(A)Inthisautopsyspecimen,centralareasareredandslightlydepressedcomparedwiththesurroundingtanviableparenchyma,creating“nutmegliver”(socalledbecauseitresemblesthecutsurfaceofanutmeg).(B)Microscopicpreparationshowscentrilobularhepaticnecrosiswithhemorrhageandscatteredinflammatorycells.(Courtesy of Dr. James Crawford.) hepatic congestion, thecentralveinandsinusoidsaredistendedwithblood,andtheremayevenbenecrosisofcentrallylocatedhepatocytes.Theperiportalhepatocytes,betteroxygenatedbecauseoftheirproximitytohepaticarterioles,experiencelessseverehypoxiaandmaydeveloponlyreversiblefattychange.Inchronic passive congestion of the liver, thecentralregionsofthehepaticlobules,viewedongrossexamination,arered-brownandslightlydepressed(owingtocellloss)andareaccentuatedagainstthesurroundingzonesofuncongestedtan,sometimesfatty,liver(nutmeg liver) (
Fig.4.1A ).Microscopicfindingsincludecentrilobularhepatocytenecrosis,hemorrhage,andhemosiderin-ladenmacrophages(
Fig.4.1B
Approximately 60% of lean body weight is water, two-thirds of which is intracellular. Most of the remaining water is found in extracellular compartments in the form of interstitial fluid; only 5% of the body’s water is in blood plasma. As noted earlier, edema is an accumulation of interstitial fluid within tissues. Extravascular fluid can also collect in body cavities and such accumulations are often referred to collectively as effusions. Examples include effusions in the pleural cavity (hydrothorax), the pericardial cavity (hydropericardium), or the peritoneal cavity (hydroperitoneum, or ascites). Anasarca is severe, generalized edema marked by profound swelling of subcutaneous tissues and accumulation of fluid in body cavities.
Table 4.1 lists the major causes of edema. The mechanisms of inflammatory edema are largely related to increased vascular permeability and are discussed in Chapter 3; the noninflammatory causes are described in the following discussion.
Fluid movement between the vascular and interstitial spaces is governed mainly by two opposing forces—the vascular hydrostatic pressure and the colloid osmotic pressure produced by plasma proteins. Normally, the outflow of fluid produced by hydrostatic pressure at the arteriolar end of the microcirculation is nearly balanced by inflow at the venular end owing to slightly elevated osmotic pressure; hence there is only a small net outflow of fluid into the interstitial space, which is drained by lymphatic vessels. Either increased hydrostatic pressure or diminished colloid osmotic pressure causes increased movement of water into the interstitium (
Fig. 4.2 ). This in turn increases the tissue’s hydrostatic pressure, and eventually a new equilibrium is achieved. Excess edema fluid is removed by lymphatic drainage and is returned to the bloodstream by way of the thoracic duct (
Fig. 4.2
The edema fluid that accumulates in the setting of increased hydrostatic pressure or reduced intravascular
Table 4.1 Causes of Edema
CongestiveheartfailureConstrictivepericarditisAscites(livercirrhosis)VenousobstructionorcompressionThrombosisExternalpressure(e.g.,mass)Lowerextremityinactivitywithprolongeddependency
DatafromLeafA,CotranRS:Renal pathophysiology, ed3,NewYork,1985,OxfordUniversityPress,p146.
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