914

Occasional Survey

ACUTE AND CHRONIC HEPATITIS REVISITED

.

Review by an International Group *

WE have defined two major subdivisions of chronichepatitis--chronic persistent hepatitis (C.P.H.) andchronic aggressive hepatitis (C.A.H.).l The basis of theclassification was histological, and its justification wasthe difference in prognosis between the two groups, par-ticularly with respect to the development of cirrhosis.When we considered the morphological features andvariants of acute viral hepatitis we were especially con-cerned with histological patterns which suggested a pos-sible transition to chronic liver disease.2 Knowledge ofpathogenesis in acute and chronic hepatitis remains in-complete. To improve communication we have reviewedour experience and re-examined liver-biopsy specimensin patients with hepatitis of known outcome.

Piecemeal necrosis has been regarded as important inthe progression from acute to chronic aggressive hepa-titis. Piecemeal necrosis was not defined by De Grooteet al. but is usually described as necrosis of hepatocytesat the junction between inflamed connective tissue andparenchyma. Various workers have drawn attention toother forms of hepatocellular damage. Boyer and Klats-kin3 indicated the predictive value of confluent necrosiswith bridging between vascular structures. Patients withbridging necrosis were more likely to die within monthsof the onset of acute viral hepatitis, or to acquire cir-rhosis. Peters4 discussed the importance of regenerationas a factor in the outcome of acute hepatitis, and empha-sised the role of spotty necrosis (hepatocytolysis) in

*The following members of the group participated in this study: Prof.L. BIANCHI (University of Basle, Switzerland), Prof. J. DE GROOTE’and Prof. V. J. DESMET (Academisch Ziekenhuis St. Rafael, Leuven,Belgium), Prof. P. GEDIGK (University of Bonn, West Germany), Prof.G. KORB (Pathologisches Institut, Stadtkrankenhaus, Weiden/Opf,West Germany), Prof. H. POPPER (Mount Sinai School of Medicine,New York, U.S.A.), Prof. H. POULSEN (Hvidovre Hospital, Denmark),Prof. P. J. SCHEUER (Royal Free Hospital, London), Prof. M. Schmid(Stadtspital Waid, Zurich, Switzerland), Prof. H. THALER (Wilhel-minenspital, Vienna, Austria), and Prof. W. WEPLER (Kassel, WestGermany). The manuscript was prepared for publication by ProfessorScheuer and Professor Thaler.

C.A.H. The pathogenesis of C.A.H. and the features whichallow a pathologist to predict the outcome of an acuteattack are controversial. Furthermore, the nomenclatureof chronic hepatitis has not been uniformly used, andpathologists and clinicians have found it difficult to com-municate and to agree on the meaning of any one termor diagnosis.

NOMENCLATURE OF CHRONIC HEPATITIS

The classification of chronic hepatitis continues to bebased on morphological criteria (table I), although clini-cal information is often essential for diagnosis. Difficul-ties may arise when the time of onset of the disease isuncertain.

The idea that the term chronic aggressive hepatitisshould be used to describe a morphological lesion andthe term chronic active hepatitis should be restricted toa clinical syndrome’ has not been universally accepted.Some physicians use chronic aggressive hepatitis as afinal diagnosis, based both on morphological and clinicalfindings, while others have objected to the word "aggres-sive" because it may upset patients and relatives. Thehandbook’ of the International Association for the

Study of the Liver and the John E. Fogarty Center inBethesda divide chronic hepatitis into chronic persistenthepatitis and chronic active hepatitis, but sanctionchronic aggressive hepatitis as a synonym (table i).Although the term chronic persistent hepatitis is notused consistently, we believe it should be retained. Itsdefinition and diagnosis are discussed later.

In 1971 Popper and Schaffner6 proposed a new cate-gory, chronic lobular hepatitis (C.L.H.), to’describe theliver lesion in those patients with prolonged hepatocellu-lar dysfunction in whom the pathological changes weremainly confined to the lobules. These changes comprisedspotty necrosis and inflammation as found in acute viral

hepatitis. We do not regard piecemeal necrosis and

bridging necrosis as part of the c.L.H. lesion. The termC.L.H. was not sanctioned by the Fogarty group, whoregarded C.L.H. as an example of prolonged, unresolved,or persisting acute hepatitis, continuing for more thansix months. In cases where portal inflammation was alsoa prominent feature, chronic persistent hepatitis wasthought to be the appropriate diagnosis. The terms per-sistent viral hepatitis and unresolved viral hepatitisdenote similar lesions.

The term carrier is most often used to describe symp-

TABLE I-FORMS OF CHRONIC HEPATITIS

c.P.H.=chronic persistent hepatitis.c.A.H.=chronic aggressive or active hepatitis.c.L.H.=chronic lobular hepatitis.

915

tom-free patients who are incidentally discovered to

carry the hepatitis-B surface antigen in their serum.Such patients often show c.L.H. on liver biopsy, some-times in a very mild form. In a few carriers more seriousliver disease is found7-9 and in others necrosis and in-flammation are entirely absent.

DEFINITION OF CHRONIC AGGRESSIVE HEPATITIS

The earlier definition’ needs modification and

explanation. It does not state that bridging necrosis3may be important in the pathological picture, and instressing the inflammatory aspects of C.A.H. it does notdeal fully with the relation between C.A.H. and cirrhosis,which represents an architectural alteration. Piecemealnecrosis, a concept central to the earlier definition, alsoneeds further discussion. Its overdiagnosis often leads tosevere acute hepatitis being diagnosed as C.A.H., a situa-tion which is apt to cause confusion in therapeutic trials.The following redefinition of c.A.H. is thought to meet

these criticisms. "C.A.H. is a chronic inflammatory andfibrosing liver lesion of varied aetiology and variable his-tological features. The features common to all untreatedexamples are: piecemeal necrosis together with new fibreformation and lymphocytic infiltration of portal tractsand lobules. Other infiltrating cells may also be found,and features of acute hepatitis, such as spotty necrosis(hepatocytolysis) may be superimposed. Passive septaformed by collapse after bridging or multilobular liver-cell necrosis may be present. Cirrhosis is not a definingcriterion but can develop. Signs of liver-cell regenerationare usually seen in c.A.H., and the borderline betweenC.A.H. and cirrhosis in the more severe cases is not sharp.The severity of C.A.H. varies with the degree of piece-meal and confluent necrosis and the density of theinflammatory infiltrate."

This definition includes patients with chronic liverdisease whose liver-biopsy specimen shows bridgingconfluent necrosis (discussed below) or multilobular nec-

Fig. I-Multilobular necrosis.

Liver cells are seen above; elsewhere there is collapsed connective-tissue framework in which portal tracts can be indistinctly seen.

Hzmaioxyiin and eosin; x 100.)

rosis (fig. 1). In addition to the defining features theremay be unrelated findings such as fatty change.

Piecemeal necrosis (fig. 2) may be defined as "the des-truction of liver cells at an interface between paren-chyma and connective tissue, together with a predom-inantly lymphocytic or plasma-cell infiltrate". Theprocess may be seen either at the edges of portal tractsor the septa of cirrhotic liver, or at the margins ofsepta resulting from collapse after confluent necrosis. Itis thus not necessarily confined to the periportal area ofthe hepatic lobules. In addition to lymphocytes and plas-ma-cells there may be segmented leucocytes and lipo-

Fig. 2-Piecemeal necrogiis.At edge of septum swollen liver cells are isolated by mononuclear

cells and connective tissue. (Haematoxylin and eosin; x 380.)

Fig. 3-Inflammatory spillover.In this example from a patient with acute viral hepatitis, a portal

tract is infiltrated with mononuclear cells. A few of these are also seenin adjacent parenchyma, but substantial liver-cell damage seen in fig.2 is absent. (Hiematoxylin and eosin; x 380.)

916

TABLE II-LIVER-CELL NECROSIS IN ACUTE HEPATITIS IN RELATION TO ACINAR CONCEPT OF HEPATIC STRUCTURE

cytes, the latter recognised in haematoxylin-and-eosin-stained slides by their elongated shape and vacuolatedcytoplasm. An important feature of piecemeal necrosis isthe close association between lymphocytes and hepato-cytes, possibly reflecting an immunological interaction.Within the lymphoid infiltrate hepatocytes, singly or ingroups, may be seen. At the advancing edge of piecemealnecrosis, hepatocytes usually show hydropic swelling,and are sometimes arranged in abnormal configurationssuch as liver-cell rosettes. Similar changes may be seendeeper within the lobules.

Piecemeal necrosis, which we regard as being centralto the pathogenesis of C.A.H., may be wrongly identified.The commonly encountered spillover of inflammatorycells from portal tracts in acute hepatitis (fig. 3) canresemble the advancing edge of piecemeal necrosis, butlacks the element of substantial liver-cell loss andfibrosis. When simple spillover is mistaken for piecemealnecrosis, acute hepatitis is likely to be wrongly diag-nosed as C.A.H. Furthermore, there are examples of self-limited acute hepatitis in which necrosis is mainlylocated in the peripheral rather than the central part ofthe lobules, and in the first few months after the onsetof acute viral hepatitis a firm diagnosis of C.A.H. shouldonly be made with great caution.

Another lesion that may be mistaken for piecemealnecrosis occurs in diseases with cholestasis, in whichthere is often swelling or necrosis of hepatocytes adja-cent to fibrous tissue. However, lymphocytes are rela-tively sparse, segmented leucocytes predominate, there isusually considerable proliferation of bile-ductules, andthe relation to morphological cholestasis may beobvious. In chronic cholestasis tissue copper is usuallyincreased and can be demonstrated by appropriate stain-ing.

Total destruction of a band of periportal hepatocytesby piecemeal necrosis, with subsequent ingrowth ofblood-vessels and bile-ductules, can mimic enlargementof the portal tract itself. Appropriate stains will identifythe latter within the necrotic zone for a long time; thetract contains thick birefringent fibres of type-i col-

lagen10 which stain strongly with collagen stains and arelighter in colour than reticulin (type-ill collagen) in un-toned silver preparations.

Piecemeal necrosis is a major characteristic of C.A.H.of viral, drug, or unproven aetiology. It is also found inprimary biliary cirrhosis, in Wilson’s disease, in alcoho-lic liver disease, and indeed in some examples of liverdiseases of many different actiologies.When cirrhosis develops in the course of C.A.H. there

is a further problem of nomenclature. "Cirrhosis with

features of C.A.H.", and "C.A.H. with cirrhosis" havesomewhat similar prognostic and therapeutic implica-tions. We suggest that the first term is the more appro-priate when the dominant clinical problem is that ofcirrhosis, and that the second should be used when theactivity of the disease dominates the clinical picture.Activity in cirrhosis is itself complex, representing thesum of the various forms of liver-cell necrosis andinflammation associated with progression of the lesion.

ROLE OF PIECEMEAL NECROSIS AND BRIDGING HEPATIC

NECROSIS IN PATHOGENESIS OF C.A.H.

Many, including the present group,’ believe that piece-meal necrosis is the most important pathological processin the development of C.A.H. However, Peters4 hasdrawn attention to the non-homogenous nature ofliver-cell damage, to focal hepatocytolysis with inflam-matory-cell infiltration, and to unevenly distributedregeneration as important features. Others3.11 have des-cribed a correlation between confluent necrosis formingbridges between the various vascular structures of theliver and progression to chronic liver disease. This situa-tion was formerly described as subacute hepatic nec-rosis, but the word "subacute" is apt to be misunder-stood and used differently by different workers. Bridginghepatic necrosis (B.H.N.)12 is a better term. This has been

Fig. 4-Diagrammatic representation of hepatic acinar struc-ture.

917

applied to all forms of necrosis in which vascular struc-tures are linked. However, these include different pat-terns of varying prognostic importance (table 11). Sincethe apparent linking of portal tracts in tissue sectionsrepresents, in our view, an example of piecemeal nec-rosis, we prefer to separate this pattern from the othersand to restrict B.H.N. to bridging between central veinsand, more important, between central veins and portaltracts. It is used in this sense in the present paper. The

topography of the different forms of necrosis is easier toexplain on the basis of the hepatic acinus than accordingto the lobular concept13,14 (fig. 4 and table n).The various views on the importance of different- pro-

cesses are not wholly incompatible. B.H.N., focal hepato-cytolysis, and regeneration are all undoubtedly involvedin the pathogenesis of C.A.H. and cirrhosis. Confluentnecrosis by itself, however, unless immediately fatal, isoften followed by healing, leaving either a scarred or asubstantially normal liver. This is well illustrated in theremarkably complete recovery of some patients fromsevere necrotising acute hepatitis," and in the equallycomplete recovery of patients from non-fatal hepaticnecrosis due to shock, carbon tetrachloride, or paraceta-mol (acetaminophen).16 In these situations inflammatoryinfiltration is likely to be relatively mild and the featuresof piecemeal necrosis are lacking. In contrast, there arepatients with acute hepatitis in whom liver biopsy showsapparent linking of portal tracts due to periportal piece-meal necrosis and intense inflammatory infiltration ofthe affected area. This lesion is more likely to developinto C.A.H. When periportal necrosis and inflammationare seen without confluent necrosis extending to centralveins, lobular architecture remains intact for longperiods (fig. 5) and the lesion may progress to cirrhosis,heal spontaneously, or regress under treatment. Incentres which distinguish between C.A.H. and chronicactive liver disease with B.H.N.17 this is the only form ofC.A.H. to be so qualified.

In other patients the inflammatory-cell infiltration

i8· 5-Chronic aggressive hepatitis without confluent necrosis.Inflammation extends from the portal tract (above) into the lobule,

and there is piecemeal necrosis. Lobular architecture remains intact.(Haematoxylin and eosin; x 150.)

and necrosis of C.A.H. are combined with portal-to-central bridging (fig. 6). It is likely that because earlierpapers on C.A.H. emphasised piecemeal necrosis, the pres-ence of B.H.N. was not always recognised.’g Conversely,in liver-biopsy specimens with B.H.N. the importance ofpiecemeal necrosis and lymphocytic infiltration has inour view been underestimated. Piecemeal necrosis andportal-to-central bridging in combination have two

effects. First, B.H.N. dissects the lobules and thus encour-ages the more rapid development of cirrhosis. The for-mation of portal-systemic shunts in the septa resultingfrom collapse of areas of confluent necrosis leads toischaemia of parts of the lobules, and may thus contri-bute to unevenly distributed regeneration. Central-to-portal bridging may also facilitate the extension of therelevant immunological reactions deep into the lobules,with the result that piecemeal necrosis is no longer con-fined to the periportal areas. However, the association ofB.H.N. with piecemeal necrosis needs further elucidation.This type of C.A.H., in which piecemeal necrosis is com-bined with bridging necrosis and regeneration, corres-ponds to some examples of the more severe variety des-cribed by De Groote et al.l (table i).

Focal hepatocytolysis, characteristic of acute viral

hepatitis, may or may not be present in addition to thefeatures described above. It is common in various formsof chronic hepatitis, but in the absence of piecemeal nec-rosis is unlikely to lead to cirrhosis in most cases. Bile-duct damage is associated with a more rapid progressionto cirrhosis’9 but the mechanism is not known.

In our view, the morphological feature of greatest im-portance in the evolution of chronic hepatocellular dis-ease is the infiltration of the tissue by lymphocytes andplasma-cells which accompanies piecemeal necrosis andprobably represents a continuing immunological reac-tion, at least in viral cases. It is probably more impor-tant than either confluent necrosis per se, or liver-cell

Fig. 6--Chronic aggressive hepatitis with bridging hepatic nec-rosis (B.H.N.) and developing cirrhosis.

Liver cells are swollen and have formed rosettes. Architecture is

destroyed. Curving septum extending from portal tract (bottom left)probably represents previous B.H.N. (Haematoxylin and eosin; x 150.)

918

regeneration. Residual liver cells may be important inperpetuating the lesion, providing continuing antigenicstimuli, perhaps in the form of neoantigens on the cellmembranes. By this hypothesis, piecemeal necrosis canbe looked on as the consequence or expression of inef-fectual elimination of viral or cell-membrane com-

ponents.

PREDICTION OF CHRONICITY IN ACUTE HEPATITIS

Two patterns of liver injury in acute viral hepatitishave been thought to indicate an increased risk of thedevelopment of C.A.H. and cirrhosis. The first is B.H.N.,discussed above.3 The second pattern is that described as"acute hepatitis with possible transition to C.A.H."2 Hereportal and periportal inflammatory infiltration are moresevere than would be expected from centriblobular

changes, and there is fibrosis in the affected areas. Truepiecemeal necrosis is seen, as opposed to mere spilloverof inflammatory cells from the portal tracts into theadjacent parenchyma. When viewed in two-dimensionalsections, the effect of the periportal necrosis and inflam-mation is to link adjacent portal tracts, since the piece-meal necrosis tends to fill the space between the limbs ofa branching portal tract. This second pattern is there-fore regarded as being the same as the "portal-to-portalbridging" included by Boyer and Klatskin3 under theheading of "subacute hepatic necrosis".

As has already been indicated, necrosis formingbridges between portal tracts and central veins, or

between adjacent central veins, is often followed by heal-ing unless some added factor prevents this or the patientdies of the acute disease. This form of bridging necrosis,when it occurs in viral hepatitis, is nevertheless clinicallyimportant. It indicates a more than usual degree of liver-cell damage and is often found in severe acute type-Bhepatitis. It may hasten the evolution to cirrhosis in

patients with piecemeal necrosis. Deficient liver-cell

regeneration in older patients with B.H.N. may explainthe relatively poor prognosis.4We believe, however, that true piecemeal necrosis

remains the most important predictive sign of impendingC.A.H. The periportal lesion may regress spontaneouslyor under treatment, but "acute hepatitis with possibletransition to C.A.H." often evolves gradually into C.A.H.of the less severe type. In a series of 500 patients withbiopsy-verified acute hepatitis,20 cirrhosis, C.A.H., or

C.P.H. developed in 28; of the morphological featuresrecorded in the acute attack, piecemeal necrosis, des-truction of the limiting plates of the portal tracts, andportal infiltration by plasma-cells proved most useful inpredicting a chronic outcome.

CHRONIC PERSISTENT HEPATITIS

De Groote et al. characterised C.P.H. as follows:"Chronic inflammatory infiltration, mostly portal, withpreserved lobular architecture and little or no fibrosis.Piecemeal necrosis is absent or slight. Features of acutehepatitis may be superimposed". The importance of thiscategory lies in its distinction from c.A.H. rather than inthe lesion itself. De Groote et al. emphasised that C.P.H.closely resembles resolving acute hepatitis and non-spe-cific reactive hepatitis. Portal inflammation, seen forexample in many livers at necropsy, is not in itself suffi-cient evidence for a diagnosis of C.P.H. Extrahepatic

causes of portal inflammation must be excluded beforea diagnosis of C.P.H. is accepted.l,4 C.P.H. implies a hepa-tic disease, usually of viral origin.When features of acute hepatitis are superimposed on

the portal lesion of C.P.H., it is difficult to distinguishbetween C.P.H. and C.L.H. (persistent, prolonged, or un-resolved hepatitis). In some systems of classification theconcepts of C.P.H. and C.L.H. are merged.21 We suggestthat the term C.P.H. should be used when the lesion is

mainly portal, and one of the other terms when thelobules are mainly affected. In comparisons between dif-ferent series of patients, for example in therapeutictrials, the portal and lobular component should be

separately assessed.The microscopical diagnosis of C.P.H. is usually not

difficult, although final diagnosis demands full clinicalinformation as well. There are, however, instances whenthe diagnosis is more difficult.

1. When the sample is small and includes only a smallnumber of portal tracts, step sections should be taken. Someportal tracts may show changes typical of C.P.H. while othersare characteristic of C.A.H., which is then the correct diagnosis.If the appearance of the biopsy specimen changes from C.P.H.in one biopsy to C.A.H. in a subsequent biopsy either a sam-pling error in the first specimen or a genuine transition toC.A.H. which takes place in a minority of patients may be re-sponsible. In either disease, all portal tracts are usually in-volved to a greater or lesser extent.

2. When the patient is on anti-inflammatory therapy. Thelesion of C.A.H. may then be temporarily modified to that ofC.P.H. Connective-tissue stains in such cases help to reveal theperiportal fibrosis which accompanies the necrosis and inflam-mation of C.A.H., and which can still be seen for some timeafter the necrosis and inflammation have been suppressed bytreatment.

3. When the sample is from a cirrhotic liver and is frag-mented, so that cirrhosis is not correctly diagnosed.

4. When the lesion lies on the borderline between C.P.H. and

very mild C.A.H. and there is genuine doubt as to the diagnosis.Step sections or further biopsies may help to resolve the

problem.

Even when C.P.H. is correctly diagnosed, the implica-tions for different patients may vary. Gudat et al. 22.23demonstrated that in some biopsy specimens with thepathological features of C.P.H. in patients with chronictype-B hepatitis, the liver cells contain only a little or nointranuclear core antigen and considerable amounts ofcytoplasmic surface antigen, while in other patients theposition is reversed and the patients may show progres-sion to C.A.H. C.P.H. thus seems to be immunologicallyheterogeneous. Some patients with C.P.H. also have morelymphocytes apparently lying within hepatocytes(emperipolesis) than usual, and C.A.H. also tends to de-velop in these patients. Emperipolesis is normally muchmore readily demonstrable in C.A.H. than in C.P.H.24 Thepresence of lymphoid follicles or damaged bile-ducts issometimes associated with progression to more seriousliver disease.25 C.P.H. is clearly not a simple entity, andthe definitions and categories may need to be changed inthe light of new information.

CONCLUSION

We have analysed the pathological features of chronichepatitis and their importance in the development ofcirrhosis. We believe that piecemeal necrosis and lym-

919

phocytic infiltration are important pathogenetic andprognostic features. However, chronic hepatitis hasmany causes and encompasses a wide variety of patholo-gical lesions, many of them found together in the sameliver. This complex situation requires careful analysis indifferent centres, so that the natural history and res-ponse to treatment of the different components can be

accurately determined.Requests for reprints should be addressed to Prof. P. J. Scheuer,

Department of Histopathology, Royal Free Hospital, London NW320G.

REFERENCES

1. De. Groote, J., Desmet, V. J., Gedigk, P., et al. Lancet, 1968, ii, 626.2. Review by an International Group, ibid. 1971, i, 333.3. Boyer, J. L., Klatskin, G. New Engl. J. Med. 1970, 283, 1063.4. Peters, R. L. Am. J. med. Sci. 1975, 270, 17.5. Diseases of the Liver and Biliary Tract; p. 9. Washington, 1976 (D.H.E.W.

publication no. [N.I.H.] 76-725).6. Popper, H., Schaffner, F. New Engl. J. Med. 1971, 284, 11547. Knolle, J., Born, M., Hess, G., Klinge, O., Arnold, W., Bitz, H., Meyer zum

Büschenfelde, K. H. Klin. Wschr. 1976, 54, 567.8. Sampliner, R.J. Am med. Ass. 1977, 237, 50.9. Simon, J. B., Patel, S. K. Gastroenterology, 1974, 66, 1020.

10. Rojkind, M., Kershenobich, D. in Progress in Liver Diseases (edited by H.Popper and F. Schaffner); vol. 5, p. 294. New York, 1976.

11. Ware, A. J., Eigenbrodt, E. H., Combes, B. Gastroenterology, 1975, 68, 519.12. Conn, H. O. ibid, 1976,70,1182.13. Rappaport, A. M. Beitr. Path. 1976, 157, 215.14. Schmid, M. Die Chronische Hepatitis; p. 59. Berlin, 1966.15. Karvountzis, G. G., Redeker, A. G., Peters, R. L. Gastroenterology, 1974,

67, 870.16. Portmann, B., Talbot, I. C., Day, D. W., Davidson, A. R., Murray-Lyon,

I. M., Williams, R. J. Path. 1975, 117, 169.17. Baggentoss, A. H., Soloway, R. D., Summerskill, W. H. J., Elveback, L. R.,

Schoenfield, L. J. Hum. Path. 1972, 3, 183.18. Boyer,J. L. Gastroenterology, 1976, 70, 116119. Poulsen, H., Christoffersen, P. Hum. Path. 1972, 3, 217.20. Dietrichson, O., Juhl, E., Christoffersen, P., Elling, P., Faber, V., Iversen,

K., Nielsen, J. O., Petersen, P., Poulsen, H. Acta path. microbiol. scand.1975, sect. A, 83, 183.

21. Ishak, K. G. Am. J. clin. Path. 1976, 65, 787.22. Gudat, F., Bianchi, L., Sonnabend, W., Thiel, G., Aenishaenslin, W.,

Stalder, G. A. Lab. Invest. 1975, 32, 1.23. Gudat, F., Bianchi, L., Stalder, G. A., Schmid, M. Schweiz. med. Wschr.

1976, 106, 812.24. Bechtelsheimer, H., Gedigk, P., Müller, R., Klein, H. Klin. Wschr. 1976, 54,

137.25. Popper, H., Schaffner, F. in Progress in Liver Diseases (edited by H. Popper

and Schaffner); vol. v,p. 531. New York, 1976.

Round the World

United StatesSTILL TOO MANY SPECIALISTS

The growing dissatisfaction of the U.S. public with themedical profession results largely from the profession’s disin-clination to provide the type of care which in Britain is mainlythe province of the general practitioner. Home visits havebecome a thing of the past, and while it is fairly easy to obtainan appointment to see a paediatrician or gynaecologist, there isno-one available to look after the patient who happens to havesome minor acute injury or illness. This state of affairs isa consequence of the relative dearth of family practitioners,whose numbers have fallen by about three-quarters over thepast 25 years. There are several reasons for the decline ofgeneral practice, not least among them being the emphasis thatwas placed on subspecialisation by the Government during the1960s and early 1970s-a policy which is now greatly regret-ted. During this period almost every teaching hospital, andmany large community hospitals, established residency pro-grammes in general surgery, neurosurgery, urology, and othersurgical specialties; the Government sponsored numeroustraining programmes for cardiology, hoematology, and othermedical subspecialties.

There seems little doubt that these policies have contributedto the surfeit of certain specialists, such as neurosurgeons,thoracic surgeons, cardiologists, and those specialising in infec-tious disease. But things are changing, and the advent of theAmerican Academy of Family Practice has led to a great in-

crease in the number of young graduates entering this field.Moreover, the federal Government has also changed its philo-sophy, and has decided that too many medical graduates havebeen entering specialty training programmes. As a result it hasbrought pressure to bear on medical schools by insisting thatat least 50% of all training programmes should be in primarycare-defined as paediatrics, internal medicine, and familypractice. If the medical school chooses to disregard the govern-ment edict, then it loses the capitation fee it receives for everyenrolled student. Since this amounts to several thousands ofdollars per student, few schools can afford not to comply. Inaddition, both the American College of Surgeons and theAmerican College of Physicians have accepted the fact that toomany specialists have been trained. The College of Surgeonshas drastically reduced the number of surgical residencies. TheCollege of Physicians has adopted a different approach, andhas been trying to foster the concept of the general internistrather than the subspecialist by persuading teaching hospitalsto offer residency training programmes in general internalmedicine and to reduce the number of subspecialty fellowships.In this they have been aided and abetted by various charitableorgariisations, in particular the Robert Wood Johnson Founda-tion, which has awarded grants of several million dollars tocertain schools for primary-care training programmes.

For a variety of reasons, and perhaps not surprisingly, theresponse has been disappointing. It is all very well to exhorttoday’s graduates to become generalists, but it soon becomesevident that the generalist places himself at a financial disad-vantage compared with the subspecialist. Unlike the cardiolo-gist with his coronary arteriography, or the gastroenterologistwith colonoscopies and gastroscopies, the generalist carries outfew invasive procedures. While a routine consultation may beworth$50, a gastroscopy is worth$150. Similarly, althoughthe immediate past-president of the College of Physicians hastoured the country giving lectures in support of the general in-ternist, as a department chairman of a well-known medicalschool he himself maintains an extensive subspecialist fellow-ship training programme which is mostly supported by theNational Institutes of Health, a fact which did not escape hisaudience. Moreover, the Veterans Administration pays a fullytrained subspecialist a far higher salary than it does the

general physician, so here again we see official Governmentpolicy pulling in two or three different directions. It is difficultnot to conclude that the status quo in internal medicine is

going to persist until the present fee-for-service system is dras-tically modified, thereby evening out the financial rewards ofthe generalist and the subspecialist.

CAMPAIGN AGAINST CIRCUMCISION

For all its problems, the United States has done a marvel-lous job of blending its diverse population. Lacking a commonheritage and culture, most Americans somehow or other

manage to live in harmony. But, by the same token and per-haps because of its diversity, the country has become a havenfor minority sects and religions, for eccentric cults, and for aplethora of far-out societies whose purposes and beliefs oftenstrain the imagination. One of the latest to hit the headlinesis Intact, an organisation whose raison d’etre is to preserve theprepuce. Routine circumcision has long been the rule in theU.S.; in fact, as one genitourinary surgeon put it, "it is asAmerican as apple pie"-and far more remunerative. Butthings are changing, and the American Academy of Pediatrics,along with Dr Spock, have come out against routine circumci-sion. The operation is slowly becoming less popular, and Intactis doing its best to hasten the process. As far as one can gather,the organisation is composed of both lay and professionalpeople, and one enthusiastic member wrote an article in TheCountry Lady’s Daybook entitled Circumcision in Social Pers-pective. Not too long ago in Washington State, a newborn in-fant was circumcised against the parents express wishes, andthe father subsequently sued those responsible. The child wasawarded$8000 damages, but, as one wag put it, had the epi-sode taken place in Texas, where things are bigger and better,goodness knows how large the award would have been.