Dog and Cat 10 Flashcards
Canine infectious respiratory disease complex clinical signs and diagnosis (when to investigate)
Clinical signs - 3-5 day incubation - Acute hacking paroxysmal cough worse with: ○ Exercise ○ Excitement ○ Tracheal pressure - Pneumonia rare ○ Puppies ○ Immunocompromised ○ Chronic airway disease Diagnosis - Usually presumptive - history and clinical signs - Investigate if: ○ Not resolving in 7-10d ○ Systemic signs ○ Uncontrolled pathogen in kennel/shelter - Thoracic radiographs, bloodwork - TTW ○ Cytology ○ Cultures/PCRs
Canine infectious respiratory disease complex treatment and complications (treatment for these)
- REST for 7 days ○ no exercise/excitement - Avoid neck pressure ○ walk on harness - Antitussives IF cough frequent/severe ○ not if productive Complications -Systemic signs - Bronchopneumonia -> Young puppies (< 6-8 wks) ○ Bordetella causes 50% bronchopneumonia - binding to cilia - mucociliary clearance failure -> Treatment - (C&S based ideally) ○ Doxycycline ○ Potentiated amoxicillin ○ 5d beyond resolution
Canine infectious respiratory disease complex prevention
1) Minimise exposure
- In shelter/kennel environments:
- Isolate puppies and recently boarded dogs from other dogs
- Disinfect cages, bowls, runs etc
- No nose-nose contact
- At least 10-15 air exchanges/hour (good ventilation) and < 50% relative humidity
2) Maintain good general health
- Good nutrition, regular deworming, limit stress
3) Vaccination
- Do not prevent infection and none are completely effective in preventing clinical signs
Collapsing trachea and tracheobronchomalacia what occurs and pathogenesis
- Narrowing of the tracheal lumen due to
○ weakening of the cartilaginous rings
○ and/or redundant dorsal tracheal membrane - and/or bronchial involvement
○ hence ‘tracheobronchial malacia’
Pathogenesis
1. underlying weakeness but trigger altere airway pressure -> weak cartilage flattens, dorsal membrane stretches -> ligament and wall contact -> cough and inflammation (results in more weakened of cartilage) -> also increased mucus and poor clearance which begins again at altered pressure eventually resulting in airway obstruction
Collapsing trachea what are some trigger factors and signalment
Exacerbating factors - Anything causing: ○ Cough ○ Increased respiratory effort ○ Airway inflammation Signalment - Middle-aged toy and miniature dogs ○ Congenital predisposition ○ 50% all coughing dogs will have this condition - Acquired in other dog breeds ○ Chronic inflammation - Rare in cats - not predisposed to cartilage weakness ○ Obstruction generally chronic
Collapsing trachea what are the main clinical presentations in history and physical examination
- History
○ Goose-honk cough
§ Excitement, Exercise
§ Neck pressure
○ Slow progression (years) to dyspnoea with
§ Excitement
§ Stress
§ Overheating - mainly - exercised in heat weather -> present in clinic with respiratory distress - Physical examination
○ Tracheal sensitivity + Extrathoraciccollapse:
§ Inspiratory obstruction, stertor, distress
§ Cough less
○ Intrathoracic collapse:
§ Cough
§ Expiratory wheeze
Tracheal collapse diagnosis what is tricky, how generally diagnosed and teh 3 others ways to diagnose
- Whole trachea is diseased however it is a dynamic disease so certain areas of the trachea will be collapsing depending on the individual
- MOST will diagnosis via clinical presentation
1. Lateral radiographs
○ Cervical (inspiration) trachea collapse
○ Thorax (expiration) trachea collapse
2. Fluoroscopy - video x-ray
○ Elicit cough - may only collapse during coughing
3. Bronchoscopy - very mild collapse
○ Light anaesthesia - won’t cough under anaesthesia
○ Evaluate URT
○ Collect wash samples - possibly secondary infections
What are the 4 main ways of treating tracheal collapse
1) acute stabilisation if in respiratory distress
2) chronic medical management
3) surgical correction of URT obstruction - stenting whole of trachea - 75-90% improvement but salvage as will fatigue overtime
4) manage cocurrent exacerbating conditions
In terms of chronic medical management for tracheal collapse what are the 6 main things involved and percentage that is controlled this way
- Weight loss! - condition score minus 1 -. Can improve clinical signs by 50%
- Avoid:
§ neck pressure
§ excitement
§ exercising in hot weather - Remove potential respiratory irritants
- Antitussives - prevent cough collapse cycle within pathogenesis
§ Long-term, lowest effective dose - Anti-inflammatory glucocorticoids - some needed initially or low ongoing doses
§ Address secondary infection first
§ Side effects of increase appetite therefore weight gain can make it worse -> if so and needs to be on longterm treatment may need to give inhaled corticosteroids - Bronchodilators -> possibly help relieve suffering doesn’t treat
Good control in 71% of cases
Canine chronic bronchitis define, what occurs and pathogenesis
- “Cough that occurs on most days for 2 or more consecutive months in the past year, in the absence of other active disease”
- Bronchial inflammation
Pathogenesis
Infection, allergy, inhalant irritants -> airway inflammation -> proteases, oxidative injury epithelium -> reduced mucociliary clearance -> chronic muscle thickening, fibrosis, epithelial hyperplasia -> retained mucous, inflammation products -> airway inflammation and repeats
canine chronic bronchitis complications and presentation
Complications
- Secondary bacterial or Mycoplasma infection
- Tracheobronchomalacia
- Pulmonary hypertension
- Bronchiectasis
○ Permanent structural airway damage/dilation
Presentation
- slow progression
- loud, harsh cough - dry or productive, possible tracheal sensitivity, often present after stress/excitement, infection, irritation
- usually well - NO HYPOXIC
- often overweight
- increased breaths sounds, crackles, wheezes, expiratory effort and end-expiratory click (TBM)
canine chronic bronchitis diagnosis 3 main ways and what are the general management and prognosis
- Radiograph
○ Can be normal but normally bronchointerstitial pattern - tram tracks and donuts - CT more sensitive
- Tracheobronchoscopy
○ Imaging - see what is going on
§ Inflammation, mucous, casts of mucous (chronic stasis of mucous)
○ +/- BAL cytology and culture (non-degenerate neutrophils - mild inflammatory reaction)
Management - general management
- medications for most dogs
- medication for some cases
- intermittent medication
Prognosis
- Cannot be cured
- Good prognosis for control for signs/good quality of life in most cases
canine chronic bronchitis what are some general management principles and medications used for most dogs
- Weight loss
- Remove irritants/improve air quality
- Reduce excitement/stress
- Maintain good oral hygiene
- Maintain airway hydration
○ systemic hydration
○ +/-humidification via a nebuliser
Most dogs: - Glucocorticoids to control inflammation - side effects not good so want to maintain on low dose - possibly inhaled
- Aminophylline/theophylline - bronchodilator
○ Anti-inflammatory
○ Mucociliary-clearance
○ -> Reduced fatigue
canine chronic bronchitis medication for some cases and what use intermittently
For some cases:
- Antitussives (opiates)
○ Cough incessant, exhausting, ineffective
○ Lowest effective dose
Intermittently:
- Antibiotics
○ Inhaled oropharyngeal flora (gram negatives)
○ C&S best
○ Need to penetrate airways and respiratory secretions (doxycycline)
○ At least3-4 weeks
Feline bronchial disease why cats predisposed 3 main diseases within and differentials
- Cats have very reactive airways
- Many diseases can cause cough, wheeze and respiratory distress
- Airway resistance -> radius to the power of 4 -> largest determinant of resistance
- Diseases within
- Asthma
- Acute bronchitis
- Chronic bronchitis
What are some differentials for coughing cats and the most common
- Allergic bronchitis
- Respiratory parasites
- heartworm disease
- Bacterial bronchitis
- Mycoplasmal bronchitis
- Interstitial pneumonias (rare)
- Carcinoma
- Aspiration pneumonia
- Toxoplasmosis
- Idiopathic feline bronchitis - most common
Idiopathic feline bronchitis most common cause of what and presentation
cough in cats presentation - cough, slowly progressive, systemically well - normal physical exam if NOT having episode - if episode - - Expiratory obstruction ○ Tachypnoea ○ Expiratory dyspnoea ○ Expiratory wheeze ○ Expiratory push \+/-Wheeze, crackles on auscultation
Idiopathic feline bronchitis diagnosis what need to do first and rule out what
1) stabilise first
2) rule out lungworm - haematology, faecal baermann (lungworm), antibody heart worm test
3) radiographs - bronchial pattern, may be normal (if normal CT)
4) endotraheal wash or BAL in referral centers for mycoplasma or lungworm
Idiopathic feline bronchitis treatment program what involved
1) first determine cause - possible allergy - then remove, lungworm - fendendazole 5 days, infection - doxcycline trail, idiopathic - improve air quality
2) most cats need ongoing glucocorticoid +/- bronchodilatory for life (prednisolone slowly taper to good dose)
3) if ongoing signs or intermittent flare up - bronchodilators such as inhaled salbutamol (ventolin)
4) refractory cases/severe - cyclosporin (experimental), crproheptadine (mild bronchodilation), antihistamine (variable)
how to improve air quality for cats
○ Eliminate smoke, aerosols and perfumed products
○ Trial sand or plain clay litter
○ Reduce dust, mould and mildew
§ clean carpets, furnishings, bedding, drapes
- Clean heating units/ducts, change air filters regularly
- Use a vacuum with a HEPA filter
- Use an air purifier
Outcome of idiopathic feline bronchitis
- If not responding… ○ Compliance? ○ Different primary disease. ○ Secondary complication. Prognosis ○ Good for control of signs in most cases, don't expect cure ○ Guarded if permanent airway damage ○ May die during acute asthma attack
In summary what are the treatment options for collapsing trachea, canine chronic bronchitis and feline bronchitis disease
- TBM: antitussives
- CCB: anti-inflammatory glucocorticoids
- FBD: anti-inflammatory glucocorticoids & bronchodilators
Lung interstitial disease what are the common signs and approach for diagnosis
Common - Cough - Tachypnoea - Exercise intolerance - Excessive panting - Increased respiratory effort - Respiratory distress Approach: 1. Thoracic radiographs 2. +/-assess oxygenation 3. Haem/chem/UA
pneumonia what are the 5 main causes and route from most to least common and the distrubution and possible pathogens within
Cause 1. Bacterial - majority 2. Viral 3. Fungal 4. Protozoal 5. Parasitic 1. Aerogenous § Airways not sterile § Aspiration/immune compromise § Cranioventral pattern - gravity dependent § Bacterial/viral -> Bordetella bronchiseptica 2. Haematogenous § Caudal/diffuse distribution § Interstitial origin § Any pathogen § Fungal, protozoal and parasitic commonly through this tract canine lungworm 3. Direct extension § Pleural space § Intrathoracic structures § Bacterial
Bacterial pneumonia wha species common in, how generally arrives, pathogens involved and puppies/kittens and adult why sick
Common in dogs - Aerogenous - Opportunistic pathogens ○ Oral flora ○ Anaerobes(mixed inf.)aspiration/consolidation ○ Mycoplasma spp.† - Bordetella bronchiseptica ○ Primary pathogen Puppies/kittens - virulent organisms (Bordetella) Why adult have pneumonia - ‘stress’ - Lack of immunity
Bacterial pneumonia some predisposing causes, clinical presentation
Predisposing causes 1. Aspiration 2. Reduced mucociliary clearance 3. Immunosuppression 4. Other primary infection 5. Inhaled/migrating FB Clinical signs - Cough (soft, productive) ○ Dogs! - Bilateral mucopurulent nasal discharge - Exercise intolerance - Respiratory distress - Lethargy, anorexia, fever and weight loss Physical exam - Fever (50%) - Tachypnoea or hyperpnoea - Nasal discharge - Focal crackles, +/-expiratory wheeze (auscultation)
Bacterial pneumonia diagnosis what are the 4 ways
evaluate primary disease when stable/recovered 1. Clinical presentation 2. Haematology ○ Neutrophiliawith left shift, toxic change ○ Normal! 3. Thoracic radiographs (3 views) ○ Alveolar pattern ○ +/-consolidation (dependent) ○ +/-bronchointerstitial 4. Cytology and culture ○ TTW - trans tracheal wash - safest way to do this ○ Septic, suppurative cytology ○ Positive culture ○ Gram stain § Guide initial therapy § Unusual organisms
Bacterial pneumonia what are the 4 treatment options and what is contraindicated
1) antibiotics
2) supportive care - airway hydration (humidify), physiotherapy
3) bronchodialtor - cat bronchospasm, dogs expiratory effort
4) oxygen therapy - PaO2 <80mmHg
Glucocorticoids and antitussives are CONTRAINDICATED
What antibiotics use for bacterial pneumonia for mild infection, severe and puppies/kittens and how long treat
- Milder infections: - relatively stable
○ Oral broad spectrum
○ Potentiated amoxicillin or TMS - Severe infections/septic:
○ IV broad spectrum
○ e.g. (potentiated) ampicillin + fluoroquinolone - Pups/kittens (Bordetella):
○ Amoxicillin or doxycycline - Treat at least a week beyond resolution
Bacterial penumonia treatment monitoring and prognosis
Monitor - clinical signs frequently - Haematology and thoracic radiographs ○ q 24-72 hrs initially; ○ 1 week after DC ○ then q 2-4 weeks after DC Prognosis is usually good
Aspiration pneumonia what due to and results in
Inhalation of solid or liquid material into the lungs: ○ Food ○ Gastric content ○ Iatrogenic - feeding tubes § bowel prep solutions § mineral oil § barium § food - Dogs>> cats - Can mimic drowning - Severe chemical injury and inflammation (first 24-48 hrs) - Secondary bacterial infection-75%, often mixed ○ Non-sterile fluid ○ Oropharyngeal flora
Aspiration pneumonia predisposing factors and radiographic changes
Predisposing causes - shouldn't get in health - Oesophageal dysfunction (regurgitation) ○ Megaoesophagus ○ Dysmotility ○ Oesophagitis ○ Obstruction - Neurologic, muscular or NM disease ○ Localised (larynx/pharynx) ○ Systemic - Depressed mentation - Iatrogenic Radiographic changes - may lag 12-24 hours - severe clinical signs - localised (cranioventral) crackles - signs of primary disease
Aspiration pneumonia treatment what are the 4 options and prognosis
- Suction
○ If observed and unconscious
○ No lavage! - Pending cultures
○ Broad-spectrum antibiotics,
○ Mixed infections, anaerobes - If respiratory distress
○ Oxygen, fluid therapy +/-bronchodilator
○ Nebulisation and coupage - If deteriorating (24-48 hr):
○ Cautious anti-inflammatory glucocorticoids
○ NOT USED IN BACTERIAL PNEUMONIA
- Investigate/manage predisposing causes when stable
Prognosis guarded if disease severe or primary cause not correctable - 80% survival rate
What are the 4 causes of pulmonary hypertension
- Left sided CHF
- Chronic pulmonary parenchymal disease or hypoxia
- Pulmonary thromboembolism
- Pulmonary arterial over-circulation
Idiopathic pulmonary fibrosis (IPF) what breed common in, what occurs, and clinical signs
- WHWT - west highland terriers»_space;SBT, JRT, Cairnterrier, Schipperkes
- Usually middle aged-older
- Severe collagen deposition in the lungs -> pulmonary hypertension
Clinical signs - Exercise intolerance > cough
- Dyspnoea, cyanosis, fainting
- Syncope (PHT)
Exam: - LOUD CRACKLES typical
- Wheezes ~50%
- +/-Tricuspid murmur, split s2 (cor pulmonale)
- +/-secondary polycythaemia
Idiopathic pulmonary fibrosis treatment and prognosis
Treatment
- Corticosteroids (cats) +/-bronchodilators (if wheezing)
- Treat PHT (phosphodiesterase 5)
○ Sildenafil (Viagra) - increase blood flow
○ PDE5 inhibitor. $$$$
- Losartan? (angiotensin II receptor blocker)
○ Antifibrotic
Prognosis
- Guarded (older literature)
- MST 18 mo in WHWT
- Cats 2/3 die within weeks, rest > 12 mo.
Eosinophilic bronchopenumopathy (EB) what diseases does it involve and presentation
- Airways or interstitium ○ Bronchitis/ bronchiectasis ○ Interstitial to nodular to alveolar ○ Large granulomas ○ hilar lymphadenopathy Presentation - Dogs > cats - Young adults - Females - Siberian husky, malamute, rottweiler - 50% peripheral eosinophilia - Allergens -> parasite treatment, diet trials - Productive cough ○ green exudate - Can be acute/severe - 50-90% eosinophils on airway wash
Eosinophilic bronchopenumopathy (EB) management and prognosis
Management
- Exclude HW or pulmonary parasites
- Treatment trial fenbendazole20-50 mg/kg PO SID 14d
- Consider inhaled or food allergens
- Idiopathic cases:
○ Prednisolone1-2 mg/kg/day
○ Taper once clinical, radiographic + haematologic remission.
○ Inhaled fluticasone?
Prognosis fair to good
- Eosinophilic pulmonary granulomatosis may need additional immunosuppression.
- Bronchiectasis some dogs.
Pulmonary neoplasia metastatic how arise, what can look like and examples of multicentric
- Lung capillaries are fantastic filters!
- Diffuse (haematogenous)
- Often multiple nodules
- Can look like - inflammatory nodules - need to rule out - needle aspirate
Screen for primary tumour +/-aspirate nodule
Multicentric - Interstitial-bronchial
○ Lymphoma
○ Mast cell tumour
○ Bronchoalveolar lavage
○ Screen elsewhere first! - Multiple nodules
○ Histiocytic sarcoma
○ Aspirate for cytology
Primary pulmonary neoplasia how common, what most common, where metastasis, clinical signs
- Less common
- Dogs > cats
- Older animals
○ Dogs median 11 yo,. Cats older! - Urban living risk
- Carcinoma most common
- Metastasis
○ Lungs (dogs)
○ Digits (cats) - 30% asymptomatic
- Non-specific signs common - hypercalcaemia, fever possible with neoplasia
- Respiratory signs
○ Cough (Dog)
○ Tachypnoea(Cat)
○ Haemoptysis
○ Exercise intolerance
Pulmonary neoplasia what are the 3 options for treatment
1. Surgical resection - ○ Treatment of choice ○ CT first ○ Screen for primary 2. Chemotherapy ○ Often little impact (primary or metastatic) ○ Intracavitaryfor effusion ○ Metronomic 3. Palliative ○ NSAIDs/corticosteroids ○ Treat secondary infection ○ Antitussives, Analgesia
Pulmonary neoplasia prognosis what need to do and dog and cat MST
Prognosis-stage first! - CT
Dogs
- MST > 12 mo if resectable, low grade - reasonable for surgery
- 1-3 mo if residual disease, high grade.
Cats
- MST 2 yrs if resectable, low grade - reasonable for surgery
- 2.5 mo if high grade.
Pulmonary thromboembolism how generally present, how respond to oxygen, what most common in and how occurs
- Acute onset severe dyspnoea
- Normal thoracic radiographs
- Hypoxaemic
- Poor response to oxygen
- +/-secondary PHT, RSCHF
- Dogs»_space; cats
- Older
- Predisposing to hypercoagulability
Virchow’s triad - thrombosis formation
1. Venous stasis
2. Endothelial damage
3. Hypercoagulability
Pulmonary thromboembolism what are the associated diseases and risk factors
Associated diseases - NEED TO FIND AND TREAT PRIMARY DISEASE - Immune-mediated haemolyticanaemia - Protein-losing nephropathy - Hyperadrenocorticism - Heartworm disease - Cardiac disease - Neoplasia Risk factors - Veterinarians can do this - IV catheters - Excess corticosteroid - Cytotoxic agents - Recent surgery - blood transfusion
Pulmonary thromboembolism what are hte 3 main treatment options and prognosis
1. Supportive - hope that the clot dissolves ○ Oxygen ○ Cautious fluid therapy ○ Bronchodilator ○ +/-sildenafil (PHT) 2. Thrombolytics - generally not used 3. Thromboprophylaxis - given ○ Platelet inhibitors § Aspirin, clopidogrel ○ Factor inhibitors § Heparin, warfarin. § Rivaroxaban? Prognosis is guarded depending on severity and cause
Pulmonary oedema what are the 4 main mechanisms for formation
- Reduced plasma oncotic pressure
○ hypoalbuminaemia - Increased pulmonary vascular pressures - most commonly
○ CHF, fluid overload - Lymphatic obstruction
- Increased vascular permeability - below
○ Acute lung injury
Non-cardiogenic pulmonary oedema wha are the 3 main causes and causes within
- Acute lung injury ○ Inhaled toxins § Smoke, aspiration, 02 ○ Systemic toxins/drugs § Cisplatin (C), Paraquat ○ Trauma § Lung or major body ○ Major systemic illness § Sepsis/SIRS, DIC - Acute CNS injury/electrocution - URT obstruction - choking
Non-cardiogenic pulmonary oedema treatment and prognosis
Treatment - Cage rest/low stress - +/-cautious sedation - Oxygen - May need ventilation with PEEP - hold alveoli open - critical ICU patients - Furosemide (CRI) - may help with shifting fluid - Care if fluids are needed - +/-bronchodilators (care) - +/-glucocorticoids? - TREAT THE UNDERLYING DISEASE where you can Prognosis - Guarded to grave - Better for neurogenic ○ Resolve over 48-72 hrs.
Pleural effusion what are the 4 ways it occurs and the 3 main occupiers
Pleural effusion how occurs
1. Increased capillary hydrostatic pressure
2. Increased vascular permeability
3. Decreased capillary oncotic pressure
4. Impaired lymphatic drainage
Pleural space occupiers
1. Air -> traumatic, spontaneous pneumothorax
2. Fluid -> transudates, modified transudates, exudates
3. Soft tissue -> diaphragmatic hernia, thoracic wall tumours
Pleural space clinical presentation what find hands off, auscultation and historical clues
Hands off:
- Tachypnoea
- Shallow breathing/decreased chest excursions (restrictive)
- Paradoxical abdominal breathing (PAM) - inward movement of abdomen during inspiration
- Dyspnoea & orthopnoea
Auscultation:
- Dull/quiet breath sounds dorsally (air) or ventrally (fluid/soft tissue)
- Abnormal sounds (e.g. gut sounds)
- Displacement of heart & lung sounds
Historical clues:
- Trauma?
- Rat bait exposure?
- Known dz? Heart (cat)
- Working dog?
Thoracocentesis 6 steps, what guided by and contraindications
- Procedure: Simple & life-saving
1. Patient: O2& minimal restraint, sit or sternal, IV catheter for low dose sedation if needed
2. Assemble equipment (sterile gloves, hyperdermic needle, 3-way tap, collecting dish, EDTA tubes) & prep patient (wide clip over 7-9th intercostal space)
3. Aim 7-9thintercostal space (8th intercoastal space)
4. Cranial to the rib - right angle to the chest wall, ventrally or caudally direct needle
○ Pneumothorax –dorsal third
○ Effusion –ventral third
5. Aspirate until negative pressure
6. Collect samples
US guided: - Aim for largest pocket & avoid heart
Contraindications - diagrammatic hernia without pleural fluid, friable lungs,
Pure transudate pleural effusion what is the cause and 4 main differentials
Causes - Decreased capillary oncotic pressure DUE TO Differentials 1. Hypoalbuminemia 2. Fluid overload 3. Right CHF 4. Left CHF (cats)
Modified transudate what are the 3 main causes and differentials
Causes - Increased capillary hydrostatic pressure - Impaired lymphatic drainage - Increased vascular permeability Differentials - Chronic CHF (dogs R>L, Cats R and L, pericardial) - Pericardial effusion - Neoplasia - Lung lobe torsion - PTE (pulmonary thromboembolism) - Dirofilariasis - Diaphragmatic hernia
Exudate pleural effusion what are the 4 main causes and 2 types
- Chylothorax
- Haemothorax
- Neoplasia (or modified transudate)
- Pyothorax
Non-septic - non-degeneration neutrophils
Septic - degenerate neutrophils
Chylous exudate colour, what rich in and causes
○ Milky white or pink
○ Lymphocyte rich
○ Lipid rich
§ Triglyceride concentration TG fluid >TG serum - how to confirm
§ Cholesterol concentration Cho fluid < chol serum
○ Causes
§ Primary -> congenital or acquired (idiopathic) - most common
§ Secondary
□ Heart disease
□ Neoplasia - thoracic duct obstruction, cranial mediastinal mass
□ Trauma
□ Lung lobe torsion
□ Diaphragmatic hernia
□ Cranial vena cava thromboebolism
Chylous exudate treatment options and complications
Medical:
§ Secondary: treat underlying disease process
§ Intermittent thoracocentesis when dyspnoeic
§ Idiopathic: low-fat diet & rutin -> if takes longer than 4 weeks to go away thing surgical intervention
Surgical:
§ Thoracic duct ligation +/- subtotal pericardectomy,
Other: Pleurodesis, pleuroperitoneal shunt, PleuralPort
Complications:
§ Weight loss, electrolyte imbalances, hypoproteinemia, dehydration, fibrosing pleuritis
Haemorrhagic exudate define, does it clot, cytological examination and causes
○ Fluid PCV of at least 25% of peripheral PCV ○ Does not clot grossly (unless peracute - within hours) ○ Cytological examination: § Erythrophagocytosis § Lack of platelets ○ Causes § Coagulopathy - rat bait most common § Trauma § Neoplasia § Lung lobe torsion § Diaphragmatic hernia § Parasitic infection § Iatrogenic
Haemorrhagic exudate treatment options what dependent on
Treatment depending on the cause
i. Oxygen & thoracocentesis: to relieve dyspnoea
□ Only thoracocentesis the amount of blood needed to allow to ventilate (can absorb all the RBC back over the next few days which is important if anaemic)
ii. Fluid resuscitation
iii. Blood products: FFP/pRBCs/whole blood
iv. Vitamin K1 –anticoagulant rodenticide
v. Surgery: penetrating trauma, neoplasia, lung lobe torsion
Neoplastic exudate types of neoplasia commonly involved, cytology and treatment options
○ Types: § Lymphoma, pulmonary carcinoma, mesothelioma, metastatic dz ○ Cytology: § Care with interpretation § FNA or biopsy often necessary for dx ○ Tx: § Surgical resection in some cases § Chemotherapy (IV or intrapleural), radiotherapy (cr mediastinum)
Septic exudate what called, how determined, signalment and clinical signs
○ Pyothorax:
§ Dx on cytology & culture - aerobic and anaerobic culture
§ Haemopurulent & often malodourous
§ Degenerative neutrophils and intracellular bacteria
○ Signalment:
§ Younger animals
§ Hunting/working: Labs, Springer Sp, B Collies, GSD, Pointers
○ Additional clinical signs:
§ Cough (<30%)
§ Fever (50% cats not pyrexic)
§ Severe: signs of SIRS or sepsis (40% cats)
Septic exudate common causes in dogs and cats and diagnosis
§ Most common in dogs - Inhaled migrating FB, penetrating thoracic injury, ruptured lung abscess
□ Pasteurella, Actinomyces, nocardia, enteric bacteria
§ Most common in cats - parapneumonic spread, penetrating thoracic wounds (cat bits), FB migration
□ Pasteurella, clostridium, fusobacterium and enteric bacteria
○ Diagnosis - thoracentesis, radiograph, CT - best to determine if surgical indication
Septic exudate what are the 2 treatment options that need to occur and when is srugery indicated
1) antimicrobial therapy - broad-spectrum initially IV (amoxicillin) then adjust according to culture results, usually 4 weeks coarse
2) tube thoracostomy - chest drains - well tolerated - require 24 hour monitoring, intermittent vs continuous
When is surgery indicated
□ Cats - most non-surgical disease, often just medical treatment
□ Dogs - more likely to have surgical disease, medical may work in some dogs, BUT surgery intervention is more common
□ Both species - lack improvement despite medication 3-7days, evidence of foreign body, pulmonary or mediastinal lesions, isolation of Actinomyces
Air pneumothorax what are the 2 things it results in
1. Increased intrathoracic pressure: ○ Lung collapse ○ Decreased venous return to the heart ○ Increased pulmonary arterial pressure 2. Hypoxemia develops: ○ Ventilation-perfusion mismatch ○ Impaired gas exchange ○ Increased pulmonary shunting
What are the 3 types of pneumothorax
1) open - communication
2) closed - no communication
3) tension pneumothorax - closed - intrapleural pressure > atmospheric pressure
What are the causes of closed pneumothorax and source of air
○ No thoracic wall defect
Causes
§ Traumatic - road traffic accident, bite wounds, stick injury, gunshots
§ Spontaneous
□ Primary - pulmonary blebs or bulae rupture
□ Secondary - bacterial pneumonia, pulmonary abscess, neoplasia, parasitic, fungal granulomas, pneumonitis
§ Iatrogenic - thoracocentesis, chest tube placement, tracheal trauma, oesophageal perforation, FNA
○ Sources of air: lungs, trachea, bronchi, oesophagus, gas forming bacteria within the abscess
Pneumothorax what causes open and tension pneumothorax
- Open - communication
○ Defect in thoracic wall
○ Air entering the pleural space during inspiration
○ Cause - typically secondary to trauma - Tension pneumothorax - closed - intrapleural pressure > atmospheric pressure
○ Pulmonary or pleural flap-like defect acts as one-way valve -> air enters pleural space during inspiration but cannot escape -> trapped air -> CV compromise -> life-threatening and required immediate action -> Thoracocentesis, emergency thoracostomy
What are the 4 diasgnostic techniques for pneumothorax
- Physical examination and history
- Ultrasound
○ TFAST = Thoracic Focused Assessment with Sonography for Trauma
§ Look for glide sign, none= supportive of PTX - Thoracocentesis - diagnostic and therapeutic
- Radiograph
○ Can be identified
SHOULDN’T HAVE TO DO - only when stable
What are the 6 steps in stabilisation of pneumothorax and what occur beyond stabilisation
Stabilisation 1. Oxygen support is vital 2. Thoracocentesis 3. Analgesia & sedation 4. Treat underlying condition 5. Plus any other concurrent injuries e.g. wound management/exploration 6. Supportive care: ○ IVFT, +/-Abx Beyond stabilisation - Place thoracostomy tube if: ○ >2 thoracocentesesin 6-12hrs ○ Failure to achieve –vepressure ○ PTX requiring mechanical ventilation - Surgery indicated: ○ Traumatic PTX: drainage >3-5d ○ Most spontaneous PTX
Diaphragmatic hernia what are the 2 main causes and what results in
Traumatic vs congenital
○ Traumatic - Causes
□ Rapid compression of the abdomen with the majority of energy dissipation cranially
□ Disruption of diaphragm @ weakest points
□ Trauma to caudal thorax & insertions of diaphragm
§ What goes through -> liver, small bowel, stomach, spleen, gall bladder, pancreas
§ Respiratory dysfunction -> increase intrathoracic pressure -> poor lung expansions -> atelectasis -> effusions, possible fractured ribs
§ Hypoxaemia due to: ventilation-perfusion mismatch, hypoventilation
What are the acute and chronic clinical signs of diaphragmatic hernia and treatment
§ Acute □ Significant dyspnoea □ Paradoxical abdominal breathing pattern □ Cardiovascular impairment □ +/- signs of GI entrapment § Chronic □ Weight loss □ Vomiting, Diarrhoea □ Pleural effusion Intermittent discomfort □ Intermittent dyspnoea Treatment - stabilise - fluid, O2, anaglesia - once stabiised - surgery
Mediastinal disease what are the general clinical signs
- Breathing pattern normal or similar to pleural space dz
- +/-Dyspnoea
- Abnormal location of cardiac impulse
- Decreased cranial thoracic compliance (cats)
- Neuro deficits: Horner’s syndrome
- Regurgitation, vomiting, gaggin
Mediastinal disease what are the main causes
1) neoplastic - lymphoma, thyoma
2) non-neoplastic
mass - bacterial abscess, fungal granuloma, cyst, lymphadenopathy
no mass - mediastinitis, pneumomediastinum
Mediastinal lymphoma from where, cell, what common finding, prognosis and treatment
○ From LNs, thymus or both ○ Commonly T-cell ○ Pleural effusion common ○ Dx: Fluid cytology +/-FNA - Dogs- Hypercalcemia(10-40%) - Cats:- Associated with FeLV in younger Prognosis: ○ FeLV–shorter survival times ○ Better pxin older Siamese, 90% remission ○ T-cell, hypercalcemia, mediastinal lymphadenopathy are –vepxindicators in dogs Treatment of choice - chemotherapy
Mediastinal thymoma how common, what leads to, treatment and prognosis
- Rare in dogs and cats
- Older (9-10yrs) espcats
- Paraneoplastic syndrome (PNS):
○ Focal/generalised myasthenia gravis (40% dogs)
○ Polymyositis
○ Skin disease (cats)
○ Hypercalcemia - Treatment:
○ Surgical resection (70%)
○ Radiation
○ Chemotherapy
Prognosis:
○ Slow growing, >6mths if no tx
○ Good if no megaoesophagus, >80% live >1y (dogs)
○ PNS may continue or reoccur despite tx
Pneumomediastinum what are some origins of the air and causes mainly in dogs and cats
1. Intrathoracic Oesophagus ○ Trachea ○ Bronchi ○ Pulmonary parenchyma 2. Extrathoracic ○ Neck ○ Abdomen Causes: ○ Spontaneous (rare) vs secondary ○ Dogs: trauma, primary pulmonary pathology, pericardiocentesis, laryngeal surgery ○ Cats: endotracheal intubation (+/-PPV), trauma, endoscopic retrieval of FB
Pneuomediastinum clinical signs and treatment
- Clinical signs: ○ Usually no dyspnoea ○ Subcutaneous emphysema ○ Lethargy, pain ○ Dysphagia, pyrexia (oesophageal rupture) - Treatment: ○ Strict rest ○ Air usually resorbs within 2 weeks ○ Rarely surgical repair required
Dog heart rule what are the 3 lateral and 1 VD for an enlarged heart
Lateral
1. Size of the heart - Two thirds height of thorax from base to apex (yellow line)
2. Cranial to caudal margin of heart -> 2.5-3.5 intercoastal spaces wide
○ Depending on the breed - IMPORTANT ONE
3. Trachea should deviate from thoracic spine at about 40degrees (blue)
VD -
1. heart should be 2/3rds the width of the thorax
Vertebral heart scale how measured and what important to remember about it
- Measure from tracheal bifurcation to apex
- Perpendicular to that - cranial to caudal margin of heart (not including left atrium)
- Place both lines on the Cranial aspect of T4 and count the amount of vertebral units
HOWEVER - large variation between breeds
THEREFORE - do not use as the ONLY way to assess the cardiac silhouette
Cat heart rule what is the main one and what to remember with heart disease
Lateral
1. 5th - 7th rib rule
- Work out distance between cranial boarder of 5th rib and caudal boarder of 7th and the heart shouldn’t be greater than that distance from cranial to caudal
CATS -> can have normal radiographs with severe heart disease
What are the main radiographic changes with cardiac disease
- Alteration to size and or shape of cardiac silhouette
- Alteration to size of pulmonary vasculature
- Radiographic Signs of Cardiac Failure:
○ Pulmonary oedema
○ Peritoneal effusion
○ Pleural Effusion (cats)
What are some lateral and VD radiographic features of cardiomegaly
Lateral
- elevation of trachea
- increased craniocaudal diameter of heart
- Heart greater than 2.3rd height of thorax -> 5 intercoastal spaces wide
- expansion of left atrium into caudal lobar area
- cranial buldging of right heart boarder and increased sternal contact
VD
- Budge at 2-3 o’clock -> enlarged left auricle
- Rounding caudal boarder of the heart
- Occupying more than 2/3rds of the thorax
- cat “valentine shaped” heart
Pulmonary vessels on the lateral and VD projection and what are some differentials for enlarged pulmonary veins
Lateral
- looks for pairs
- Dorsal to ventral - artery, bronchus, vein
VD
- Vessels travelling through caudal thorax
- Veins are central to the arteries
Veins are ventral and central to the arteries
Enlarged Pulmonary Veins Causes
- Mitral insufficiency
- Volume Overload
- Patent Ductus Arteriosus
- Primary Myocardial Disease
- Left Atrial Obstruction (neoplasia, thrombosis)
Enlarged vessels how to tell on the VD and lateral projection and why may you need see it in left sided heart failure
Look at vessels when cross the 9th rib
VD
1. Can be 1.2 times width of the rib when cross the rib
2. The artery and vein should be the same width
Lateral
- Proximal portion of the 4th rib -> harder to do
- May not always be seen in left sided failure
Why?
○ Inability to see veins due to the pulmonary and or pleural opacity
○ Pre-treatment with furosemide
○ Venous constriction due to sympathetic stress
Pulmonary arterial hypertension leading to larger arteries and altering ratio
Enlarged pulmonary arteries how common, 3 main causes and what can cause enlargement of both arteries and veins
Enlarged Pulmonary Arteries - not as common
- Parasitic arteritis - heartworms disease
- Thromboembolic disease
- Chronic lung disease with pulmonary hypertension
Enlarged Pulmonary Arteries & Veins
- Iatrogenic Fluid Overload
- Left to Right Shunting
- Fluid Retention
- Peripheral Arterio-venous Fistula
What are 4 differentials for small pulmonary vessels
Small Pulmonary Vessels
- Hypovolaemia
- Right to Left Shunting
- Severe Pulmonic Stenosis
- (Pulmonary Overinflation)
Assessment of heart with echo what need to assess
- can look at chambers relative sizes and the function
- Aorta to atrium ratio - determine whether enlarged -> Atrium should be the same size of aorta 1-1.2 times
Enlargement of atrium and ventricle what see on radiograph
Atrium - increase opacity in caudal areas - left atrial wedge on lateral view - valentine hear appearance in cat Ventricular - straightening of caudal boarder - generally occurs with left atrial enlargement
right ventricular enlargement what are the 2 differentials and radiographic finding
- Pulmonary hypertension
- PDA
- Two budges from aorta and main pulmonary artery - PDA
What are some radiogrpahic findings of cardiogenic pulmonary oedema - heart failure
- Increase opacity in the caudodorsal lungs
- Large heart
- Can also have pleural effusion in failure
once determined the animal is in heart failure how to differentiate the cause and what are some findings for DCM
- Echocardiology ○ DCM Enlarged left atrium - DCM Heart isn't contracting well - Decreased fractional shortening ○ Calculating size of chamber in diastole and systole
How to grade a cardiac murmur and locate
Grade - Mild - hearing S1 and S2 - grade 1,2 - Moderate - No S1 and S2 - grade 3,4 - Severe - thrill grade 5,6 Location LEFT - pulmonic, aortic, mitral RIGHT - tricuspid - Need to go from apex cranial under the axillary region
Myxomatous (mitral) valve disease (MMVD) what is it, cause, how common and signalment
- Myxomatous degeneration of mitral +/-tricuspid valve
- Defect in valve connective tissue
- Could be deterioration with age (12 to 13 years old)
Causes 75-80% of cardiovascular disease in canine small practice
Signalment - small breed, older dogs - most common patient - heritance proven in CKCS and Dachshunds
- less common in large breeds
Caviler kind charles spaniel how common is mitral valve murmur and in large breeds what is the other differential more common and differences in murmur and prognosis
§ Murmur in 10% < 1 y.o.
§ Murmur in >50% by 4 y.o. -> Problem is showing now AFTER already bred from this animal - also multiple genes involved
□ Need to look at linage of dogs to figure out which is better to breed from (older the parents without CHF the best)
§ Almost all by 10 years!
○ 15-20% die of CHF <10 yrs
Large breed
§ Major ddx dilated cardiomyopathy more common - eccentric hypertrophy - pulling apart of the valves so softer murmur
□ If loud murmur over left apex more likely to be mitral valve disease - not as common in large breeds
§ Worse prognosis
□ Atrial fibrillation - larger heart so more predisposed -> increased HR -> CO falls as no time for filling
Myxomatous (mitral) valve disease (MMVD) pathogenesis what valve, what occurs and early, mild and severe
○ 60% mitral only
○ 10% tricuspid only
○ 30% both valves
- Collagen degeneration of the valve causing the issue
○ Mucopolysaccharide accumulation -> mitral tip becomes thicker -> holes within
Early disease: grade
○ Initial stretch/prolapse of valves - see via echo
○ No regurgitation so NO MURMUR at this stage
Mild-moderate:
○ Discrete nodules form
○ Regurgitation begins
Severe: grade 5-6
○ Gross fibrosis, distortion, retraction of valves
○ Severe regurgitation
Myxomatous (mitral) valve disease (MMVD) what does it result in and some late and acute complications
Left heart volume overload
○ Atrial dilation
○ Jet lesions - degeneration of valve
○ Mitral annulus dilation
○ LV eccentric hypertrophy (compensate for extra volume - stretch)
Late and acute complications
- Left atrial tear - leads to pericardial effusion (blood)
- Primary Chorda tendinea(CT) rupture - valve flips the wrong way back into left atrium - increase regurgitation
- both usually fatal
Myxomatous (mitral) valve disease (MMVD) clinical signs
- Incidental detection of a regurgitant murmur:
○ Loudest mitral region
○ Louder S1
○ ↑ Intensity = ↑ severity - not always
○ +/-tricuspid murmur
○ May still have respiratory sinus arrhythmia (increase HR expiration, decrease HR inspiration)
Explain how in Myxomatous (mitral) valve disease (MMVD) eccentric hypertrophy results
- SNS activation due to:
- Regurgitation
○ Blood goes backwards into the left atrium
§ Slowly enlarges
- Less blood goes forward
○ Lower systemic BP
○ Less renal blood flow
- Baroreceptors activate the SN -> acts inappropriately in this situation
○ Increase HR, increase Cardiac contractility, vasoconstriction (afterload) - MAKES HEART DISEASE WORSE - Fluid retention
- Salt + water retention (preload) - increase
- Vasoconstriction (afterload) - increase
- Tissue RAAS (Aldosterone -> inflammatory function as well - bad) - Eccentric hypertrophy
- (volume overload)
- Enlarged heart on imaging
- Increased HR
- Murmur
- Otherwise well
Define eccentric and concentric hypertrophy, when occurs, will you see changes on radiograph
- Eccentric Hypertrophy
• Occurs in response to elevated ventricular end diastolic pressures
• Ventricular dilation occurs as new sarcomeres are added in-series to existing sarcomeres
• Mechanically, dilation increases the ventricular compliance - will see increase in size in X-ray - Concentric Hypertrophy
• Occurs due to chronic pressure overload - increase afterload
• The ventricular chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres - adding of new cells
• This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress. - won’t see in radiographs but will see with ultrasound (walls)
CASE 10 year-old Miniature Poodle (FS) Coughing past 4 weeks and less keen on exercise Physical examination: - Grade 5/6 mitral murmur - HR 110/min - Respiratory rate 32/min in hosp - Temp 38.8ºC - No abnormal respiratory sounds - Pink mm, CRT < 2 seconds - Equal and normal pulses RESPIRATORY OR CARDIAC
- Do we have pulmonary oedema - IMPORTANT
○ First clinical sign is respiratory rate
○ LOW RR -> likelihood of this being cardiac reason - LOW
○ ALSO -> HR is normal -> CHF -> heart rate over 120 so UNLIKELY - RESPIRATORY most common
Pathophysiology of heart failure - how does heart disease lead to heart failure
Regurgitation worsens… - Output (perfusion) near normal - Heart can’t enlarge more - Fluid still being retained… ○ ↑ Diastolic LA pressures ○ Pressures ‘behind’ the heart increase → Pulmonary oedema - Congstive or backwards failure
