The effects of edema vary, ranging from merely annoying to rapidly fatal. Subcutaneous edema is important to recognize primarily because it signals potential underlying cardiac or renal disease; however, when significant, it also can impair wound healing and the clearance of infections. Pulmonary edema is a common clinical problem. It is seen most frequently in the setting of left ventricular failure, but also may occur in renal failure, acute respiratory distress syndrome (Chapter 11), and inflammatory and infectious disorders of the lung. It can cause death by interfering with normal ventilatory function; besides impeding oxygen diffusion, alveolar edema fluid also creates a favorable environment for infections. Brain edema is life threatening; if the swelling is severe, the brain can herniate (extrude) through the foramen magnum. With increased intracranial
Edemaresultsfromthemovementoffluidfromthevasculatureintotheinterstitialspaces;thefluidmaybeproteinpoor(transudate)orproteinrich(exudate).
Edemamaybecausedby:
Increasedhydrostaticpressure(e.g.,heartfailure)
Increasedvascularpermeability(e.g.,inflammation)
Decreasedsynthesis(e.g.,liverdisease,proteinmalnutrition)
Increasedloss(e.g.,nephroticsyndrome)
Lymphaticobstruction(e.g.,inflammationorneoplasia)
Sodiumretention(e.g.,renalfailure) pressure, the brain stem vascular supply can be compressed, leading to death due to injury to the medullary centers controlling respiration and other vital functions (Chapter 23).
Hemorrhage, defined as the extravasation of blood from vessels, is most often the result of damage to blood vessels or defective clot formation. As described earlier, capillary bleeding can occur in chronically congested tissues. Trauma, atherosclerosis, or inflammatory or neoplastic erosion of a vessel wall also may lead to hemorrhage, which may be extensive if the affected vessel is a large vein or artery.
The risk of hemorrhage (often after a seemingly insignificant injury) is increased in a wide variety of clinical disorders collectively called hemorrhagic diatheses. These have diverse causes, including inherited or acquired defects in vessel walls, platelets, or coagulation factors, all of which must function properly to ensure homeostasis. These are discussed in the next section. Here we focus on clinical features of hemorrhages, regardless of the cause.
Hemorrhage may be manifested by different appearances and clinical consequences.
• Hemorrhage may be external or accumulate within a tissue as a hematoma, which ranges in significance from trivial (e.g., a bruise) to fatal (e.g., a massive retroperitoneal hematoma resulting from rupture of a dissecting aortic aneurysm) (Chapter 10). Large bleeds into body cavities are described variously according to location— hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis(in joints). Extensive hemorrhages can occasionally result in jaundice from the massive breakdown of red cells and hemoglobin.
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Fig. 4.4 (A)Punctatepetechialhemorrhagesofthecolonicmucosa,aconsequenceofthrombocytopenia.(B)Fatalintracerebralhemorrhage.
Petechiae are minute (1 to 2 mm in diameter) hemorrhages into skin, mucous membranes, or serosal surfaces (
Fig. 4.4A ); causes include low platelet counts (thrombocytopenia), defective platelet function, and loss of vascular wall support, as in vitamin C deficiency (Chapter 8).
Purpura are slightly larger (3 to 5 mm) hemorrhages. Purpura can result from the same disorders that cause petechiae, as well as trauma, vascular inflammation (vasculitis), and increased vascular fragility.