Respiratory: Pathology - Atelectasis, pulmonary oedema and congestion Flashcards
Describe the layers of the alveolar walls, from blood to air
- Capillary endothelium
- Basement membrane and surrounding interstitial tissue
- Alveolar epithelium (95% type I pneumocytes, 5% surfactant-producing type II pneumocytes)
- Alveolar macrophages
Describe each of the three types of atelectasis in brief, including what happens to the mediastinum in each
- Resorption: due to complete obstruction of an airway (e.g. excessive secretions, bronchial neoplasm, foreign body aspiration); mediastinum shifts towards affected lung
- Compression: pleural space partially or completely filled with fluid exudate, tumour, blood or air; mediastinum shifts away from affected lung
- Contraction: due to local or generalised fibrosis of lung or pleura, preventing full expansion
How is pulmonary oedema classified according to its cause?
- Haemodynamic pulmonary oedema: due to increased hydrostatic pressure, decreased oncotic pressure, or lymphatic obstruction
- Oedema due to microvascular injury (increased capillary permeability)
- Undetermined origin
Seven broad causes of oedema due to microvascular injury
- Infection
- Inhaled gases
- Liquid aspiration
- Drugs or chemicals
- Shock, trauma
- Radiation
- Transfusion-related
Two causes of oedema of undetermined origin
High altitude
Neurogenic (CNS trauma)
Five examples of drugs and chemicals which can cause oedema to microvascular injury
- Chemotherapeutic drugs (e.g. bleomycin)
- Amphotericin B
- Kerosene
- Paraquat
- Heroin
Give four examples of haemodynamic oedema caused by increased hydrostatic pressure
- L-sided heart failure
- Mitral stenosis
- Volume overload
- Pulmonary vein obstruction
Give four examples of haemodynamic oedema caused by decreased oncotic pressure
- Hypoalbuminaemia
- Nephrotic syndrome
- Liver disease
- Protein-losing enteropathies
Describe the morphological changes seen in ARDS (acutely and in the organising stage)
Acutely:
- Heavy, firm, red, boggy lungs
- Congestion with interstitial and alveolar oedema
- Inflammation with fibrin deposition
- Diffuse alveolar damage (DAD)
- Alveolar walls lined with hyaline membranes
Organising stage:
- Proliferation of type II pneumocytes
- Granular tissue response (resolves in most cases)
What is dependent oedema and why does it occur?
Dependent oedema is when fluid accumulates in the basal regions of the lung
Due to haemodynamic oedema (higher hydrostatic pressures occur in the basal regions at baseline)
Describe the morphological changes seen in haemodynamic oedema
Engorgement of alveolar capillaries
Intra-alveolar granular pink precipitate
Alveolar microhaemorrhage
May see haemosiderin-laden macrophages (“heart failure cells”
Brown induration occurs with long-standing oedema
What is the hallmark of ARDS?
Diffuse alveolar damage (DAD)
Describe the clinical course seen in ARDS
Profound dyspnoea and tachypnoea
Cyanosis, hypoxaemia and respiratory failure
Hypoxaemia can be refractory to O2 due to V/Q mismatch (ARDS is not homogenous - poorly aerated areas remain perfused)
Loss of functional surfactant causes increased stiffness of lungs
May result in longterm interstitial fibrosis in the minority
Describe the pathogenesis of ARDS
Damage to alveolar capillary membrane results in increased vascular permeability and alveolar flooding, causing loss of diffusing capacity and loss of surfactant (type II pneumocytes damaged)
Nuclear factor κB (NF-κB) shifts balance to pro-inflammatory state
IL-8, IL-1, TNF released -> neutrophil chemotaxis and activation, endothelial activation
There is also coagulation system dysregulation
What are the most common causes of ARDS? What % of all cases do these account for?
Most common causes, accounting for >50% of cases:
1. Sepsis
2. Diffuse pulmonary infection (viral, Mycoplasma, PJP, miliary TB)
3. Gastric aspiration
4. Mechanical trauma (including head trauma)
