Document 4aDgJ6gwbDmoE8EGovgJ16e61

' 2 Annals New York Academy of Sciences t Chcmic. W. Focrst, Ed. Vol. Id: 306. Urbnn <5t Schwnrzcnbcrg. Mllndicn, West Germany. '-------------------- 100. Ostejt, R. H.. C. J. Carr A J. C. Krantz. 1947, Anesthesia. XXVII. Narcosis with vinyl chloride. Anesthesiology 8: 339. 101. Ostermayer, H. 1967. Vinylchlorid. In Ullmanns Encyklopadie der (ecltnisclien Chemie. W. Foersl, Ed~Vol. 18: 82_Urban & Schwarzenberg. MUnchen, West Germany. 102. Otto, P., P. II. Krause, H. G. Jester, F. \V. Schmidt A K. H. Gutzel. 1972. Idiopathische portale Hypertension. Med. Xlin. (Munich) 67s 447. 103. Parmeooiani, L. A C. Sassi. 1933. Kischl e paiologia professional nella pro- duzione c nella lavorazione di alcune materie plasiichc. Med. Lavoro 46: 14. 104. Patty, F. A., W. P. Yant A G. P. Waits, 1930. Acule response of guinea pigs lo vapors of some new commercial organic compounds. V. Vinyl chloride. Public _ Health Rep. 45: 1963. | -cip)fc-3n<Fedih-lniefs<iAnce-EutJlsh&ss-JdeAu-3torkr-N^Vi-----T^oOrlOG--Pat11, rr~A:, Sdr-t963. Industrial Ilygiene-and-ToRieolegyi Voir Hi Tom'cofogyrIrL-'"'' - D, W: russLtt dL~OrO. I<i:h7-Eder-2nd-edih-lnierscience-PublishcrTrNw-Yock,-- -NrY. 107. Peoples, A. S. A C. D. Leaks. 1933. The anesthetic action of vinyl chloride. J. Pharmacol. Exptl. Ther. 48r 284. 108. Polish, ., J. Christie, A. Coiien A B. Sullivan. 1962. Idiopathic presinusoidal portal hypertension (Band's syndrome). Ann. Internal Med. 56t 624. 109. POPPER, H., F. Paronetto, F. Schaffwer A V, Perez. 1961. Studies on hepatic AbroJiJ. Lab. Invest. JOi 263. /*,oo1 110. PerfCR, Il:-1968. Pathoiogyuf yuiul liy pcilcnsioii. In Tlie Tlieiapyuf Portal-- s'/^' --HyptfinflllilOII. |4.~Ov MjTfcuffrTEii. Gcorg-Thiemc-VcriJg. 3luilg4irr3Ycst-Ocr-uiiiiyr 111. Popper. H. A F. Hutterer. 1970. Hepatic (ibrogenesis and disturbance of hepatic circulation. Ann. N.Y. Acad. Sci. 170: 88. 112. PorrER, II. AS. Udenfrieno. 1970. Hepatic fibrosis. Correlation of biochemical and inOiphologic investigations. Am. J. Med. 49: 707. 113. Pusiiin, G. A. 1965. O porashenii pe(cnl I zclinyikh putei u raboiikh' zan- jalyikh w proizwodstwe nekatoryikh widow plaslmass. Sov. Med. 28: 132. 114. PVC producers see good business shcad. 1969. Chem. Eng. News August 4: 18. 113. Quooss, H. 1939. Gcsundheilsgefahren in der KunststofTindustrie. Johann Am broses Barth Vcrlag. Leipzig, East Germany. 116. Ramaainoaswaku, V., K. L. Wto A S. K. Sama. 1962. Cirrhosis of the liver In ,t Northern India--a clinicopalhoiogical study. Arch. Internal Med. 110: 350. ;~1I7. Ramaunoaswami, V. A N. C. NaYak. 1970. Liver disease In India. In Progress In i'" l LNievwerYDoisrke.asNe.Y1.1. Popper A F. SchatTner, Eds. Vol. Ill: 222. Grune A Stratton. 118. Raffafort, A. M,, M. Knoblauch, R. G. Black A S. Oiiiaa. 1970. Hepatic microcirculatory changes leading to portal hypertension. Ann. N.Y. Acad. Set. 170: 48. 119. Ravenna, P. 1940. Band syndrome (fibrocongeslive splenomegaly). Definition, classification and pathogenesis. Arch. Internal Med. 66i 879. 120. Remmer, H. 1970. The role of the liver in drug metabolism. Am. J. Med. 49r 617. 121. Reynolds, T. D. A A, G, Redeicer. 1965. Hepatic hemodynamics and portal hy- |>ertension^i^^^^^^^^^^^^^Mc^4^onrier A F. Schaffncr, Eds. Vol. .......... r 123. Rousselot, L. M.4940. Yhe late phase of congestive splenomegaly (Band's syn drome) with hemafemesis but without cirrhosis of the liver. Further observa tions on the etiology of Band's syndrome and rhe effect on prognosis of certain variations in the portal venous pattern^Surgcry 8t 34.-- . 423. SARAOOCA^^rw^s^kVARES^^^AllROOnnjniLVOToRTA? 1972. Some clinical and laboratory findings in patients Injected with thorium dioxide. Study of 155 cases. Am. J. Gastroenterol. 57s 301. U6. ScttAFfNER, F. A H. Poffer. 1963. Capillarizadon of hepatic sinusoids In man. Gastroenterology 44: 239. VjOTSSV?- Marstcllcr et al.: Splcnomcgalic Liver DUcOic iJ-3 127. Sciiaumann, O. 1934. Ueber die llerzwirkung einiger InhRl2t:or.sr.irko:j;a. Medizin A Chemie. Abhandlungcn aus den Medizinisch-chemischeft Fo.-schungjjlilten der l.G. Farbeninduslrie A.G. Vol. II. Bayer-Meister Lucius. Leverkusen, West Germany. 128. ScifAUMANN, O. 1938. In Toxikologie und Hygiene der technischcn LSjungsmillel. K. B. Lehmann A F. Flury, Eds. p. 130 (Monochlorathylen). Julius Springer. Berlin, Germany. 129. Scmuo, M. 1968. Zur Leberhislologie der verschiedenen Formen des portalen Hochdruckes. In The Therapy of Portal Hypertension. N. G. Markoff, Ed. Georg Thieme Verlag. Stuttgart, West Germany. 130. SctiwoT, F. W. J969. Geringer Aktiviratsanslieg der Serum-Transaminasen. Deut. Med. Wochschr. 94: 2250. 131. Sciinack, 11., L. Stockinoer A F. Wewalxa. 1967. Adventitious connective tissue cells in the space of Disse and their relation to fibre formation. Rev. Intern, ' Hipatot. 17: 855. - i32. CmoNUS. 11. R'., A. 1. Weiiw-A-M-H^-flictLouL-1949.-HimUbuu>.~uf PUStlu7~2IIU -~<1it. D -van-Norfiand C.U.. Inc. I'llnocMir, MX. 'v K- 133. Slater, T. F. 1972. Free radical mechanisms in tissue injury. Pion Ltd. London, England. 134. Smoron, G. L. A H. A. Battifora. 1972. Thorotrast-induced 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. 11. Baccenetoss, L. J. Sciioenfield et of. 1971. Observer error and sampling variability tested in evaluation of hepatitis and cirrhosis by liver biopsy. Am. J. Digest. Diseases 16: 1082. 137. Stein, G., S. JOiie, C.-E. Lance A G. Veltman. 1973. Bandffirmige Osteolysen in den Endphalangen des I landskeletls. Forrschr. Cebieie Rocntgenstrahlen Nu- Mearmed. 118: 60. 138. Stencer, R. J. 1965. Fibrogenesis along the hepatic sinusoids In carbon-telra- chloride-induced cirrhosis. An electron microscopic siudy. Expil. Mol. 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Klatskii bleeding esophageal varic hepatic and exlrahepatic o nn. 1959. Portal hypertension and ice in (he absence of both inlraorlal vein. New Engl. J. Med. 261: 209. 147. Torkeison, T. R., F. Oven as determined by repealed >61. The toxicity of vinyl chloride alory animals. Am, Ind, llyg. As- soc. J. 22: 354; Dull. Hyg. J 148. Tridukii, S. L., N. P. Tikiiom truda i mcropriyaliya po a A L. A. Kozlov. 1949. Usloviya i pri proizvodslve I ixpol'tovanii khlorvinilovykh ploslitcski'. nnit. 10: 38. 149. Truffert, L. 1959. Aspects i I'induslrie dcs malices plastfqucs. Arch. Maladies Profess. 20t ... 150. U.S, Department of Health, Education, and Welfare--Pudlic Health Ser vice: Center for Disease Control. 1974. Angiosarcoma of the liver imoni polyvinyl chloride workers--Kcniucky. Morbidity Mortality Weekly Rep. 23(6): 49. Q) BFG36687 BFG36689 NOncE THIS MATERIAL MAT BE PROTECTED BY COPYRIGHT LAW (IT T L E J 7 U.S.CODE) THE LATE PHASE OP CONGESTIVE SPLENOMEGALY (BANTI'S SYNDROME) WITH 1IEMATEMESIS BUT WITHOUT CIRRHOSIS OP THE LIVER Further Observations on the Etiology op Banti's Syndrome and the Effect on Prognosis of Certain Variations in the Portal Venous Pattern Louis M. Roussklot, A.B., M.D., Mkd.Sc.D., New York, N. Y. (From the Deportment* of Surperit, Vveshptrrian Hospital and Habits Hospital, and the. Spleen ('linic of the Vanderbilt Clinic) THE early descriptions of Banti1-3 and his concept of the etiology and clinical course of so-called Banti's disease are so entrenched in medical literature and text that it becomes difficult to alter that which so long has received the sanction of common usage. The follow ing quotation from Cecil3 epitomizes the generally accepted textbook version of the disease: "Splenic anemia (Banti's disease) is a chronic disease of unknown origin, probably toxic, and primary in the spleen, and is characterized by splenomegaly, anemia, and leukopenia, a tend ency to gastric hemorrhage, increased formation and destruction of blood colls, and later by cirrhotic changes in the liver, with ascites and jaundice." The clinical sequence as described by Banti of (1) primary spleno megaly, toxic in origin, (2) an intermediate stage, and (3) finally, the third stage with cirrhosis of the liver, of course, has often been dis puted. The German concept of SUiuuwjsmilz* was an early attempt to controvert Banti's theory. This in general precludes the possibility of a toxic substance producing primary splenic enlargement and predi cates the existence of chronic portal stasis as a precursor of the spleno megaly. It is surprising to find how little convincing evidence has been presented to prove either of the two aforementioned contentions. The Spleen Clinic of the Presbyterian Hospital has presented a scries of papers5'7 in recent years supporting the view that the picture pre sented by Banti is confusing and misleading in respect to etiology, clinical course, and treatment. Our group is firmly convinced that the etiology of Banti's syndrome may be entirely explained on a mechan ical basis; i.e., portal bed obstruction with an associated "portal hyper tension."8 The site of the. obstructive factor causing the portal hy pertension and splenomegaly may be intra- or extrahepatic. The term "congestive splenomegaly" suggested by Larrabec," wc believe, is more descriptive than Banti's disease or Banti's syndrome. The usual intrahepatic lesion producing congestive splenomegaly is, of course, cirrhosis of the liver. This paper, however, is solely con- Presented at the meeting of the Society of University Surgeons at New York, N. Y.. February 9 and 10, 1940. zoozsepz 34 noussELOT: LATE phase of congestive splenomegaly 35 corned with a selected group of 15 patients, all presenting ttie typical-i symptoms, signs, and blood studies usually associated with thissyn-) f drome. Severe gastrointestinal bleeding occurred. in each of these' patients, yet in no case was there coexistent liver cirrhosis. We shall demonstrate that in most of these patients an extrahepatic obstructive' factor was present in the portal venous bed. In every instance in which splenic vein pressures were taken at operation, a "portal hyper tension" could be determined. The nonexistence of liver cirrhosis in all was established by most of the available methods at our command. These procedures include various liver function tests carried out beforo j operation, gross examination of the liver at operation, and liver biopsy i on one or more occasions in the same patient. Furthermore, evidence j will be -advanced to show that cirrhosis not only was absent at the L time of operation, but did not develop as established by the subsequent j clinical course and further laboratory studies for varying periods up to nineteen years after operation. In four instances this lack of liver-, disease has had additional confirmation by autopsy as well. evidence demonstrating the absence of liver cirrhosis IN Tilts GROUP OF CASKS Tabic I will clarify the statements as to the nonexistence of liver ', ,(t'il. ' cirrhosis in all these cases. In the first 2 patients operated upon in 1920 and 1922, there is the least evidence. In each instance there is' only the surgeon's operative description of a normal liver. However, H, in each of the succeeding .13 patients, almost ail of whom were operated , ; : upon by Allen 0. Whipple or myself, at least two forms of corrobora- .^, live evidence are presented. Histologic proof of normal liver tissue ' Jr was available in 10 of the 15 cases. Liver biopsy was done at opera- il. tion in 7 instances and 1 of these also had subsequent autopsy con- I Urination. Autopsy was also obtained in 3 additional patients who had t .j:; no liver biopsy at the time of operation. <?j:: ft is our experience that the bromsulphthalein test is a reliable index " 1 of hepatic damage. We have felt particularly secure in our interprets- : tion of these tests because in every case no retention or only a slight trace of the dye was present in the blood nftcr thirty minutes and no '' equivocal or border line determinations occurred. Bauman and OrrV* recent report on the accuracy of the bromsulphthalein test is of in-,,' ' terest In not one instance in our scries was there any inconsistency ' between liver function test, liver biopsy, or necropsy findings. '' ,v nature of the extraueuatic lesions As designated in Tabic I an extrahepatic obstructive factor wss de-1[ monstrable in the portal venous system of 8 of the 15 patients examined (Cases 4, 5, 6, 7, 9, 11, 12, and 14). This was recognized at the apenU ing table in 4 instances and 4 times it was only demonstrable at autopsy. The failure to discover an obstructive factor in the other 7 cases is not Od aTl u> On On NO O 36 SURGERY W) ccc 8G V. # fa!1i c e ss. 11 1 1*111 (u ? U i 1 1111 i 1 32 t/.hS 2U t"o 11 11 11 LIVER SI AFTER w A S 111 h 1 1 1 V(J, wu 111 111 ii ii ii iiitti iiiiii t ii iiii a *s II fc 1, sti : i ill o <V"* X 02 iii iii1i1 i iii ii ii >2 g*5-.^4BS} --*f, ^ N W i -> 2B a.41 V to i iiii 1 ii i iii % * * a.? 8.1 Isti j -e *3 -- -M 2 . 1Sio..." . |SEo.."3.*.30 l1i 1 ii1l 2-0 III ii i i ii1 ii iii tii i i i iii ji iii ! i1i nsfor1 vein kh \es 2o Bi e'g ~ i< 91 an, <n o w :i 5r " SB-> ^o.24t*^ XiOguLrt. |Sc Ifii Xu 111 1111 11 11 11 11 >1l1 11 J1 11 i1 11 111 1 t1 t11 111 6g Q^ E8w owtJoca &/.* gC 39 2tC.*` .>Vc2j,. _//. >an. >, L iUoem 2 >X. *4->> o X X X X X ca c _ _/ u scH. Uf*<t <S ptN- OaMs _2 < H -- o8k ftJ e _, t25 &&> XD p *5 st XD c ~ 2*t- M XD a *2. 2 ii XD occ.Sa*> -1-5 SHi c4 i 3 ii O.- * a Xf* X D 2 Ji o = XD 111 11111111 1 111 1111 1 1f1 1 1111 1 M 1. a a .a 73 a fl haft.. --!> -d S 13 2 gl oa X& o CO CO 72S " %W CO CO CO t- pleni mm 50 1ii iii iii i i i i 1i 1 1 i i rt ^ 0* 1 i .2 in to A .5 OV 1 1-- 1 r-it 2 i i i 2i i i i t l i ^ in n i-J ^ 1 i 2 o}-i ft w> i i i ii i i 1 1 i s a IB . .i i i *; .g i i i i i OG ,B 1 i i i i i 1 1 1 i i "e. o J= 32S 1 OS -w 03 Ml 3 g i ii i i i 1 1 ii L L 1. P it L it L CO rf) CO CO CQ I^S CO 70 UW Q i--i rt C /1 'I* > N eoorsepg KOUS8KI-OT: LATH PHASE OK CONGESTIVE SPLENOMEGALY 37 <' 8 , Splenectom y; L . H p itk m o f splenic vessels; E , exploratory celiotom y. I II j. tI II f Ii BFG36691 38 SURGERY necessarily a weakness in our hypothesis but is due rather to the tech nical difficulties involved in an operative examination of the portal venous bed away from splenic hilum, particularly behind the head of the pancreas. In this connection it is of interest to note that one patient (Case 4), although reported in two previous papers in 1936 and again in 1939 as having an "obstructive factor" undetermined, has recently died, and a post-mortem examination was made. This patient had had a splenectomy at 5 years of age and was subsequently followed for thirteen years. During this period he continued to have recurring hematemeses and rnelena and was admitted to the Presbyterian Hos pital twenty-four times. Bleeding was always severe and occurred approximately twenty-one times via the esophageal route and ten times per rectum. Because of (1) the normal appearing liver at operation, (2) the normal blood count between bleeding episodes, (3) normal liver function tests at the ninth, eleventh, and twelfth years after splenectomy, we felt secure in our belief that cirrhosis never did exist and that it subsequently had not developed. This patient finally died only seven months ago. Before section was started, one of our staff, William P. Thompson, predicted the finding of a normal liver and also an obstructive lesion in the portal vein (dose to liver. Both predictions were confirmed. The nature of the cxtrahepatic lesions responsible for obstruction to splenic blood in this series are listed as follows : 1. Thrombosis of splenic vein (traumatic) Case 5 2. Thrombosis of splenic ut junction with portal vein (traumatic) Case 11 3. Thrombosis of splenic vein (nontruumntic) Case 9 4. Thrombosis of splenic vein (nontraumatic) Case 14 0. Stenosis of portal vein (uppor end) just below liver Case 4 6. Stenosis of portal vein (lower end) above entranco of splenicvein Cose 12 7. Cavernomntous transformation of portal vein Case 6 8. Caverronmtous transformation of junction of portal vein and splenic veins Case 7 The extrahepatic obstructive lesions just detailed occurred in the respective sites indicated on Fig. 1. THE ANATOMICAL PORTAL VENOUS PATTERN AS A DETERMINANT OE SYMPTOMATOLOGY AND PROGNOSIS In an analysis of the long-term results following splenectomy in this entire group, one rather interesting observation has become apparent. From an examination of Fig. 2 it will be seen that 9 of these patients continued to have intestinal bleeding following operation for periods varying from eight months to thirteen years; whereas, 6 were imme diately relieved of this serious complication and have remained so for long periods of time, in Case 1 for as long as nineteen years. Why $hould such a marked variation in clinical behavior occur? This phase tooTseirz ROUSSEIXIT; LATE PHASE OP CONGESTIVE SPLENOMEGALY i ! 89'^' ' of the problem has been given a good deal of thought and it is our belief that we may have the answer. It is our purpose to demonstrate ' that (1) the site of the obstruction and (2) variations in the anatomical ' distribution of the veins forming the portal system may be the determining factors governing symptomatology, course, and eventual prog-- " nosis in any individual case. Referring again to Fig. 1, it seems obvious^ ; that a lesion occluding the portal vein close to the liver will impede the flow of a much greater volume of blood than a similar1 stenotic process located in the splenic vein close to the hilum of the spleen. Case 4 ,1 Fig. 1.--Sc/iem&tfc drawing: (after F. Paltre, H. Lacaxe, S, Pupret), Indicating the . n sites of the obstructive factor In the case# designated. Tho former involves tho entire return flow of the porta) system; whore* as, the latter affects only the splenic fraction, or approximately 20 per cent. This question of the site of the obstruction is further qualified,' , we believe, by the second consideration just alluded to. This second consideration is the variations that occur in the anatomy of the veins forming the portal system. Fig. 3 portrays six different anatomical patterns taken from six standard sources. Even cursory inspection of these figures will show that an obstructive lesion as indicated in B will produce much more profound alterations in intestinal physiology than the identical lesion .. . ''a BFG36692 40 SURGERY CASE NO- AFTER OPERATION 4 CEassDoooooo S ooooceoaieawowMMWMM 12 < icva*. ~)oa S oocooaCZ--j 14 QiaSDoLoeoaaececnaea to r 8VRS- ~tooooooooooo* S mml col oeeooo 9 3 MMOMW S MOMOM 13 ij'yrs .IDm S OOO 2 C-A*gL3tooo--E Cm 7 r,--------xvfm ~) S0Ao* 6 03*0 S 13 YRS. 13 YRS. 7 YRS. b YRS. 4 YRS IVIbYRS 8 'nos8 MOS. 3 CAYS 1 C5HD* S ocooooooocooocoooooocxxcjocoooo 3 r bvw--T3 S aacooDooooccaxiOocoooo 5 c--- ~ "TSVIK ~") s 0300000000000 8 r >yrs -~t >ooooo>oooMOCoa S ooooo It ! H.VKV ) 0 S OOCO 15 r -tavm ) S OO 19 YRS. 13 YRSbV2YRS2 ViYRS 2 YRS. 10 MOS- EACH CIRCLE DENOTES A SIX MONTH PERIOD 5-SPLENECTOMY L-LIGATION OF VESSELS A-OMENTOPEXY O-SYMPTOM FREE -INTESTINAL BLEEDING CHEMATEMESIS OR MELENA) -DEATH FIZ. 2. fertal V (.Inf-. HticnNrK V- "R* Gastrocpiplotc V -Sup. Mmntvric V (After henrahan) A Portel V. Jnf MmnHric V -Sup Mesenteric V> (After Spalteholz) B p&rtel V. Gastroepiploic V Coronary VPyloric V \lnf. Meeentenc Vft Sup Mesenteric V* (After Gray) C PjHtel V // J^-lnt. Mesenteric V. Y Alnf Mesenteric V. >lnf Mesenteric V- ^SupMeecnteric V- Sup Mesenteric V- Rt Gasf Sup Mesenteric V. (After Peitre) (After Sobotte) epiploic (After Piersol) Dl F howFi'ga.n 3.--Variations in the anatomical aUpaet'Ttenrn"dloferethnei fpi.odrltvalldus.y1s.temmayIlluresatrua.ttinIgn marked differences In clinical behavior. ROIJRRRIXtT! liATK PHARR OP CONORRTIVR BPLKNOMROALY >'* occurring in an individual possessed of a portal system as illustrated in A. Additional observations along these lines will explain many of the vagaries and alterations in clinical behavior in these patients./ To quote specific examples from our series: Case 4 showed a stenotic lesion of portal vein immediately subjacent to liver, and Case 32 lower down in the portal vein. Regardless of the venous pattern in such a situation the entire portal flow is imipeded. Splenectomy, although returning the blood picture to normal, will only remove a small burden of the already overloaded collateral circuit. Intestinal bleeding in this type of case, of course, will continue and will not only evolve from esophageal varices but also from small and large bowel. The latter is duo to blockage of the superior and inferior mesenteric venous outflow. These are the cases in which melena will always be a dominant feature. , In Cases 5 and 11, however, the obstructive factor was a thrombosis of the splenic vein. This involved only the splenic contribution to the portal flow. Establishment of a collateral circulation via the vasa brevia resulted in bleeding esophageal varices. Following splenectomy, this recurring thrust on the varices was removed. These patients had subsequently no, further bleeding. Between these two extremes'all' gradations in clinical behavior are possible and are dependent, as men tioned before, on (1) the site of the obstruction and (2) the disposition of the accessory veins supplying the portal vein. SUMMARY A group of fifteen cases is presented, all with the characteristic features of Banti's syndrome and all with gastrointestinal bleeding as a dominant symptom. Although exhibiting the presumably late symp tom of hematemesi8, none of these cases had cirrhosis of the liver at operation or subsequently for long periods of time up to nineteen years after operation. The etiology of the splenomegaly can be en tirely explained on a mechanical basis with a primary obstructive factor in the portal bed and an associated portal hypertension. The evidence presented therefore contradicts the sequence described'by Buiiti of a primary splenomegaly and a subsequent cirrhosis due to a hypothetical toxic agent. A variety of oxlrahepatie lesions liavo been listed, all capable of producing venous stasis. In the four instances in which splenic vein pressures were determined a definite venous hypertension was recorded. This confirms similar observations previously reported by this clinic in other forms of Banti's syndrome. The frequency of anomalies in the portal system is stressed. In this group of cases of congestive splenomegaly due to extrahepatic obstructive lesions, the prognosis and variations in clinical bohavior BFG36693 42 ' SURGERY ,' * :> i' l.'i"' are dependent on two factors: (1) the site of the obstructive lesion and (2) variants in the anatomy of the venous pattern. To the best of our knowledge, this latter concept is herein presented for the first time. REFERENCES 1. Banti, Guido: Splenomegalie mit Levercirrhose, Beitr. z. path Anat. 24: 21, 2. Ba1n8ti9,8G. uido: Ueber Morbus Banti, Folia haemat. 10: 33, 1910. 3. Cecil, R. L.: A Text Book ol Medicine, Philadelphia, 1937, W. B. Saunders 4. EppCion.ger, H.: Die Stauungsmilz beim Measchen: Die Hepatolienalen. Er- krankungcn, Berlin, 1920, Julius Springer, pp. 384-493. 5. Bousaelot, L. M.: The Bole of Congestion (Portal Hypertension) in So-Called Banti's Syndrome. J. A. M. A. 107: 1788, 1930. 6. Bousselot, L. M.: Congestive Splenomegaly (Banti's Syndrome), Bull. New 7. BouYsosrekloAt, cLa.d,MM., eadn.d16T:ho1m88p,so1n9,39W. . P.: Experimental Production of Congestive Splenomegaly, Proc. Soc. Exper. Biol, k Med. 4: 705, 1939, 8. Thompson, W. P., Canghey, J. L., Whipple, A. 0,, and Bousselot, L. M.i Splenic Vein Pressure in Congestive Splenomegaly (Banti's Syndrome), J. Clin. In 9. Larvreabsteigea, tiBon. C16.:: 5C7h1,ro1n9ic37.Congestive Splenomegaly and Its Belationshjp to Banti's Disease, Am. J. M. Sc. 188; 745, 1934. 10. Bauman, L., and Orr, L.: Bromsulphalein Test, New York State J. Med. 38: 11. Ha1n7ra, h1a9n3,8.E. M., and Vincent, B.: Surgery of the Spleen, Lewis' Practice of Surgery VI, Hagerstown, Md., 1939, W. P. Prior Co., Chap. XV, p. 74. 12. Spalteholz, W.: Hand Atlas of Human Anatomy, ed. 7, Philadelphia, J. B. 13. GraLyip, pHin.c: otAtnCaoto.,mvyol.oIfI,thpe. H4u77m. an Body, ed. 23, Philadelphia, 1936, Lea and 14. PaFitreeb,igFe.r,, Lpa.ca6z7e5,. H., and Dupret, S.: Pratique Anatoma-Chirurgicale Illustrie, Paris, 1934, G. Doin et Cie, vol. I, p. 277. 15. Sobotta, J.: Human Ahatomy, ed. 4, New York, 1936, G. E. Stechert and 16. PieCrsoo.,l:volH. uIlml,anp. A8n9.atomy, ed. 9, Philadelphia, 1930, J. B. Lippincott Co., p. 919. SS&Z THE PROPHYLACTIC USE OP SULFANILAMIDE IN ABDOMINAL SURGERY John S. Lockwood, M.D., and I. S. Ravdin, M.D., Philadelphia, Pa. (From the Surgical Clinio of the Hospital of the University of Pennsylvania' the Laboratory of Surgical Bacteriology of the Harrison Department of Surgical Research, Schools of Medicine, University of Pennsylvania) V v IN VIEW of the dramatically successful results of chemotherapy in .such diverse infections as hemolytic streptococcic peritonitis, cellulitis, and septicemia, colon bacillus pyuria, gonococcic urethritis, and pneumo- coccic pneumonia, the question has logically arisen as to the possible . effectiveness of sulfanilamide or one of its derivatives in peritonitis of intestinal origin. The literature on the surgery of the colon has been ' concerned to a large extent with measures designed to minimize the threat of peritonitis as a complication of such operations. That peri- tonitis continues to occupy the major position among the causes of death following surgical procedures on the large intestine is shown in Table I. . The operative mortality of radical procedures averages about 18 per cent and about 40 per cent of the deaths are due to peritonitis. The i data of Rankin' show that, while the mortality following simple | colostomy may be very low, almost 60 per cent of the deaths that do | occur are attributable to peritonitis. If sulfanilamide can be safely ' employed to reduce the incidence of postoperative peritonitis, a major i advance will have been achieved. In a previous publication,' dealing with the use of sulfanilamide in^ hemolytic streptococcic infections, expression was given to the opinion 7 that the effectiveness of sulfanilamide in any lesion is conditioned more ' by the pathologic character of the infectious process than by the . degree of susceptibility of the infecting organisms. As a result of.a^ i three-year experience in the use of sulfanilamide in the prevention and treatment of peritonitis on our surgical service at the Hocfpital /- of the University of Pennsylvania, we are inclined to reaffirm this`If-; opinion. In this paper we will undertake to supply a rational basis foriefe sulfanilamide therapy in polymicrobic peritonitis and to present "a summary of our experience to dato. '"fy bacteriolooio considerations in peritonitis of intestinal origin Peritonitis of intestinal origin is usually a mixed bacterial infection > in which the organisms most frequently found are the Bacillus cold, the',;! '' green or nonhemolytic streptococci, and the Welch bacillus. The care- v ful studies of Meleney, Harvey, and Zaytseff-Jern10 on the bacterial flora of peritonitis, in which sound bacteriologic methods were used, showed ----------- * Presented at the meeting of the Society of University Surgeons at New York, N. 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