Interstitial edema

Pulmonary surfactant decreases surface tension of alveolar fluid. Reduced surface tension leads to a decrease in the collapsing pressure of the alveoli, an increase in pulmonary compliance (less elastic recoil), and a decrease in the work required to inflate the lungs with each breath. Also, pulmonary surfactant promotes the stability of the alveoli. Because the surface tension is reduced, the tendency for small alveoli to empty into larger ones is decreased (see Figure 17.2, panel b). Finally, surfactant inhibits the transudation cf fluid out of the pulmonary capillaries into the alveoli. Excessive surface tension would tend to reduce the hydrostatic pressure in the tissue outside the capillaries. As a result, capillary filtration would be promoted. The movement of water out of the capillaries may result in interstitial edema formation and excess fluid in the alveoli. 

The thickness of the blood-gas interface is normally less than 0.5 (im. This extremely thin barrier promotes the diffusion of gases. The thickness may increase, however, under conditions of interstitial fibrosis, interstitial edema, and pneumonia. Fibrosis involves the excess production of collagen fibers by fibroblasts in the interstitial space. Edema is the movement of fluid from the capillaries into the interstitial space. Pneumonia causes inflammation and alveolar flooding. In each case, the thickness of the barrier between the air and the blood is increased and diffusion is impaired. 

Cardiovascular Effects. One of the patients described by Letz et al. (1984) (see Section 2.2.3.1) who had a terminal cardiopulmonary arrest had acute myocardial interstitial edema, myocardial inflammation, and Gram-positive sporulating rods at necropsy. The second patient initially had a normal electrocardiogram, but as his renal and hepatic function deteriorated, eventually developed supraventricular tachycardia and asystole. 

Three pulp mill workers died after inhalation of fumes for approximately 10-15 minutes from a nitric acid tank explosion (concentrations not available). No significant respiratory complaints were apparent during initial examination. However, 4—6 hours later they became cyanotic with frothy fluid escaping from the nose and mouth. All died in less than 24 hours. Necropsy showed bronchiolar epithelial necrosis, marked capillary engorgement, and slight interstitial edema of alveoli the lungs were five times heavier than normal and released abundant frothy fluid from all lobes. The delayed manifestations of lung injury were consistent... 

A common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney. This reduction is sensed as insufficient effective arterial blood volume and leads to salt and water retention and edema formation. Judicious use of diuretics can mobilize this interstitial edema without significant reductions in plasma volume. However, excessive diuretic therapy may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying illness. 

Rat Inhalation 20 ppm 20 h Lung morphology changes included cytoplasmic blebbing in type I class, swelling and hyperplasia of type II cells, and interstitial edema at 5-15 d after exposure. Lungs normal at 35 d. Hayashi et al. 1987... 

Fig. 7 (a) Diffusion-weighted MRI of a patient with laige middle cerebral artery stroke. There is involvement of the entire vessel territory with possibly some hemorrhage in the basal ganglia. The image was made within hours of the infarct and there is minimal compression of the ventricles, (b) CT days after the infarct shows the massive shift of the midUne structures away from the evolving mass lesion. Compression of the CSF outflow tracts causes the hydrocephalus with interstitial edema in the white matter adjacent to the ventricles... 

Interstitial edema is seen in the periventricular regions in patients with hydrocephalus (Fig. 9). The widened extracellular space is the site of transependymal flow of CSF. The movement of ISF into the frontal white matter leads to difficulty walking and incontinence in the syndrome of normal pressure hydrocephalus. 

Fig. 9 Cerebellar infarct with secondary hydrocephalus and transependymal fluid movement (interstitial edema), (a) Initial diffusion-weighted image with cerebellar infarct in the territory of the left posterior inferior cerebellar artery, (b) Echo-planar T2 axial image shows enlargement of the ventricles prior to surgery for hydrocephalus. Arrow shows transependymal movement of fluid...

Initial painless papulovesicular lesion surrounded by massive interstitial edema eschar develops within 2 to 5 days (Freedman et al., 2002). 

Electromyography and saccadic velocity studies demonstrated that the mechanical restriction of the eye is caused by interstitial edema and fibrosis of the muscles rather than by myopathy. However, in the acute phases of Graves orbitopathy saccadic velocity testing demonstrates a neuropathic state, which resolves on fibrosis. 

Pulmonary features of the adverse effects of aldesleukin include lung opacities, diffuse pulmonary interstitial edema, pleural effusions, alveolar edema, and hypoxemia, with full and rapid recovery after treatment withdrawal (29,30). 

There is no significant association between pre-existing clinical dysfunction and radiological interstitial edema (30). Very severe adult respiratory distress syndrome requiring double lung transplantation has been reported in one patient (32). 

Interstitial edema and local fluid retention resulting from increased vascular permeability has been suggested to... 

Findings on autopsy and endomyocardial biopsy have shown diffuse, interstitial edema, intracytoplasmic vacuolization of myocytes, and no inflammatory infiltrate (34). Acute myocardial infarction has been demonstrated pathologically in some, but not all, patients with clinical infarction (10). 

---