Pulmonary Oedema
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- 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