Pulmonary Pathology Online
Pathology of Pulmonary Edema
Pulmonary edema, is a common clinical and pathologic condition.
Hemodynamic disturbances or change in microvascular permeability can cause pulmonary edema.
When the capacity of the lymphatics to drain the interstitial fluid is exceeded, interstitial edema develops.
There is loss of lung compliance.
When there is further rise in interstitial pressure the tight junctions between the alveolar epithelial cells open and fluid moves into the alveolar spaces causing alveolar edema.
The ventilation stops at this stage.
Chronic edema predisposes to infection.
Alveolar edema fluid is a good culture media.
Secondary pneumonia may occur.
There is impairment of normal respiratory function.
The outflow of fluid is determined by the difference between the capillary hydrostatic pressure and the interstitial hydrostatic pressure, the hydrostatic pressure being higher.
Resorption of fluid is determined by the difference in oncotic pressure between the two compartments.
The amount of fluid exuded is modulated by the permeability characteristics of the alveolar capillary membrane.
Thus, there may be hydrostatic, oncotic, or permeability pulmonary edema, and several forms of edema may be present at the same time.
Interstitial Pulmonary edema : Represents the earliest phase and is an exaggeration of the normal process of filtration.
Alveolar Pulmonary edema: When the fluid can no longer be contained in the interstitial space, it spills into the alveoli, a condition termed alveolar edema.
Hydrostatic edema is due to increased capillary pressure usually as a consequence of left-sided heart failure from any cause.
Fluid overload during transfusion or resuscitation may lead to hydrostatic edema.
A rare form of edema follows rapid aspiration of large pleural effusions and occurs on the side of the aspiration.
It has been suggested that the interstitial pressure rapidly becomes more negative, drawing fluid into the interstitial space and then the alveoli.
Damage to the endothelium, the epithelium, or both increases capillary permeability.
In addition, many chemicals and therapeutic agents, and fat metabolism, produce edema without affecting neutrophils.
Primary epithelial damage results from near drowning, aspiration of gastric contents, inhalation of toxic gases, and the viral infections.
The presumed sequence of events is similar to that in hydrostatic edema, but it has not been well studied.
Oncotic Pulmonary Edema:
Although systemic edema is a well-recognized complication of low capillary oncotic pressure, notably in starvation or hepatic failure, it is not commonly recognized in the lung, which suggests that the lung tends to keep its interstitium dry.
Thus, low capillary osmotic pressure is not often significant in the lung.
However, osmotic effects may occasionally play a role in pulmonary edema that is due to kidney disease, cirrhosis, or overhydration
Gross features: Lungs become heavy, wet and subcrepitant. Fluid accumulates, especially in the dependent, basal regions of the lower lobes.
Microscopic features: There are engorged capillaries and filling of the intra-alveolar air spaces by a granular pink precipitate.
In chronic congestion and edema (as in mitral stenosis), there may be interstitial fibrosis, associated with numerous hemosiderin-laden macrophages (brown induration).
Classification and causes of Pulmonary Edema:
1. Hemodynamic Edema:
-Increased hydrostatic pressure: cardiac & pulmonary causes ;
-Decreased oncotic pressure: Nephrotic syndrome, hypoproteinemia ;
2. Edema due to microvascular injury:
-Diffuse infections (virus, mycoplasma etc) ;
-Inhalation of oxygen, smoke, cyanates etc ;
-Near drowning (salt or fresh water) ;
-Aspiration of gastric fluid ;
-Drugs and chemicals, colchicines, gold, heroin, paraquat ;
-Shock, trauma, sepsis ;
-Miscellaneous ; Acute pancreatitis, embolism (fat, air, amniotic fluid), extensive burn, uremia, heat, diabetic ketoacidosis.
3. Edema of undetermined origin:
Example: High altitude, neurogenic .
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