SA LRT Disease Flashcards
1
Q
Why do we see respiratory problems?
A
- URT obstruction
- Something in the middle of it that is blocking it.
- Loss of thoracic capacity
- Structure of airway: pleural space or mediastinum gets blocked and crushing lungs.
- Pulmonary parenchymal disease
- Non-CRS conditions
- Metabolic/physiologic
2
Q
What can cause airway obstruction and what signs to we often see?
A
Causes
- F.B.
- Acute
- Neoplasia
- Trauma/haemorrhage etc
- Acute
- Laryngeal paralysis/trauma/granuloma
- BOAS - long soft palate, stenotic nares, larynx collapse etc
- Not classically acute, but if have laryngeal collapse, can be.
- Tracheal or bronchial collapse
- Extra-luminal mass lesions - thyroid, abscess, lymphoma
- Asthma/bronchospasm (cat)
- Nasopharyngeal polyp (cat)
- Chronic
Often see cough, cyanosis and noise
3
Q
Causes of loss of throacic capacity?
A
- Not always acute.
- Have changes in ability of chest.
- Pleural effusion
- blood, pus, chyle, true/modified transudate
- Pneumothorax
- Neoplasia - pleural or mediastinal
- Ruptured diaphragm
- Cats RTA
- Abdominal abnormality - severe ascites/mass
- Gross cardiomegaly
- Animals that have pericardial effusions.
4
Q
Clinical signs of pulmonary parenchymal disease
A
- Usually increased inspiratory and expiratory effort
- Some interstitial lung diseases however limit compliance and so inspiratory effort predominates
- Cannot breathe in because cannot expand lungs – they are stiff due to fibrous tissue.
- Cough may or may not be present
- As disease process may be too deep for cough receptors to be activated.
- Can see less frequently hemoptysis, collapse/syncope or cyanosis
- Cyanoses with parenchymal disease = very severe.
- Occasionally minimal signs of respiratory disease are noted even with severe pathology
- Particularly in cats
5
Q
What are you looking for on physical exam if you suspect pulmonary parenchymal disease?
A
- Are there other signs of systemic disease?
- Pyrexia, lymphadenopathy, lameness
- Cyanosis
- Crackles
- Increased/decreased bronchovesicular sounds
- If patient is in respiratory distress immediate oxygen therapy is indicated
- Regardless of underlying cause.
6
Q
Explain aspiration pneumonia
A
- Inhalation of material into the lower airway
- Stomach contents with variable amounts of particulate matter
- Acid, fluid +/- bits of food.
- Stomach contents with variable amounts of particulate matter
- Care with nursing recumbent patients
- Esp. feeding recumbent patients – don’t tube or syringe feed them as will increase risk of this.
- Outcome depends on nature and amount of aspiration
- pH, bacterial contents, volume, particle size
- Chemical aspiration – pneumonitis
- Large volumes of fluid – drowning event
- PEG fluids (bowel prep) – pulls interstitial fluid into the lungs
- Primary infection due to aspiration is less common
- This usually occurs as a secondary event due to damage to the lungs.
- pH, bacterial contents, volume, particle size
7
Q
Signs of aspiration pneumonia
A
- cough, harsh/reduced (dull) lung sounds, tachypnoea, pyrexia
- Pyrexia is a tell-tale sign.
- Check oxygenation – serial evaluation
8
Q
Diagnosis of Aspiration pneumonia
A
- Radiographs alveolar infiltrate (patchy/focal)
- Most common affected lobes are right middle, right cranial and left cranial
- BAL to confirm diagnosis
- In human’s pepsin used in BAL fluid
9
Q
Treatment of aspiration pneumonia
A
- Supportive – oxygen therapy, antibiotics
- Care with oxidative damage to already fragile lung
- Treat any underlying cause
- E.g. laryngeal paralysis, mega-oesophagus
- Consider anti-acid medication if frequent occurrence
- May increase gastric bacterial load therefore caution…
- Metoclopramide to improve motilty and increase LOS (lower oesophageal sphincter) tone
10
Q
Explain Pulmonary oedema
A
- Consequence of various conditions: stuff/ fluid etc. gets into the lungs.
- Increased hydrostatic pressure
- Reduced oncotic pressure
- Increased vascular permeability
- Seen with inflammation.
- Impaired lymphatic drainage
- Seen with lymphatic obstructions.
- This leads to fluid accumulation in the interstitium of lung (where transfer occurs) and subsequently it gets into the alveoli at a rate that exceeds removal.
- Ventilation perfusion mismatching and hypoxaemia
- Blood supply is going wrong – get hypoxaemia.
- Ventilation perfusion mismatching and hypoxaemia
11
Q
Cardiogenic vs. non cardiogenic pulmonary pneumonia
A
- Main difference is type of fluid
- Cardiogenic oedema is low protein due to increased hydrostatic pressure without increased vascular permeability.
- Due to increased hydrostatic pressure, so fluid is low protein, a lot more watery.
- Non-cardiogenic is the result of lung damage which increases vascular permeability
- Associated with damage to lung, leading to increased permeability, so not just fluid – higher protein, so have much greater problem. Increase interstitial pressure, get compression of airways because fluid accumulates and get much more severe hypoxia.
- If have damage to epithelial cell surface due to lung injury, process of removing fluid means non-cardiogenic oedema is harder to treat as lung damage needs to be addressed. Cardiogenic – they respond well to diuretics.
- This leads to a higher protein fluid in the pulmonary parenchyma
- This alters fluid dynamics and the resultant increase in interstitial pressure also alters perfusion causing ventilation perfusion mismatch
- Alveolar fluid accumulation, reduced compliance, airway compression all increase pulmonary vascular resistance
- This all contributes to the hypoxaemia
- Removal of the fluid requires active transport of sodium and chloride from the luminal surface across epithelial cell to the basal surface
- This is an active process – if the epithelium is damaged this cannot occur
- So the damage to the epithelium leads to fluid accumulation and reduced the ability to remove the fluid which makes non-cardiogenic oedema more refractory to therapy than cardiogenic oedema
12
Q
Non-cardiogenic causes of pulmonary oedema?
A
- Importantly hypoalbuminaemia rarely causes pulmonary oedema due to efficient pulmonary lymphatics
- Lymphatic damage is more likely to cause a chylous effusion (chylothorax) rather than pulmonary oedema
- Neurogenic form (along with electric shock) – pathophysiology unclear but thought to be due to intense pulmonary vasoconstriction and inflammation both increase vascular permeability
- Most common cause is pulmonary epithelial injury
- Hypoalbuminaemia can exacerbate fluid accumulation if vascular permeability is compromised
- End up with either acute lung injury or ARDS. The severity is what differentiates the two and it is to do with oxygen concentration.
13
Q
Clinical signs of pulmonary oedema?
A
- Signs may be delayed after insult for up to 72 hours – so don’t say to O they are going to be fine!
- Clinical signs:
- Moist cough (may produce froth), orthopnoea, cyanosis
- Harsh BV lung sounds with crackles are typical
- Radiographs – unstructured interstitial pattern and peri-bronchial can progress to alveolar, often caudo-dorsal.
14
Q
Treatment of Pulmonary oedema?
A
- Address underlying cause, treat ARDS/ALI
- Oxygen supplementation
- Sedation may be required (caution with resp depression)
- To keep them calm.
- May need active cooling as they cannot thermoregulate
- Support – keep affected lung dependent
- Diuretics less effective for non-cardiogenic oedema but still indicated.
15
Q
Explain physical lung injury
A
- Thoracic trauma
- Pulmonary contusion - ventilation perfusion mismatch
- Chest wall damage and pain
- RTAs, dog fights etc.
- Thoracic radiographs to evaluate all thoracic structures
- Lag phase
- Supportive care with supplemental oxygen ASAP
- Other treatment as required – e.g. stabilisation of the thoracic wall, analgesia
