Document Ozap0Bg3GG6yp14JG6NxnazvK

13.2 Annals New York Academy of Sciences . Chemie. W. Foersl, Ed. Vol. 14: 306. Urban St Schwarzenbcrg. MUnchcn, West Germany. 1-------------------- 100. Ostia, R. II.. C.i J. Cara St J, C. Kaantz. 1947. Ancslhcsin. XXVII. Narcosis . with vinyl chloride. Anesthesiology S: 339. 101. Osteamayer, H. 1967. Vinylchlorid. In Ullmanns EncykJopldie dec technischen Chemie. W. Foerst, Ed-Vol. 18: 87--Urban & Schwarienbcrg. MUnchen, West Germany. 102. Otto, P., P. H. Krause, H. G. Jester, F. W. Schmidt St K. H. Glatzel. 1972. ldiopathische portale Hypertension. Med. Klin. (Munich) 67: 447. 103. Parmegoiani, L, A C. SASSt. 1933. Rischl e patologia professional nella pro- duzione e nellailavorazione di alcune materie plasliche. Med. Lavoro 46: 14. 104. Patty, F. A., \V. P. Yant it C. P. Waite. 1930. Acute response of guinea pigs to vapors of some new commercial organic compounds. V. Vinyl chloride. Public Health Rep. 45: 1963. 105. PaW, Fi Ah Bdi I9tg. Jnduatrial Hygiene anrl-T-oxIrologm-Uol, l.-Qencral-Prin- ~^To<>l04<-i,lTl, PrA:,' CJ. I963| IndusttieV-Hygienc-and-Toiiieolegyi Valr lli Toxicolog/i- O' Wi ra'ssctnfc-DrOrlrlshr-Edsr-ind-edltT-Intersclene^PubllshersrNaw Yorlt,.. 107. PeorLM, A. S. it C. D. Leaks. 1933. The aneslhelic action of vinyl chloride. J. Pharmacol. Expti. Ther. 48: 284. I0t. Polish, E., 3. Christie, A. Coiien it B. Sullivan. 1962. Idiopathic presinusoidal portal hypertension (Qanli's syndrome). Ann. Internal Med. 56t 624. 109. PorrgR, H.j F. Paronetto, F. sciiaffner it V. Perez. 1961. Studies on hepatic fibrosis. Lab. Invest. IOi 263. Pofferi Hr i960: ratliuiugyi3t~punal lin*nK.inlou. fn *nie~Tlieiavy~ot~Porta IlypetlEIISIOn: N.-O. hlxikulT, Cdj Geerg-Thieme-Verlagr'StnngirTTrWeTt-QeT- -many: . hi. PorrER, H. it F. Hutterer. 1970. Hepatic fibrogenesls and disturbance of hepatic . circulation. Ann. N.Y. Acad. Sci. 170: 88. 112 PorrER, H. it S. (Joenfriend. 1970. Hepatic fibrosis. Correlation of biochemical ' and morphologic Investigations. Am. J. Med. 49: 707. 113. Pusiiin, G. A. 1963. O porashenii peteni i zcISnyikh pule: u rabofikh' zan- jatyikh w proizwodstwe nekatoryjkh widow plastmass. Sov. Med. 28: 132. 114. PVC producers see good business ahead. 1969. Chem. Eng. News August 4: 18. 113. Quooss, H. 1939. Gesundheitsgefahrcn In der Kunsistoffindustrie, Johann Am- brosiui Barth Verlag. Leipzig, East Germany. 116. Ramajlinoaswamj, V., K. L. Wio it S. K. Sama. 1962. Cirrhosis of the liver in Opt'-Wl. Northern India-- clinicopathological study. Arch. Internal Med. HO: 330. Ramaunoaswami, V. it N. C. Navak. 1970. Liver disease In India. In Progress in Liver Disease. H. Popper it F. Schaflner, Eds. Vol. Ill: 222. Grune it Stratton. New York, N.Y. U 9' RAMd;,rr B.l"U `/"dTojne (fibrocongestive splenomegaly). DefinilibiT l.c.l.a.s..s.ificiai_tion tndpalhoaTenersiifs-/Alrrc^/i. iInte.i_rn__a_l_M__e_dl.-6,6:T87.9 ,* i ,w|itM iii uTti unessem II: 457. Grune it Stratton. New York, N.Y. 122. Rorrt, F. 1957. Arsen, Leber, Tumoren (HVmangloendothellom). Z. Krebsforsch. 6Ji 468. 123. RousscuoT. L. M. 1940. The late phase of congestive splenomegaly (Dantl's syn drome) with hematemesis but without cirrhosis of the liver. Further observa tions on the etiology of Band's syndrome and the effect on prognosis of certain variations in the portal venous pattern. Surgery 8: 34.' 124. Sama, S. K., S. Bharoava, N. Gofi Nath, J. R. Talwar, N. C. Nayak, B. N. Tanoon & K. L. Wto. 1971. Noncirrhotic portal fibrosis. Am.). Med. 51: 160. 123, Saragoca, A., M. H. Tavares, F. B. Barros St J. Da Silva Horta. 1972. Some clinics) and iebsracon' findings in patients injected with thorium dioxide. Study of 155 cases. Am. J. Gastroenterol. 57: 301. 126. Sciiaffner, F. it H. Popper. 1963. Capillarizatlon of hepatic sinusoids In man. Gastrocnlcrcicgy 44: 239. Xmift&oz .Marstcllcr el ai: Splenomcgalic Liver Disease 135 127. Sciiaumann, 0. 1934. Ueberdie Herzwlrkung einlger Inha!t!!j;s:.t..'.,:i:ica. Medllln it Chemie. Abhandlungen aus den Medizinisch-chemisther. ro.-jchunjsstSllen der I.O. Farbcninduslrie A.G. Vol. II. Bayer-Melsur Lu:i..s. Ls/sfEusen, West Germany. 128. Sciiaumann, O. 1938. In Toxikologie und Hygiene der techr.itchen LoS'JRgsmittel, K. I). Lehmann it F. Flury, Eds. p. 130 (MonochlorSthyler.). Julius Springer. Berlin, Germany. 129. Schmid, M. 1968. Zur Leberhislologie der verschiedenen Formen des porUlen Hochdruckes. In The Therapy of Portal Hypertension. N. G. MarkolT, Ed. Georg Thicme Verlag. Stuttgart, West Germany. 130. Sciimiot, F. W. 1969. (jeringer Aktivitiitsanstieg der Serum-Transaminasen. Dent. Med. Wochschr. 94: 2250. 131. Schnacx, H,, L. SroCRiNOER St F. Wewxlxa. 1967. Advenlltlous connective tissue cells in ihe space of Disse and their relation to fibre formation. Rev. Intern. iJ-L-GiNHO6NpaPtsorlH. .17K:.8T3A5T. ir^Verrii A M^Hr-0ictLow^lP49iTHndboq>nrt-PhmUJ.*2HU n jLMiwMfltnmill l'U. liif UlliiugNuw-MJ,----- v 133. Slater, T. F. 1972. Free radical mechanisms in tissue Injury. Plon Ltd, London, England. 134. Saioron, G. L. A H. A. Battifora. 1972. Thorolrast-lnduced hepatoma. Cancer 30: 1252. 135. Smyth. H. F., Jr. 1956. Improved communication. Hygienic standards for daily inhalation. Am. Ind. Hyg. Assoc. J. 17: 129. 136. Soloway, R. D., A. II. Bagoenstoss. L. J. ScttoturteLD a at. >971. Observer error and sampling variability tested In evaluation of hepatitis and cirrhosis by liver biopsy. Am. J. Digest. Diseases 16r 1082. 137. Stein, G., S. JOna, C.-E. Lanoe it G. Veltman. 1973. Bandlbrmige Osteolysen in den Endphalangen des Handskeletls. Fortschr. Gebiele Roenlgenstrahlen Nu- klearmed. 118; 60. 138. Stenoer, R. J. 1965. Fibrogenesis along the hepatic sinusoids in carbon-tetra- chloride-induced cirrhosis. An electron microscopic study. Expti. Mol. Pathol. 4< 357. 139. Stutz, F. H., D. C. Tormey it J. Blom. 1973. Hemangiosarcoma and pathologic rupture of Ihe spleen, Cancer 31; 1213. 140. Suctu, 1., I. Drejman it M. VaLaskai. 1963. Contributll la studiul imbolnavirilor produse de clorura de vinil. Med. Interna 15s 967. 141. Suciu, I., I. Dreiman Sl M. Vauskai. 1967. Etude des maladies dues au chlorure de vinyle. Med. Lavoro 58: 261; Abstr. Hyg. 43: 430 (1968). 142. Summerskill, W. U. 3. 1974. Chronic active liver disease reexamined: prognosis hopelul. Gastroenterology `"l.'"' 143. Sussman, -E. -B., 1. Nydick i W ===%) w gwthe liver and hemochromi 144. Svmanski, H. Ed. 1963. Ha Ed. Vol. JV/2: Arbeitshy 4. Hemangioendothelial sarcoma of I. 97: 39. tlen Arbeitsinedizin. E. W. Baader, :hwarzenberg. MUnchen, West Ger- many. 145. Tanoon, D. N., R. Laksiimi 1970. Ullraslrudure of I pertension. Gut 11: 905. 146. Tisdale, W. A., G. Klats: bleeding esophageal var hepatic and extrahcpatlc aroava, N. C. Nayak St S. K. Sama. rhotle portal fibrosis with portal hy- '.enn. 1959. Portal hypertension and ence in the absence of both intraportal vein. New Engl. 3. Med. 261: 209. 147. Torkelson, T. R., F. Ov* as determined by repetl 1961. The toxicity of vinyl chloride loritory animsls. Am. Ind. Ilyg. As- soc. ).22t 354; Bull. Hy 148. Tribuich, S. L,, N. P. Tiki Iruda i meropriyatiya khlorvinilovykh plastiii 149. TRuffert, L. 1959. Aspe vina it L. A. Kozlov. 1949. Usloviya niyu pri proizvodslve i izpol'zovanil ia Sanit. 10: 38. de I'industrie des maliires plastiques. Arch. Maladies Profess 150. U.S. Defartment of He and Welfare--PunLid llEAiTii Ser- vice: Center for Diseaac ' ,/74. Angiosarcoma of (lie liver among polyvinyl chloride workers--Kentucky. Morbidity Mortality Weekly Rep. 23(6): 49. kL i | BFG36606 ARCHIVES OF INTERNAL MEDICINE clinic the values lay within normal limits. The lesions tended to run a chronic course, and neither local therapy nor, in the case of diabetics, general management tended to speed their healing. In some cases the lesions slowly receded and left depressed scars. Two ideas regarding the pathogenesis of this condition have been considered: (1) that which assumes the occurrence of a primary vas cular injury, possibly by circulating toxins, with secondary thrombosis, necrosis, and fat imbibition and (2) that which assumes a local lipoid disturbance in the skin, based on a general disturbance in fat metab olism. Neither hypothesis has proved satisfactory in the light of studies made both here and elsewhere. Therefore, the pathogenesis of this condition remains obscure. BANTI SYNDROME (FIBROCONGESTIVE SPLENOMEGALY) DEFINITION. CLASSIFICATION AND PATHOGENESIS PAOLO RAVENNA, M.D. CHICAGO The Banti syndrome is still an unsolved problem. The question of cardinal importance is whether the splenomegaly is primary or secondary to portal or hepatic changes. Banti1 2st3at4ed the belief that the trouble lay primarily in the spleen and that the portal and hepatic changes were dependent on the splenic ones. The idea that the splenomegaly was the consequence of circulatory disturbances was put forward by Dock and Warthin * and further devel oped with the description of the thrombophlebitic splenomegaly.* This theory occupied a position of definite advantage when it was recognized that the structure of Banti splenomegaly was chiefly congestive * and that 1. Banti. G.: La splcnomegalia con cirrosi epatica, Spcrimentalc (sei. biol.) 48:407, 1894; I-a mvcc cirrltotc du Me, Scmoinc i>i4< 14:318, 1B94; Ueber Morbus Banti, Folia haemat. 18:33, 1910. 2. Dock, G., and Warthin, A, S.: A Clinical and Pathological Study of Two Cases of Splenic Anaemia, with Early and Late Stages of Cirrhosis, Am. J. M. Sc. 127:24, 1904. 3. (a) Cauchois, A.; Splenomegalies chroniques d'originc pylithrombosique, Thesis, Paris, no. 422, Paris, G. Steinheil, 1908. (6) Dfv, F.: Splnomgalie chronique avec animie d'origine pyllthrombosique, Normandie md. 21:109 (March) 1908. (c) Warthin, A. S.: The Relation of Thrombophlebitis of the Portal and Splenic Veins to Splenic Anaemia and Band's Disease, Internet Clin. 4:189, 1910. (<0 Eppingcr, H.: Hepato-Henale Erkrankungen, Berlin, Julius Springer, 1920. (*) Frugoni, C.: La splcnomegalia tromboAcbitica primitive, Arch, di pat. e din. med. 8:574 (Dec.) 1924; La spltoomlgalie throrabophMbitique, Rev, beige sc mid. 14:227 (April) 1938. (/) Ccconi, A.: La splenoraegalia tromboflebidca, Gass. d. osp. 44:265 (March 3) 1929. (p) Klemperer, P.: Cavcmomatous Trans formation of the Portal Vein, Arch. Path. 4:353 (Sept) 1928. 4. (a) Greppi, E.: II tuuore di milza cootrattile emorragiparo come probabfle forma di aplcnoangiopatia primitiva, Minerva med. 2:644 (Sept. 22) 1928; Die contractile Mil*tumor und seine Besiehungen stir thrombophlebitischen Splenonegalie, Verhandl. d. deutsch. Gcseltsch. f. inn. Med. 44:615, 1928. (b) Villa, L: II signiheato semiologico della contraaione di volume della milxa mediante adrenalina par la diagnosi delle iplenomegalie voluminose, Boll. d. soc. med.-chir., Pavia 8:479, 1928; Cuore e circolaz. 12:465, 1928. (r) Larrabcc, R. C: Chronic Coogestive Splenomegaly and Its Relationship to Banti's Disease, Am. J. M. Sc 188:745 (Dec.) 1934. (d) Rousselot, L. M.: The Role <of Congestion (Portal Hypertension) in So-Called Banti's Syndrome, J. A, M. A, 147:1788 (Nov. 28) 1936. NOTICE THIS MATERIAL MAY BE Z00.t6lZ BFG36609 880 ARCHIVES OF INTERNAL MEDICINE the pressure in the splenic vein was highly increased.9 But these same signs of portal hypertension were found to be present when an obstruc tive factor was missing. This fact was responsible for the widest gap in the support of the theory of venous congestion as the causative agent and formed an apparent paradox of great interest.* It is my opinion, however, that this apparent contradiction may be explained if the portal congestion is considered to be the effect of an increased flow of blood into the spleen ("primary acute congestion"). In 1936 I published a detailed study1 in which I suggested this inter pretation. I believe that some important recent contributions by other observers and my successive experience have brought further evidence to the support of this view. The object of this paper is to correlate these various arguments, thus bringing up to date an idea which may have some bearing both on the understanding of the physiology of the spleen and on the clinical manage ment of its circulatory dysfunctions. Before proceeding, it seems advis able to suggest a definition and a scheme of classification of the Banti splenomegalies; these preliminary considerations should be constantly borne in mind, as they form the premises of any discussion on the pathogenesis of the syndrome. DEFINITION Banti's conception of a symptom complex which is dominated by chronic splenomegaly, characterized by certain particular anatomicohistologic changes, due to an unknown agent and recognizable as a separate, dearcut disease can no longer be maintained. Many conditions presenting the clinical and pathologic features described by BarUi have been shown to be dependent on various known causative agents.* The term "Band's disease" has thus been discarded and "the Banti syndrome" used in its place, though even recently an author,*' with 5. Thompson, W. P.; Catighey, J. L.; Whipple, A. O., and Roussclot, L. M.: Splenic Vein Pressure in Congestive Splenomegaly (Band's Syndrome), J. Clin. Investigation 14:571 (July) 1937. 6. (a) Whipple, A. O.: The Combined Spleen Clinic, Surg., Gynec. & Obst, 4}296 (Feb.) 1937; (fr) The Medico-Surgical Splenopathies: Introduction, Bull. New York Acad. Med. 18:174 (March) .1939. (0 Rousselot, L. M.: Congestive Splenomegaly, ibid. 15: IS# (March) 1939. 7. Ravenna, P.: La splenomegalia fibroso-congestizia primitiva con ctrroii epatica e la sua sistemazionc fra le sindromi bantiane, Minerva med. 1:225 (March 10); 255 (March 17); 276 (March 24); 306 (March 31) 1936. 8. (a) Micheli, F.: Contributo clinico ed anatomopatologico alio studio della variety luetica del morbo di Banti, Soc. ital. per il progr. delle sc. 7:962, 1913. (t>) Durr, R. : Bantimilz und hepatolienale Fibrose, Bcitr. t. path. Anat. u. z. alls. Path. 74:418, 1924. S'. Patrassi, G.: 11 morbo di Banti intcso come cirrosi splenomegalies a dccono protratto, Arch, per le sc. med. 49:259 (April) 1940. C004.V6S2 I RAVENNA--BANTI SYNDROME 881 remarkable lack of criticism, insisted on the term Uuuti's disease, in spite of the fact that he admitted the multiple etiologic considerations. Even the idea of a Banti syndrome has been the object of repeated criticisms until recently. It must be granted, however, that chronic splenomegalies not related to any typical disease of the blood, to intrasplenic deposits of lipoids or to tumors are a matter of universal experience, though their existence has been noted more often in certain countries than in others. Banti1 and several other Italian authors* emphasized that this type of splenic enlargement is more or less frequently associated with hepatic cirrhosis. As to the relation between splenomegaly and cirrhosis, it was noted that the same degrees of splenic enlargement are found without any lesion of the liver, or with diverse stages of typical cirrhosis. There was enough evidence, it was believed, to warrant the assumption that this splenomegaly is either autonomous or coordinated with, but not dependent on, the hepatic lesion. This intimate relation between splenomegaly and cirrhosis of the liver, in which the splenic enlargement constitutes, apparently at least, the primary lesion, forms the basis of the modern idea of the Banti syndrome.1 To the Banti syndrome can therefore be ascribed the con ditions in which the morbid picture is dominated by a considerable chronic splenic enlargement, nonhemolytic anemia and leukopenia. The clinical course is often punctuated by repeated severe hematemeses and sometimes by transitory or permanent ascites. More or less constantly these symptoms are couple^Twith cirrhosis of the liver. Splenomegalies due to diseases of the blood, to intrasplenic deposit of lipoids or to tumors must not be confounded with Banti syndrome. Splenic anemia, a term which from Griesinger'g times up to recent years 11 1h2as pooled all these and other various morbid conditions, is really void of any par ticular meaning.1' Almost all chronic splenomegalies are, in point of fact, associated with such a type of anemia. 9. (a) Micheli, F.: Sul morbo di Banti, Arch, per le sc. med 15:351, 461 and 495, 1909; Sistemazionc e patologia delle splenomegalie primitive, Turin, Unione tlpogra/ico editrice torinese, 1910. (b) de Vcechi, B,, and Zanotti, P,: Su di una particolare splenomegalia primitiva, Sperimentale, Arch, di bio). 12:217, 1928. 10. (a) Greppi, E.: La maladie de Banti. Evolution et 6tat actuel du probl&me. Rev. beige sc. mid. 10:237 (April) 1938. (6) Ravenna.T 11. Hanrahan, E. M.: Splenic Anemia; A Study of End Results With and Without Splenectomy Based on Thirty-Five Cases, Arch. Surg. 19:639 (March) 1925. Mayo, W. J.: Certain Blood Dyscrasias Dependent on Pathologic Condi tions of the Spleen, J. A. M. A. 88:815 (Sept. 13) 1924. 12. (a) Naegeli, P.: BJutkrankheitcn und Blutdiagnostik, ed. 5, Berlin, Julius Springer, 1931, p. 560. (b) Klemperer, P.: The Pathologic Anatomy of Spleno megaly, Am. J. Clin. Path. 9:99 (March) 1936; The Spleen, in Downey, H.: Handbook of Hematology, New York, Paul B. Hoebcr, Inc., 1938, vol. 3, pp, 1591-1728. 882 ARCHIVES OF INTERNAL MEDICINE CLASSIFICATION Actual classifications arc mainly founded on morphologic bases. Macroscopic and histologic examinations have decided whether the splenomegaly had to be classified as fibrous or fibroadenic/ congestive 4 or siderotic.1* Naegeli'sl* and McNee's143 *classifications were based on which tissue was prevalently damaged The concomitant presence of hepatic cirrhosis or of thrombophlebitis gave rise to other classes (Eppinger*4 and Rousselot44). All these classes do not differentiate nosologic entities hut merely point to characteristics and courses which may depend either on the same or on different causative agents. In syphilitic patients with the Band syndrome, for instance, all the aforementioned aspects have been recorded (Micheli*4 and Minot2*), either with or without histologic signs of syphilis (Ravenna T). The only correct diagnosis would be that of Banti syndrome of syphilitic origin, which offers a comprehensive definition of the disease and not only one particular aspect. One of the best schemes for classification was suggested by Klemp erer,1** and it was based on pathogenetic criteria. But a lasting classifica tion should be based on the etiology. Only conditions of which the cause is not determined may be divided, somewhat arbitrarily, from the standpoint of morphologic aspects. It would then be correct to make a diagnosis of primary or cryptogenetic splenomegaly with prevailing con gestion (hemorrhages or siderosis) or with prevailing fibrosis (fibroadenia or cirrhosis). The latter class evidently includes instances presenting all the etiologic and morphologic characters described by Banti, and it therefore may conserve the name of Band's disease. The following scheme may be suitable for a simple classification. infective A. Of known origin' toxic syphilis leishmaniasis schistosomiasis malaria tuberculosis alcohol lead phosphorus B. Of undetermined origin with prevailing congestion (primary fibcocongestivc with prevailing fibrosis (Band's disease) splenomegaly with cirrhosis) 13. Canuta, C.: Contribute alia conoscertzs della splenomcgalia primitive, Haematologica 4; J29, 1923. 14. McNee, J. W: The Spleen: Its Structure, Function ami Diseases, Uncct I i95l (May 2); 1000 (May 9); 1063 (May 16) 1931. I RAVENNA--BANTI SYNDROME m 'Flic progress of the general knowledge of etiology will enlarge class A, with the inclusion of other causative agents, while the number of cases ascribed to class B is bound to decrease and ultimately disappear. CLINICAL AND PATHOLOGIC NOTES For a long time great importance was attributed to the anemia which almost constantly accompanies Band's syndrome. It is of moderate degree, normocytic and nonhemolytic and is associated with well marked leukopenia, relative or absolute monocytosis, and frequently with decrease of blood platelets. Its significance decreased considerably when it was generally recognized that this type of anemia, as pointed out by Micheli in 1903,14 is usually associated with any considerable splenic enlarge ment, from whatever cause. Lately attention has been drawn to a condition of splenic and portal congestion of high degree, and it has been noted that, being (ess con siderable or absent in splenomegalies from oilier causes, thin congestion forms a salient and typical feature of Band splenomegalies. Its presence is inferred from (I) the pronounced decrease of splenic volume after injection of epinephrine ir or after hemorrhage; (2) the frequent occur rence of copious hemorrhages from the gastrointestinal tract; (J) the frequency of transitory or permanent ascites, and (4) the hypertension in the splenic veins, as determined during surgical intervention.* The spleen is invariably greatly enlarged but shQws no specific char acteristics, and this fact accounts for the long opposition that Band's idea met with when morphologic criteria were dominating morbid anatomy as well as clinical diagnostics. A certain similarity of lesions, however, was noted, consisting in connective and elastic hyperplasia of the capsule and trabeculae and fibrosis and hyperplasia of the reticular framework of the splenic pulp. The liver is normal in some instances but mostly presents various degrees of Laennec's cirrhosis. Moreover, careful examination showed many definite signs of portal congestion, represented by (1) the gross and histologic aspect of the spleen; dilata tion of the sinuses, intrasplenic hemorrhages and their residuals and the siderotic nodules 14; (2) the dilatation of small vessels inside the spleen, 15. Minot, G. R.: Anemias, in Christian. H. A.: Oxford Medicine, .New York, Oxford University Press, 1932, vol. 2, p. 642. 16. Micheli, F.: Note ematologiche sulta malattia di Banti, Riv. di cliu. med. 4:65 (May); 81 (June); 97 (July) 1903. 17. Grcppi.** Villa.*b 18. B. dc Vecchi, B. Picchi and G. Patrassi (Ricerche sistematiche sulla genesi e sul valore delle icsioni spleniche conosciute col nome di arte di Gamna, Arch, di pat. e clin. med. 8:17 (Jan.) 1929) and C. Overling (Le role pathoginc de \a mycoae sp)huquc de Nanta, Presse mdij. S4:2 (Jan. 4) 1928), examining some of Ranti's own slides, observed siderotic nodules also in Ins original cases. 884 ARCHIVES OF INTERNAL MEDICINE of the splenic veins and its roots and of porta! and mesenteric veins,1" and (3) the dilatation of collateral portal-general paths of circulation. The aforementioned frequence of gastroesophageal hemorrhages and ascites is, of course, a pathologic as well as a clinical sign of portal congestion. Pathologists usually evaluate the state of congestion front the anatomic aspect of the spleen removed surgically or at necropsy. This criterion is misleading, as the spleen is larger during life than after death and is subject to shrinkage as an effect of various operative pro cedures, of anesthetics (both ether and chloroform) and of epinephrine, which is often purposely given. A further amount of blood flows out of the splenic tract of resected veins. That is possibly the reason why the presence of congestion had been so long overlooked by pathologists and by Banti himself. But, once, recognized, the importance of splenic and portal hypertension was stressed increasingly.u Some authors have used the term congestive splenomegaly as synonymous with Band's syndrome. Piney ** wrote: "There seems to be little doubt that Banti's disease is essentially a pathological state of the vascular system of the spleenand Greppi" noted that the vascular factor was becoming the "Leit-motif" of splenic pathology. Thrombosis of the splenic and portal veins, their cavernomatous transformation and their stenosis by external compression due to various causes or various stages of hepatic cirrhosis were often noted and referred to as possible or probable causes of the splenic and portal congestion. Experimentally, however, attempts to produce chronic splenomegaly by means of varied derangements in the portal or splenic circulation have l>cen uniformly disappointing.1" Only Rousselot and Thomson** have claimed positive results; obviously, their experi ments must be confirmed independently before definite conclusions be drawn.19 20 21 22 23 19. McMichael, J.: The Pathology of Hepatolienal Fibrosis, J. Path. 4 Bact. 89:481, 1934. Rousselot." 20. (a) Villa, L.: Sulla retrattiliti splenica, Rassegna med. 15:127 (Sept. 30) 1935. (b) McNee, J. W.: Croonian Lectures on Liver and Spleen: Their Clinical and Pathological Associations, Brit. M. J. 1:1017 (June 4) ; 1068 (June 11) ; 1111 dune 18) 1932. McMichael." 21. Greppi." Larrabee." Rousselot." 22. Pincy, A.: Recent Advances in Haematology, ed. 4, London, J. & A. Churchill, Ltd, 1939, p. 294. 23. Greppi, E.: Morbo di Banti 1938, Riv. di din. med. M:52 (Jan.) 1939. 23a. Castiglioni, G, and Peperc, M-; Ricerche spcrimentali intese a modificare il circdo splenico. Arch. ital. di anat. e istol. pat. 11:14 (Dec.) 1939. 23b. Rousselot, L. M, and Thomson, W. P.: Experimental Production of Congestive Splenomegaly, Proc. Soc. Expcr. Biol. St Med. M:705 (April) 1939. i RAVENNA--BANTI SYNDROME 885 A (act of the utmost importance fur the proper understanding of this vascular condition was the observation that all these clinical and patho logic signs of congestion could also be found in the absence of any obstructive factor in the portal vessels. Such an event was rarely con sidered in its real significance, though it clearly resulted from the patho logic records of most of the instances of what was described as Banti's disease in the old and modern literature, and McNeehad already noted that in Banti's disease high portal pressure and changes in the spleen precede the onset of marked fibrotic changes in the liver. Shortly thereafter Klemperer1,11 wrote that chropic portal stasis is not the sole cause of splenic enlargement and that cases have been observed in which the splenomegaly becomes clinically manifest at a period when there is no indication of a hepatic disorder. In other cases, he stated,'11* the splenomegaly occurs concomitantly with the hepatic alterations, and not subsequently; it is not dependent on or secondary to them. Six recent cases of congestive splenomegaly without peripheral obstacle to the venous return from the spleen were cited by me,1 and 2 others have since come to my attention. Two similar instances were referred to by Larrabee." Twenty-two others have been collected by Rousselot," from a total of 55 cases of congestive splenomegaly under his observa tion in the spleen clinic of the Presbyterian Hospital of New York. If it were borne in mind that often the obstacle to the venous return from the spleen could not logically have accounted for the splenomegaly (fre quently old splenomegalies are associated with slight cirrhosis or with recent thrombosis, as observed by Davies14 and myself1), the number of cases of apparently nonsecondary splenomegaly would increase considerably. Also the observations in cases of schistosomial splenomegaly are rather against the idea of ascribing the splenomegaly to the local deposition of ova and the subsequent fibrosis or to the thrombbsis of large portal veins, which is extremely rare in this condition.11 ' MECHANISM OF SPLENIC CONGESTION The absence of any obstruction in the portal bed is too frequent to be considered an insignificant exception; it forces one to the conclusion that an obstacle to the venous return from the spleen cannot be the first and common cause of the Banti syndrome in all cases and that the 24. Davies, J. C.: Splenic Anaemia and Portal Thrombosis, Lancet S:498 (Sept. 8) 1928. 25. Onsy, A. B.: The Pathogenesis of Endemic (Egyptian) Splenomegaly, Tr. Roy. Soc. Trop. Med. 4 Hyg, 19:583 (April) 1937. Shafi, A. M.: Hiatorical Review of Egyptian Splenomegaly and Allied Conditions, J. Egyptian M. A. 191 561 (Oct.); 631 (Nov.); 652 (Dec.) 1936. BFG36611 00&TCtZ '9C6t (SZ JCOIt l'l'l! 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)a s^uiteaoa >9u;doaie 4t^snitqmrt(oX `xneuuou suatqa saj xaip ii t\ ap auinjoA np t)uauia8uvqa ia tap^j^jn suou^jtoxg :*q 'Jajqo^ put '*jf mi ( *V) 6111 ill P!q* `Mld poom OI uottmay ui uaaids aqi jo XiiamupXira ; 0 '3 `PI'0 Pub ' J [ `BapjaH ' H f 'X|puiJ0 6C61 (*"V) 90t:KI -|0>Xyi f -my `UMjds aip jo Moy pools ay) jo )uauiajmcajy ; 3 j `uuBjy pus ' j f jjaijjaH !'H i ,<'(PU!J0 -8C6I (61 PO) t99!*I U!D ox'M `lB HS aoij `Xpnjg jBjuauiuadx^ oe jo tjodajj Ajutitutuajj :uaajdg aq) jo unpXq^ puB uopaunj jjoAasa^ poo|g MX : '3 ( `ijaujaH pu* ' H 'f 'X1P"U0 '6Z 6C61 (""O CZ!> >"> I>! a aeus ip *jb)i -ipjy '(auotznpuouajds B|jns a auoiZBJiuoaouajdi Bjjnt tuotxBJapjs -oo3) aq3siSo|0)8d mouipuoa asjaAtp ui oaiuajdc biuojjs ojjap aJBpsfmu-oapieja oiBjedds.-t :-q 'yonig (</) '<59z d 'gT6I `Juuduio^ uapunns a 'M 'B!qd|3po|!qj '( pa 'A8ojo|t<n jo qooqixax V I'M 'u>oo|fl puB '-y -y 'Mounxtjy (o) -gz 'SC6t '00c: t !A!lBsg `aijBSautouajds aunajs tp tcaua8o)d sjjau Bzjtut Bjjap ajyiBJiuoa ajBjossnui ojRjBddBjjap BiuoiBjjns nioizBjapisuo^ : y 'jauna tjjssao SC6t `Wr'-t B!>)D ' Jiqa-paiu 'aog ijog `wna a naira* -ojnf 'oisayiuSit : (siuo) up) aizi)sa*uoa atjeSaiuouajdg : '3 `iddajij *zz a')ojassnog zZ d `BC6I, -03 )j 005 s.uoltiijBig -j `ttqdfapEjiqg 'A3o|oieara{j jo qooqixax V "AV `'oiOrj^4 jZl-411 dd `gpdt *S3j(j XiisjaAiuf) pJojxo jjjoa N 's*>u>auy qi jo uoyduooQ JE31U1I3 pue ASojoisAqg iBOfSojoqicg : g 3 'louyy pus ` g 'A\ 'j|SB3 yz uonsaSuoD aiuajds aq) papaaajd sjassaA jBjjod aq) jo sjjbm aq) jo suoisaj )sq) paiejjsuoiuap aq ji pjnoa JOjq X)(ai|ob aqij-jBijauB Jiaq) jo aauapiAa ou st ajaq) `Xjijipbj) -uoa q3;q qijM paMopua puB sjaqtj ajasnui ui qaiJ ajB sjassaA jBjiod qSnoqi ')tig 'uoysaduoa aq) jo asnsa aq) si uoi)aunj siq) jo Xauaiayjnsui aq) )uq) pa)sa3Sns sem )i `snqx 'JaAij aq) jo aauB)sisai jBiaqduad aq) auioajaAO 01 poojq aq) sdjaq XjaAi)aB qaiqM uoyaunj aqij-jBuaviB `aji)aBj)uoa b aABq paq jB)jod aq) jo sbiaA aq) )Bq) j)sa33ns uaaq SBq )i sjaqjo Xg ,,'M0|J poojq aqi ill suoiicijba auuqiXqj Xq jnq uaajds aq) jo qjoMauiBJj jBjnasmu qjoouis aq> jo uoijBXiqaj puB uoiianjtuoa a;ui -q)Xqj b Xq )ou pasnea bjb auinjoA aiua|ds jo saSusqa aiuiq)Xqj aq) osjy ti |nj)qnop si uotiaujjuoa jjaqi jo Xanayja aqi pern `uaajds UBumq aqj ui pajnqujsip X|aajsas bjb *Jaqy ajasnui mg poojq a;ua|ds jo Moymo aq) paju|n3aj uaajds atjj jo qjoMaumjj jBjnasniu ajsutj)ui aq) jo uotpuj) -uoa aq) )Bq) uoiujdo aq) uo pasixj sum siqj, `uaajds aqi jo qjoMaiuBjj jBjnaaqsj) puB jsjnsdBa aq) jo X)ijipBj)Uoa pasBajaap aq) jo aauanbasuoa aq) sbm )uama3Jo3ua aiuajds aqi mqi jaqaq aq) pa)B)s ,, |auiag sijusa^ pus iddajQ paq |B)jod aq) ui uoipnjisqo ub uiojj Xjmapuadapui uo|isa3uoa aqj uisjdxa oj pagmiqns uaaq aABq sasaqjodXq Maj y *a|qBjiBAB masajd )b aauapiAa aiSojoqjsd aq) q)iM Sui)SBJ)Uoa SB papjvasip aq pjiinqs ,,'9joi|inu jo Xiuofmu aqi Xq p|aq jjiis `XjBJjuoa aq) o) uoniido ZNI3M3H iyN8-U.Nl 80 S3AIH08V 98ft BFG36612 archives of internal medicine further development of the disease. They are complications or asso ciated morbid conditions and not the first cause of the congestion, because --as should always be remembered--splenic congestion may .be found independent of either. Obviously, the favorable effect of splenectomy or of ligation of the splenic artery (Greppi and Kemp *'J), which often, besides relieving the general and hematologic conditions, diminishes the tendency to gastroesophageal hemorrhages and ascites, is due to the removal of the primary cause of portal congestion. But some failure, often cited in the literature,should have been foreseen, as splenectomy cannot remove the eventual thrombosis or the cirrhosis, nor can it always modify the state of gastroesophageal varices '* or of the widespread dilatation of submucous and subserous small vessels of the esophagus and the stomach, which is frequently seen in cases of this kind (Ravenna * and Fiessinger, Albeaux-Fernet and Varay **). COMMENT It seems to me particularly significant that the present conception of primary splenic congestion is based on the undisputed presence of lesions in the small splenic arteries. Their fibrosis had been described by Banti1; the presence of regressive lesions in their walls and of endoarteritis had been noted by Gamna11 and by myself.' The siderotic nodules themselves are the direct consequence of periarteriolar hemor rhages, as pointed out in 1902 by Marini,** the first author who described such lesions, and his interpretation was substantially confirmed by successive observers." The significance of arteriolar lesions in the* 23 32. Kemp, R.: Recurrent Haematcinesis in Band's Disease, Brit. M. J. J: 222 (Jan. 29) 1938. 33. Pemberton, J. dej.: Results of Splenectomy in Splenic Anemia, Hemolytic Jaundice and Haemorrhagic Purpura, in Collected Papers of the Mayo Clinic and tlie Mayo Foundation, Philadelphia, W. B. Saunders Company, 1931, vol. 23, p. 539; Ann. Surg. 84:755 (Oct.) 1931. 34. Hines, L and Fitzgerald, li.: Splenomegaly of the Banti 'I'ytto: Uei>orl Of a Case with Postmortem Observations Four Years After Splenectomy, Arch. Path. 38:155 (July) 1938. Kemp." Grccmvidd, 11. M., and Wasch, M. G.: The Roentgenologic Demonstration of Esophageal Varicea aa a Diagnostic Aid in Chronic Thrombosis of the Splenic Vein, J. Pediat. 58:57 (Jan.) 1939. 35. Fiessinger, N.; Albeaux-Fernet, and Varay, A.; A propos des lidmorrhagies peraiatantes apria splincctomie. Bull, et mem. Soc. rofd. d. hop. de Paris 84)494 (March 18) 1938. 36. Marini, G.: Sopra un caio di aplenomegalia con cirrosi epatica, Arch, per le sc. med. 38:105, 1902. 37. Gandy, C.: Ldiiona particulierci de la rate en un cas de clrrhose blltairc, Bull, ct mfm. Soc. anat. de Paria 88:872, 1905. Eppinger.u Gamna.1* Cfirtsteller, E., and Puskeppelies, M.: Die periarteriellen Eisen- und Kalkinkrugtationenx in der Mils, Virchows Arch. f. path. Anat. 388:107, 1924. de Vecchi i ravenna--banti syndrome mechanism of cougcsiiui), however, hud never Iwcii considered before in human pathology, but recently Greppi ,w and Lend,** accepting the arguments discussed in my previous paper, admitted that the first lesion responsible for the splenic congestion might be an arteriolar one. Some experimental attempts to produce active congestion of the spleen were made by Henschen and Hovvald.1** They denervated the spleen of 3 dogs, in 2 of which splenomegaly was obtained. In view of their importance, these experiments should be repeated and enlarged, with the study of the alterations, if any, secondarily produced in the portal circula tion and in the liver itself. Episodes of Gastroesophageal Hemorrhages and Ascites.--Often this frequent and serious event in the course of the Banti syndrome puzzled the physicians by whom it had been attributed to an organic obstacle in the portal bed, which could not be found at the necropsy.19 Hemor rhages and ascites may depend on the breakdown of the portal circula tion, due to an anatomic obstacle (thrombophlebitis or cirrhosis), as well as to the progress of arteriolar lesions in the spleen and to a transitory increase of hepatic resistance, due to digestive or cardiac exigencies. In many cases ascites appeared and disappeared quickly (Frugoni '*), and I think that this fact is rather against the idea of ascribing the con dition to a definite anatomic obstacle, such as that represented by thrombosis or cirrhosis. The influence of digestive requirements on splenic circulation is great indeed, as it is proved by the increase of splenic volume during the normal digestive process, and therefore in splenomegalic patients the relation of the hematemeses to digestive phases should be investigated with greater attention. Splenic Shrinkage After Administration of Epinephrine.--The shrinkage may depend on the stimulation of the splenic arterioles, the unl /.juiuIII "i* O. M., uim| OacIliultH'c, G.: K*ui dr r^priMliitiion meuiale dcs nodules de Gaiwly-Gamna, Presse mid. *7:1136 (Autf. 31) 1929. Jaeger, IS.: tfeber Stainingimilz, Verhandl. d. deutsch. path. Geiellsch. 28:334, 1931; Milzbuii und Kreiilau/storuntf, Virchows Arch. f. path. Anat. 28#:531 and 552, 1937. Alexandre, A., and Valducci, E.; Fallon chc determinant) le Micros- tuaion! lideroticbe della miUa nei focolai sdcrosidcrotia, Pathologica *7:321 (May 30) 1935. 3d, bensi, F.: Sintlromc Bantiana-splenomcgalia fibrosq-congestiiU prevaleute- mente fibrosa-Contributo clinico-Ipotesi patogcnetlcbe, liaeinalologica 12:47, 1940. 38a. Henschen, C., and Howald, R.; Die analomtichen und Iciinisch-physio- logiichen Folgen der operadven Entnervung tier Mila. ExperJmentclle Untertuchungen, Arch. f. klin. Chir. 187:667, 1929. 39. Cellina.1* de Castro and dall'AcQua.*9 Lucchi, G.: Morbo di Banti a hmghissimo tkcorso e splenomegalia tromboflebitica con trombnsi della vena mesenteries superior*, Riv. di din, med 18:421 (July 15) 1934, BFG36613 Q6P6&Z |0 pom^n mi (pe 'on) srs-'ci f n "^hiv <vns '!iov iCq MttEl01UOU3]d5 psinon ) 1U3UJ1E3J L qt UO !pn|g JRIU3U1 -uadxg : f 'onjq p ouipojj -g[gj *pjq '*inos nijqnu *ipp oiumubih.ii pu niuipuojpe-ouiuiqi auoticraonv g 'EAotnqj gjdi 'IfI:gl piqi `BAiimiMd 3ltuuninr-0Ans3 eticpui *)pu coiuqnnjpo Eidtjaj njjni oipjaoijj : -j 'pjopanN 'Kfit `TZl'-Lt *Pjq* 'eatJiqBiu 3U0!Z3JU1 eipp qousyn !P *Jna *[lnS : '3 'KKojq '4E61 'CZl:tl (I ra) 'loyrejwu tp MJI `oauEittn omt z]pp ooniipinjp* oitntu -DIWI a nucput n|S3uiot|dt jpp pttptojiuoo ip oiMipuos : H `01109 'zt '8C61 '1W P* M!il PIP! *)> 3uoii3jui cjpp t|oov K !P "IP'S "9 XC6! `pf:| TP! `ral"i Mioizsjm E|pp i|ov n !P >"0 ns -d `opm XE6I '06Z:l (I '*) W*!*TM ip 'Aig 'muipsui auoiojui t|pp I|03v W IP bjiu *ns - 9 `oiptrtMiy,p '9E6I (PI tpj*n> ISC t9 Pi![i buijojijj `niuoio nuigrat auotnjuypp Jta zips - n `flossy `Ip sjuapBd apjBjadouou ut stsauiajBtuaq snotjps jo igSuep sqj asra-nap ospt jqSttu justuiEaij siqj 'ajnssajd [Bjjod aqj sjaMO] auuqdauida aq) JI 'ssaasns JO S30UBq3 M3J SJ3JJ0 U33]ds 3fl) UO UOtJUaAjajUt ]B3l3jnS qoiqM Ut S3SB3 111 1U3UllE3.il JO pOl(13UI S,t[03Sy Xj) OJ 3[IqM qjJOM 3q Xbui jt lEiji )Sa33ns o) qstM j jnq 'pajinbaj st aauauadxa jaqjjng TJBJS |EJ3U33 aqj JO JUautaAOjdtUt XjOJ3BJSt)BS pUB 3U1UJOA 3Uedaq JO 3SE3J33P Jq3t]S B `aZIS 3IU3(ds JO 3SB3J3ap luaUBttUad pasnBS XdBjaq) I|03Sy qllM jaqja3oj JUatUJB3J) 31)l|!qdXsllUV *Xm0133U3fds p3)B3tpUIEJJU03 uotjipuoo Jood sjh 'SijipqdXs sbm aq imp paoojd suotjasaj d;3o|oj3s aq) pue `bub|Eui uiojj pajajjns psq sq 3JOJ3q sjboX ; 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It is suggested that the congestion may be due to primary lesions of the small splenic arteries which regulate the blood flow into the spleen ("primary active congestion''). The human spleen should be considered as an elastic rather than as a contractile organ. Its variations in size depend on variations in volume of the inflowing blood, rather than on active contractions of the smooth muscle of its supporting framework. From a mechanical point of view, the spleen might be defined as an automatic controller which regulates the pressure of the splenic venous blood in order to maintain the balance between the volume of inflowing blood and the amount which can be discharged through the hepatic resistance.' Normally, and within certain limits, in pathologic conditions, the splenic elasticity guarantees a pressure sufficient to secure the further progress of venous portal blood. Congestive splenic enlargement is therefore a mechanism to counterbalance either increased volume of portal blood or increased peripheral resistance to the dis charge of a normal amount of blood. The Bants syndrome is a symptom complex dominated by chronic fibrocongestive splenomegaly, accompanied by portal hypertension and complicated by, or associated with, hepatic cirrhosis or thrombosis of the splenic and portal veins. It may depend on various causative agents, either infective or toxic. A scheme for its etiologic classifica tion is presented. The splenic changes of Banti syndrome arc probably due to primary lesions of the splenic arterioles, the regulating power of which becomes insufficient to control the inflow of blood. The consequent congestive splenomegaly is the cause of the circulatory disturbance in the portal bed. Secondarily, hepatic cirrhosis and venous thrombosis may aggra vate the state of portal circulation. 2900 Ellis Avenue. sootbevz Progress in Internal Medicine GASTROENTEROLOGY REVIEW OF LITERATURE FROM JULY J9J9 TO JULY 1940 CHESTER M. JOKES, M.D, Physician, Massachusetts General Hospital; Clinical Professor of Medicine, Harvard Medical School boston The widespread interest in gastroenterologic problems and their clinical importance is evidenced by the multiplicity of articles appearing in the world literature on all phases of the physiology of the alimentary tract, normal and abnormal, and the therapeutic applications directed thereto. Some new data have been added, particularly to the knowledge of the physiologic response of the digestive tract to various drugs, many of which are actively employed at present. In this review allusion will be made to strictly new discoveries and to' new applications of old principles. It will also be my purpose, however, to call attention to many articles of clinical importance for the sake of reemphasizing recog nized or partially recognized concepts of gastrointestinal disease. PHYSIOLOGIC ASPECTS Interest continues in the various factors influencing gastric secretion. In fact, attempts are still being made to obtain a satisfactory normal gastric sccrciory curve by varying technics. Wilhelmj and Sachs * still pursue their studies of gastric secretion following a test meal consisting of a specially prepared solution of Liebig's meat extract and a standard amount of phcnolsulfonphthalein (phenol red). They believe that after such a test meal it is possible to determine what proportion of a given sample is fluid of the test meal remaining in the stomach and what pro portion is due to secretions. The total secretions entering the stomach can be separated into acid and nonacid fractions, and the acidity of the total secretions can be determined independent of the acidity of the mixed gastric contents. Multiple curves on given subjects show a rather remarkable agreement, and the amount of acid secretion is usually constant in the same person. The increase in nonadd secretion due to regurgitation from the duodenum varies considerably even in the same1 1. Wilhelm), C. M., and Sachi, A.: The Characteristic! of the Normal Human Gastric Secretory Curve Using an Improved Gastric Test Meal, Am. J. Digest Oil. 529, 19.19. 893 9 V70094 BFG36616 ii " ii i:;;" >Z / iS'is 99 '1..... C /l. T :K.. T f-'u ii;. ........ it i Nwa 6 E i 13 ;--di z sjusr.osg 4u5ijj i MUSiiMj **'N J5P-u V*?ij SWhijAjiAiMMMhii'iMNhiMMhiMhiMMkiMH m3 '"4"N iiuna ; 'P5XfT-j _.f. --uaSrSg; Piluuuuuuvuuuuuuuuuuuuu'S c t..i j '.! 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