect -Prednisone -Not a cure, manages disease on a long-term basis |
|
Aerosolized drugs for Dogs with airway disease
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-Not always needed if oral drugs are well-tolerated
-Delivers drug directly to site of disease -Little systemic absorption of the drug -May have insufficient delivery of the drug to most severely affected areas -May be more labor intensive -May be more expensive |
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Inhaled Drugs in animals with Airway Disease
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-Albuterol: can be used intermittently as part of emergency management
--B agonist -Fluticasone: must be given consistently for several days before can see effect --less useful for crisis management --Steroid Good for diabetic animals with chornic bronchitits or a dog with combination of chronic bronchitis and heart disease |
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Coughing due to tracheal collapse, chronic bronchitis, and mainstem bronchus compression
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-Use combination of anti-tussives, bronchodilators, and corticosteroids
--different combination in every dog -Decrease body weight -Minimize inhaled stresses -Minimize exercise and excitement -Use harness instead of a collar -Manage concurrent diseases |