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| − | ==Pulmonary oedema== | + | ==[[Pulmonary Oedema]]== |
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| − | *Excessive fluid in the lung
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| − | *Normally, mechanisms are in place to protect the lung from the entry of circulatory fluid into alveolar spaces (See [[Respiratory System General Introduction - Pathology#Lungs|functional anatomy]])
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| − | *Occurs when exudation of fluid from vessels into interstitium or alveoli exceeds the rate of alveolar or lymph removal
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| − | *Generally a sequel to or part of congestion or inflammatory process
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| − | *Generally begins as '''interstitial oedema''' characterised by expansion of perivascular and peribronchial and peribronchiolar fascia and distension of interstitial lymphatics
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| − | *Only when this interstitial compartment is overwhelmed does fluid flood the airspaces causing '''alveolar oedema'''
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| − | *Gross pathology:
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| − | **Heavy wet lungs which do not properly collapse
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| − | **Subpleural and interstitial tissue distended with fluid
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| − | **Foamy fluid oozing from the cut surface and airways
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| − | *Micro pathology:
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| − | **Pinkish fluid in alveoli and airways in association with air bubbles, and also in dilated lymphatics of the interstitium
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| − | **Colour of the fluid enhanced in cases where the endothelium is damaged - more protein present
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| − | **In slowly developing cases, macrophages contain haemosiderin
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| − | *The major causes of pulmonary oedema are:
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| − | **Increased capillary or type I epithelial permeability caused by
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| − | ***Systemic toxins
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| − | ***Shock
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| − | ***Inhaled caustic gases
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| − | **Increased capillary hydrostatic pressure ('''cardiogenic oedema''' - left-sided or biventricular heart failure, sympathetic stimulation in acute brain damage)
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| − | **Decreased plasma oncotic pressure (hypoalbuminaemia)
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| − | **Overloading in excessive fluid therapy
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| − | **As part of inflammatory process
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