- Excessive fluid in the lung
- Normally, mechanisms are in place to protect the lung from the entry of circulatory fluid into alveolar spaces (See functional anatomy)
- Occurs when exudation of fluid from vessels into interstitium or alveoli exceeds the rate of alveolar or lymph removal
- Generally a sequel to or part of congestion or inflammatory process
- Generally begins as interstitial oedema characterised by expansion of perivascular and peribronchial and peribronchiolar fascia and distension of interstitial lymphatics
- Only when this interstitial compartment is overwhelmed does fluid flood the airspaces causing alveolar oedema
- Gross pathology:
- Heavy wet lungs which do not properly collapse
- Subpleural and interstitial tissue distended with fluid
- Foamy fluid oozing from the cut surface and airways
- Micro pathology:
- Pinkish fluid in alveoli and airways in association with air bubbles, and also in dilated lymphatics of the interstitium
- Colour of the fluid enhanced in cases where the endothelium is damaged - more protein present
- In slowly developing cases, macrophages contain haemosiderin
- The major causes of pulmonary oedema are:
- Increased capillary or type I epithelial permeability caused by
- Systemic toxins
- Shock
- Inhaled caustic gases
- Increased capillary hydrostatic pressure (cardiogenic oedema - left-sided or biventricular heart failure, sympathetic stimulation in acute brain damage)
- Decreased plasma oncotic pressure (hypoalbuminaemia)
- Overloading in excessive fluid therapy
- As part of inflammatory process
- Increased capillary or type I epithelial permeability caused by
- In the normal state, pulmonary alveoli are kept dry by three mechanisms:
- Normal "push-pull" mechanism at capillary level.
- Efficient lymphatic drainage by rhythmic pumping action near airways.
- Integrity of the alveolar epithelial basement membrane is relatively impermeable.
- Unlike the capillary basement membrane, which is relatively permeable.
Pathogenesis
- The pumping efficiency of the lymphatics is exceeded.
- Fluid accumulates in connective tissue adjacent to airways.
- The alveolar walls fill with fluid.
- The alveoli abruptly and severely fill with fluid.
- Associated with the disintegration of alveolar epithelial junctional complexes.
Haemodynamic type
- Fluid leaks into alveoli via junctional complexes BUT the alveolar basement membrane remains intact.
- I.e. is due to elevated pulmonary venous pressure.
- Potentially reversible.
- Causes:
- Cardiogenic
- Usually left ventricular failure.
- Also occurs with cardiac overload due to valvular disease.
- Mechanical
- Large primary pulmonary tumours.
- Severe metastatic disease.
- Granulomatous infections may raise pulmonary venous pressure.
- Neurogenic
- Seizures or CNS disorder.
- Rare in domestic species.
- Cardiogenic
Permeability type
- Fluid fills the alveoli following damage to cells or junctional complexes, or permanent ionic alteration of the alveolar basement membrane.
- Irreversible.
- Causes:
- Toxins
- Bacterial
- Chemical
- Paraquat.
- Aspiration/inhalation
- Gastric contents (low pH)
- Smoke.
- Excess ozone.
- Oxygen.
- Toxins
- There may be a combination of haemodynamic and permeability types in electrocution syndromes and "shock" lung.
- E.g. in Adult Respiratory Distress Syndrome (ARDS).