1.1.3: Lung disease - alveolar disease Flashcards
Where do you localise respiratory problems to?
- URT obstruction
- Loss thoracic capacity (pleural space disease)
- Pulmonary parenchymal disease (alveolar/interstitial)
- Non-CRS conditions (metabolic/physiologic)
Clinical signs of pulmonary parenchymal disease
- Increased inspiratory and expiratory effort
- Some interstitial diseases limit compliance -> increased inspiratory effort predominates
- Cough may/may not be present -> only happens when disease has moved into terminal bronchi
- Less common signs: haemoptysis, collapse/syncope, cyanosis
- Occasionally minimal signs of respiratory disease noted even with severe pathology (esp cats)
Where are cough receptors present: alveoli or airways?
Airways.
There are no cough receptors in the alveoli.
What do crackles tell you?
- There is something wrong in the lung and you need to image them
- Crackles are produced by air being dragged through fluid
- These are not definitive for alveolar disease
Clinical signs of aspiration pneumonia
- Cough
- Harsh/reduced lung sounds
- Tachypnoea
- Pyrexia
- Check oxygenation -> serial evaluation
How do you diagnose aspiration pneumonia?
- Radiographs show alveolar infiltrate (patchy or focal)
- Most commonly affected lung lobes: right middle, right cranial, left cranial; in aspiration penumonia, material tends to enter cranial lung lobes
- Need BAL to confirm diagnosis: cytology, check for neutrophils/toxic neutrophils
You suspect aspiration pneumonia and confirm the diagnosis with BAL and cytology. What antibiotics will you treat with?
- Ideally based on C&S
- Broad spectrum antibiotics as often not sure what we’re dealing with e.g. amoxicillin or amoxy/clav, OR TMPS
Examples of alveolar disease
- Aspiration pneumonia
- Pulmonary oedema (may be cardiogenic/ non-cardiogenic)
- Pulmonary haemorrhage
- Eosinophilic lung disease
- (Pulmonary parasites)
- (Pulmonary neoplasia - primary or metastatic)
- (Infectious pneumonia)
Histological appearance of bronchopneumonia (e.g. aspiration pneumonia)
- The airway and alveoli are full of neutrophils
- There are no air-filled spaces evident at all in a fully consolidated area)
- Other areas may be less severely affected
Treatment of aspiration pneumonia
- Supportive care: oxygen therapy, antibiotics (take care not causing oxidative damage to already fragile lung)
- Treat any underlying cause
- Consider anti-acid medication if frequent occurence (caution with this; it may increase gastric bacterial load)
- Metoclopramide improves motility and lower oesophageal sphincter tone
What is pulmonary oedema?
Pulmonary oedema: when there is fluid accumulation in the interstitium and subsequently in the alveoli at a rate that exceeds removal.
* This in turn leads to V:Q mismatching and hypoxaemia (areas of lungs are still being perfused, but can’t be ventilated)
What (physiologic) conditions can pulmonary oedema be a consequence of?
- Increased hydrostatic pressure
- Reduced oncotic pressure
- Increased vascular permeability
- Impaired lymphatic drainage
Describe how pulmonary oedema develops
- Initially there is fluid accumulation in the interstitium
- This quickly floods the alveoli
- There is then ventilation: perfusion mismatch
What are the two types of pulmonary oedema and what types of fluid are formed in each?
- Cardiogenic - due to increased hydrostatic pressure; fluid is building up behind the failing heart - fluid formed is low-protein
- Non-cardiogenic - the result of lung damage that increases vascular permeability and so protein leaks out - fluid formed is high protein
Possible causes of non-cardiogenic pulmonary oedema
Most commonly: pulmonary epithelial injury
* Choking
* Near-drowning
* Electric shock
* Head trauma
* Smoke inhalation
* SIRS
Pulmonary oedema
