128

Lymphology 16 (1983) 128- 137 ©Georg Thieme Verlag Stuttgart · New York

Preservation of the Spleen

M.H. Witte, M.D., Ch.L. Witte, M.D., D.B. Van Wyck, M.D., K.J. Farrell, M.D.

Departments of Surgery and Medicine, University of Arizona College of Medicine, Tucson, Arizona

"Beside your stomach may be seen A pulpy organ called the spleen The body seems to perk without it But, since its role is still in doubt, it Is prudent on the part of man To keep it in him if he can . .." (1)

Summary hyperfunction. Historically, less radical pro­ Because the spleen can no longer be considered cedures such as incision of the spleen (spleno­ readily dispensable, a variety of alternatives to total tomy), repair (splenorrhaphy), flxation (spleno­ splenectomy (splenic repair, partial resection, auto· transplantation, ischemic therapy, reticuloendothelial pexy) and partial resection enjoyed sporadic blockade and irradiation) have been developed to success most notably for management of trau­ preserve functioning remnants in trauma and hyper­ ma and fibrocongestive splenomegaly associat­ splenism. It remains unclear how much spleen ade­ ed with portal hypertension (Banti's syndrome). quately protects against OPSI or under persistent workload stimulus leads to recurrence of hyper­ But as operative technique and anesthetic safe­ splenism ty advanced, these options were progressively shunted into the background. Indeed, it be­ came almost axiomatic that splenic repair and Growing recognition of the risk of overwhelm­ reconstruction were unthinkable even with ing sepsis after splenectomy (OPSI) and short­ minor injury, and non-resective operations comings of measures to prevent or treat this quickly faded from the surgical scene. Now, complication have generated widespread en­ with increasing recognition of the spleen 's role thusiasm for retaining some splenic tissue. in host defense against infection, these alterna­ These attempts at preservation (Fig. 1) carry tive procedures are coming back into favor (2). not only important practical implications but Ultimately, for acceptance in the therapeutic also provide insight into what exactly the armamentarium, splenic preservation must spleen does and how its functions relate to prove as safe as splenectomy while minimizing blood flow , workload, mass , resident cell po­ the risk of fulminant sepsis and at the same pulations, the rest of the reticuloendothelial time controlling symptomatic hypersplenism. (RE) system, and intercurrent disease. After blunt trauma, careful observation is gra­ Because the spleen was long considered readi­ dually replacing "routine" splenectomy in ly dispensable, total splenectomy gradually children with injured spleens and more recent­ evolved during the past 50 years as the treat­ ly this approach has been cautiously extended ment of choice for injury and symptomatic to adults (Fig. 2). If unstable vital signs, dete­ riorating abdominal fmdings, and declining Supported in part by USPHS Grants No. HL20086 blood hematocrit dictate early operation and and AI16926 a ruptured spleen is confirmed at laparotomy,

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A B c

Fig. 1 Schematic diagram depict­ ing various methods of splenic pre­ servation : A) suture repai r or splen­ orraphy (e .g. after trauma), B) re­ striction to splenic arterial inflow (ischemic therapy or circulatory D F control), C) partial resection leav­ ing the remnant in situ with vascu­ lar supply intact, D) implantation of splenic fragments in the perito­ neal cavity or subcutaneous tissue (autotransplantation), E) irradiation, F) chemical splenectomy through

Au\Oiransplarllatlon lrradlallon various antimetabolic-alkylating agents or particulate reticuloendo­ thelial blockers

Fig. 2 Posterior (left) and left anterior oblique views (right) of splenic scintiscans (99mTc sulphacolloid) within a few hours (upper) and 4 weeks after (lower) trauma t:J the spleen from a high speed motor ve­ hicle accident. Note the "filling in" of defects as splenic repair proceeds. Treatment was non-operative

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Fig. 3 Serial anterior views of splenic scintiscans (99mTc sulphacolloid) one week (left), four weeks (middle) and 12 weeks (right) after omental wrapping and splenorrhaphy for splenic disruption following a motor ve· hicle accident. Note gradual improvement in the splenic scintiscan the entire spleen may not need removal. Sim­ "circulatory control" or "induced splenic an­ ple tamponade, topical application of throm­ gina") limits splenic function and thereby abil­ bogenic agents (e.g. microcrystalline collagen) ity to respond to a particulate workload. Dur­ and suture repair (Fig. 1A and 3) often con­ ing the past decade it has been clearly docu­ trol minor bleeding. Because splenic blood mented that marked restriction to splenic flow is segmental in distribution and collate­ blood flow reduces splenic mass (visualized ralization rich via the celiac and superior mes­ by reticuloendothelial uptake on splenic scinti­ enteric arteries, the splenic artery may be scan) and initially raises one or more depressed ligated preferably close to the hilum (Fig. lB cellular elements in peripheral blood associated and see Circulatory Dynamics, Fig. 9) thereby with hypersplenism. Early success was gained lowering the arterial pressure head and arrest­ by selective catheter infusion of vasoconstric­ ing bleeding. Alternatively, partial splenecto­ tor drugs (e.g. vasopressin), intraarterial balloon my (Fig. 1C) with resection of the pulpified occlusion, and distal ligation of the splenic ar­ fragment leaves behind a remnant of architec­ tery (see Circulatory Dynamics, Fig. 8) (9, 10), turally intact spleen (Fig. 4) (3, 4). Splenic but more prolonged effects follow transcathe­ fragments (free grafts (Fig. lD) too, may be ter blockage of the splenic artery especially in implanted into the peritoneal cavity or conjunction with embolization using autolog­ wrapped in omentum simulating spontaneous ous blood clot, fme steel coils, and gelatin autotransplants found after traumatic rupture sponge (see Circulatory Dynamics, Figs. 6, 7 (splenosis) (5 , 6). Subsequent splenic scinti­ and 10) (11 - 13). Unfortunately maneuvers scans are helpful in documenting continued that sharply reduce splenic blood supply so reticuloendothelial trapping by the remnant as to minimize collateralization and limit re­ as well as growth and reconstitution of a re­ growth of the segment may be complicated paired, ischemic, amputated or transplanted by potentially life-threatening infection in fragment. Several large clinical series now do­ the ischemic, infarcted fragment. Other opera­ cument the safety of these alternatives, and tive approaches include partial splenic resec­ the number of total splenectomies for trau­ tion (Fig. 5) (13, 14) and transplantation of ma has sharply declined ( 4, 7, 8). small splenic remnants within the peritoneal On the other hand, in patients with hyper­ cavity or abdominal wall (Fig. 6) (15- 17). splenism, who are even more vulnerable than Subtotal splenectomy in staging operations for injured patients to sudden uncontrolled sepsis lymphoma may, however, inadvertently over­ after removal of the spleen, splenic preserva­ look small foci of cancer and misrepresent the tion has received scant attention largely be­ true extent of tumor progression (18). Although cause of concern over recurrent hyperfunc­ splenic irradiation (Fig. 1E) temporarily also re­ tion. Theoretically, restriction of arterial in­ duces splenomegaly, it has been generally inef­ flow (synonyms include "ischemic therapy", fective in controlling hypersplenism (19).

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Fig. 4 large splenic remnant left in situ (left) after resection of pulpified fragment of spleen (middle) in a young man following an automobile collision. A substantial splenic remnant (right) is visible on 99mTc sulphacolloid scintiscan 3 months later

Fig. 5 Splenic scintiscans (99mTc sulphacolloid) before (left) and 6 months after (middle) partial resection of the spleen for relief of painful splenomegaly and hypersplenism following occlusion of a distal splenorenal shunt (SA) in a 12 year old boy with histiocytosis X and portal hypertension. At 12 and 24 months the splenic remnant on scintiscan was unchanged. Peripheral white blood cell (WBC) and platelet counts (right) before and after SR shunt for bleeding esophageal varices and subsequent splenectomy, showing eventual im­ provement of leukopenia and thrombocytopenia. (Reproduced with permission of the Brit. J. of Surg.) (13)

A different approach to splenic preservation and both are suppressible by these potent cy­ - "chemical splenectomy" (Fig. IF) - is sug­ totoxic agents. Among the various mechanisms gested by salutary effects of immunosuppres­ proposed to explain the beneficial clinical re­ sive (cytotoxic) agents in treatment of hyper­ sponse, interference with macrophage function splenism and other splenopathies associated leading to impaired destruction of sensitized with neoplastic and non-neoplastic disorders. platelets is particularly germane. For example, Thus, azathioprine, cyclophosphamide, 6-mer­ to enhance delivery of vincristine or vinblast­ captopurine, vincristine and vinblastine, have ine to impede macrophages, the ability of pla­ been tried for immune thrombocytopenic telets to bind vinca alkaloids has been exploit­ purpura (ITP) refractory to glucocorticoids ed in refractory ITP (20) and in autoimmune and splenectomy and for low platelet counts hemolytic anemia (21). While the long-term accompanying disseminated lupus erythema­ efficacy of this particular treatment is unclear, tosus, lymphoma, leukemia, carcinoma and the concept of using a particulate vehicle for bone marrow aplasia. Circulating antibodies targeted delivery of cytotoxic agents to hyper­ to platelets or abnormalities in cell-mediated functioning macrophages is intriguing. What is immunity are implicated in these disorders, needed now are ways to enhance loading or

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Fig. 6 Serial splenic scintiscans (technetium labelled heat-damaged red blood cells) in young boy with idio­ pathic thrombocytopenic purpura fa il ing to visualize immediately after (left) but revealing a substantial splenic fragment 2 years after (middle, right) autotransplantation in the abdominal subcutaneous tissue. Lateral veiw (right) shows the palpable remnant under the abdominal wall. Platelet.count is 335,000/mm3 (Courtesy of Drs. P. Crowe and J.J. Corrigan, Jr.)

binding of the cytotoxic agent onto particles suspension of ethyl palmitate administered targeted for the macrophages, to reduce the intravenously produces rapid and marked sup­ circulating levels of unbound drug thereby pression of phagocytic function and widespread minimizing undesirable side effects, to iden­ necrosis of the spleen. By and large, however, tify drug analogs that are rapidly metabolized the bone marrow, thymus and liver are spared. and eliminated in an unbound state, and to This curious affinity of Ethpalrn for splenic deliver high concentrations of the particle macrophages suggests regional differences in selectively into reticuloendothelial organs. RE function or possible metabolism ("detoxi­ Where the underlying disorder is thought to fication ") in the liver. While applicability to reside primarily in the spleen, loading of bleo­ patients is as yet undefined, this substance mycin onto red blood cells (22) and selective may be potentially useful when administered splenic arterial infusion of particle-bound cy­ via superselective splenic arterial infusion in totoxic agents (as previously for unbound cy­ patients with life-threatening peripheral cyto­ totoxic agents in chronic granulocytic leuk­ penias. emia or 9o yttrium microspheres in malignant Despite mounting evidence of advantages to lymphoma) (23) hold promise for the future. possessing a spleen and growing clinical appli­ Reticuloendothelial blockade probably also cation of various methods of splenic preserva­ underlies amelioration of refractory ITP with tion, it is unclear how much spleen is needed. high-dose intravenous polyvalent intact immu­ On the one hand, the rarity of OPSI and the noglobulin (24), which presumably interferes frequency of functional splenosis in patients with phagocyte-Fc receptor-mediated immune splenectomized for trauma have prompted clearance by the spleen. High dose long-term speculation that small splenuli (so-called "born corticosteroid therapy may also exert thera­ again spleens") (Fig. 7a) restore host resistance peutic benefit in these derangements by im­ to infection (26- 28). On the other hand, ful­ pairing splenic phagocytosis. minant pneumococcal septicemia and death Several decades ago, ethyl palmitate (Eth­ have occurred in patients following splenecto­ palm), an esterified long-chain fatty acid, was my for blunt injury despite large ectopic splen­ shown to profoundly inhibit the ability of ses­ ic fragments and innumerable minute splenic sile cells to remove particulate matter from nodules (splenosis) found at autopsy (Fig. 7b) the bloodstream (25). In mice, a colloidal (29, 30). Similarly, patients with small or hy-

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Fig. 7 Extensive splenosis (arrows) visualized on hepatosplenic scintiscan (left) in a healthy 1 ~ year ~ld bo_y 8 years after splenectomy for traumatic rupture, who also showed a low percent~ge (0.8 %) of pttted ctr~ulatt~g red blood cells. This finding is contrasted w ith similar splenosis in the retropentoneum of another pattent ~nght) who succumbed to fulminant pneumococcal sepsis 10 years after splenectomy for trauma. (Reproduced wtth per­ mission of New Engi.J.Med.) (28, 20) . pofunctioning spleens from sickle cell anemia, a fraction of the original spleen size and cell ulcerative colitis, sarcoid infiltration and fol­ populations, difficult to quantify for multiple lowing thorotrast administration or splenic ir­ fragments , and gradually declines with advanc­ radiation have also succumbed to pneumococ­ ing age . cal sepsis (see Clinical Disorders of Splenic While these ectopic implants have been re­ Function). Together, these fmdings suggest ported to retard BartoneUa infestation (36), that small or severely hypofunctioning splen­ restore gamma leukophilic opsonin levels (37) ic remnants cannot be relied upon to protect produce antibodies to particulate antigen (38) against the spectrum of sudden and fulminant as well as reduce the number of pitted red infections characteristic of the asplenic state blood cells (26), the bulk of evidence indicates (see Overwhelming Postsplenectomy Infection: that they do not provide adequate protection OPSI). against pneumococcal septicemia. Experimental autotransplantation of splenic In a rat model of incremental partial splenic fragments has been reported by some to pro­ resection permitting early and quantitative tect (31 - 33) and by others to offer little or determination of remnant function over a no protection against intravenous live pneu­ precisely graded range of mass, both ear~y mococcal challenge (34). These implants, antibody production to intravenous particu­ which closely resemble clinical splenosis, late antigen (sheep red blood cells) (Fig. 8a) first undergo central necrosis but over the (39) and LD after intravenous pneumococ­ ensuing 6- 12 weeks gradually enlarge emerg­ 50 cal challenge (Fig. 8b) (40) vary directly with ing as splenuli histologically resembling an in­ residual splenic mass. In these experiments, tact spleen (35). Moreover, they take up ra­ remnant spleens of less than one-third the diocolloid and trap damaged red blood cells. original spleen size fail to improve host survi­ Blood supply, however, derives from penetra­ val over the spleenless state. Furthermore, in tion of the capsule rather than.hilar arteries rats depleted of complement by parenteral and in the absence of an abnormal workload cobra venom factor, a substantial splenic mass (e.g. liver injury or circulating particulate an­ (approximately one-third to one-half normal) tigen), regrowth is unpredictable, limited to

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! 3.0

I .. . \ .. {01 ... r• 08\ocO.Cll:n ,.. \------,.e.,. w•t80•0.002Z. . tO •

00)200300.00!10)6007008001001000tOJ Spleen We.gH lmg)

Fig. 8 Demonstration that various splenic functions bear a close relationship to splenic mass. Left, direct relationship between splenic weight and serum hemolysin titers in intact rats (sham-operated) and rats after partial splenectomy (Sx) following intravenous challenge 5 days earlier with sheep red blood cells. Hemoly­ sin activity in totally splenectomized rats was barely detectable. Middle, survival plot and LDso in adult rats with varying size spleens after administration of virulent S. pneumoniae (Type Ill) intravenously. The model represents a form of the generalized logistic equation to predict mortality from log dose . Note that the smaller the remnant spleen mass left in situ the lower the LD50 . Right, survival rates of ra ts challenged with low doseS. pneumoniae (Type Ill) (102 bacteria) 24 hours after complement depletion with cobra venom factor. A substantial protective advantage was offered by partial spleens (PS) of greater than 200 mg left in situ (approximately one-third whole spleen (WS) weight). (Reproduced with permission of Surgery, J . of Surg. Res. and J. Jnf. Dis.) (39-41)

is needed to restore host resistance in this value of different methods of splenic preserva­ highly susceptible state (Fig. 8c) (41). Sophis­ tion. ticated statistical analysis by failure-time mo­ In contrast to individuals undergoing splenec­ delling of the experimental data ( 42) indicates, tomy for injury where "the more spleen the however, that even a small remnant left in si· better", in patients with hypersplenism, reten­ tu has some small protective value but large tion of a splenic fragment for immune protec­ remnants provide an exponential increase in tion raises the spectre of eventual recurrence host resistance. No significant protection is of splenic hyperfunction. In a sense, the phe­ provided by ectopic remnants, either single nomenon of hypersplenism and associated or multiple, in this highly sensitive bioassay splenomegaly is an appropriate reaction of system. splenic RE tissue to an abnormal stimulus or "workload" (e.g. increased numbers of defec­ Because "born-again spleens" rarely achieve tive red blood cells, abnormal lipids or foreign the critical threshold of substantial protection particulate antigens) (35). As treatment direct­ provided by the splenic remnant with intact ed at eliminating or reducing the excessive blood supply and architecture, their ability workload, enhancing hepatic function , or im· to protect against OPSI remains in doubt as proving a stagnant congested splenic interme­ does the efficacy of attempts at splenic pre­ diary circulation is difficult or impossible, the servation which leave behind small remnants spleen is usually removed despite the even of insufficient functioning cell density. While greater risk of OPSI in patients with diseased deaths from fulminant sepsis have occurred compared to normal spleens. Although recur­ in patients with extensive spontaneous sple­ rence of hypersplenism has occasionally been nosis, long-term follow-up of patients with reported with a small accessory spleen, the splenic preservation carried out by a variety frequency of such relapses and the time period of techniques for trauma and particularly for for recurrence are both unclear and open to hypersplenism is still limited. Accordingly, reinterpretation (43). Most presumed recur­ meaningful population studies to examine rences from accessory spleens have been asso­ changes in incidence of OPSI are not yet pos­ ciated with ITP (a special disorder character­ sible, and experimental studies remain the ized by a normal size spleen, circulating anti­ main source of information about survival platelet antibodies, spontaneous remissions,

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Hypersplenism (_.,rbc, wbc, plataleto)

.,., ..... """" ,...... Eusplenlsm "" ...... "":ill: Hyposplenlsm Fig. 9 Titering of splenic function Asplenlsm ,...,.,""' through manipulation of splenic mass. ( 1'HJB, % piHed rbc While a fine line exists between sus­ '!'Fulminant Sepolo _.,Immune AE Function) ceptibility to fulminant sepsis (hypo· splenism and asplenism) on the one hand and recurrent hypersplenism on the other, splenic mass and func­ tion can be titrated by a variety of preservation techniques (partial splen­ ectomy, ischemic therapy, RE block­ ade). Conversely, splenic mass and function can also be " boosted" by increasing workload, immunopoten­ .... tiating agents, and splenic remnants to attain eusplenism - the ideal bal ­ ...... 0 • Workload ance of splenic immunologic and lmmunopotentlators hematologic function (see text for Remnants expansion of these concepts, HJB = Howell-Jolly bodies)

and recurrence even in the absence of detect­ between susceptibility to fulminant sepsis on able splenic tissue), and even the favorable re­ the one hand and recurrent hypersplenism on sponse to accessory splenectomy reported by the other, splenic mass can be reduced gradu­ some in ITP has been disputed (44). In the ally by a variety of preservation techniques al­ few instances of recurrent anemia from acces­ ready described; conversely, splenic function sory spleens in hereditary spherocytosis, the can also be "boosted" in several ways. For ex­ original diagnosis has been questioned. Be­ ample, immunopotentiators such as vaccines sides, accessory spleens are detected on occas­ prepared from anerobic coryneform bacteria sion in this disorder without reappearance of stimulate the normal spleen (and even the ru­ reticulocytosis and anemia. Nonetheless, there dimentary spleen of immunodeficient CBA-N is little doubt that if a substantial remnant is mice) to enlarge several-fold and provide "su­ left behind in situ, as after splenic arterial li­ pernormal" resistance against bacterial, viral gation where collateralization continues and and protozoan infestations as well as certain workload of abnormal red cells persists, re­ neoplasms (45). Thus, while preservation of growth of the remaining spleen to greater maximal splenic tissue may be desirable after than normal size takes place with recrudes­ trauma, careful "titration" of mass in hyper­ cence of splenic hyperfunction (see Circulato­ splenism to optimize the balance between im­ ry Dynamics, Fig. 8 and Clinical Disorders of munologic protection and hematologic remis­ Splenic Function, Fig. 2) (10, 13). sion is appropriate. Splenic remnants may be Despite these limitations, it is likely that the "boosted" by stimulation from particulate an­ goal of "titering" splenic function through tigen or immunopotentiating agents, recruit­ manipulation of splenic mass is attainable ment of new blood supply to ischemic r~m­ (Fig. 9). While one may tread a fme line nants (e.g. wrapping in omentum), auxiliary implantation of subcutaneous and omental

Permission granted for single print for individual use. Reproduction not permitted without permission of Journal LYMPHOLOGY. 136 M.H. Witte, Ch.L. Witte, D.B. VanWyck, K.J. Farrell autografts preserved in a frozen state, injec­ 6 Patel, J. , J. Williams, B. Shmigel, J. Hinshaw: Pre­ tion of spleen cells, and ultimately by selec­ servation of splenic function by autotransplanta­ tively replacing identifiable splenic immune tion of traumatized spleen in man. Surgery 90 (1981) 683 "protective factors" (e.g. with cryoprecipitate). 7 Grosfeld, J.L., M.A. Malangoni: Blunt splenic trau­ More precise control and tailoring of remnant ma: assessment of surgical therapy based on labora­ mass and function will likely follow greater tory and clinical observations in Surgery Annual elucidation of specific spleen cell populations 1980, L. Nyhus (ed.), Appleton-Century Croft, New York, 1980, pp. 123 (e.g. macrophages, T and B lymphocytes) and 8 Pachter, H.L. , S.R. Hofstetter, F.C. Spencer: subpopulations and their participation in the Evolving concepts in splenic surgery: splenorrha­ spleen's pitting and culling functions, ftltering phy vs. splenctomy and postsplenectomy drainage: capacity, and antibody production. experience in 105 patients. Ann. Surg. 194 (1981) 262 From this brief analysis, it is apparent that a 9 Witte, C.L., M.H. Witte, W. Renert, R.E. 0 'Mara, wide array of preservation techniques are now D.L. Lilien: Splenic artery ligation in selected pa­ feasible. While the technical aspects are rela­ tients with hepatic cirrhosis and in Sprague-Daw­ ley rats. Surg. Gyn. & Obstet. 142 (1976) 1 tively simple, straightforward, and safe, major 10 Witte C.L., J.J. Corrigan, M.H. Witte, D.B. Van unanswered questions remain about the long­ Wyck, R.E. O'Mara, J.M. Wolfenden: Circulatory term value of these remnants in terms of pro­ control of splenic hyperfunction in children with tection from sepsis and,'in hypersplenism, peripheral blood dyscrasia. Surg. Gyn. & Obstet. risk of recrudescent hyperfunction. Nonethe­ 150 (1980) 75 11 Witte, C.L., T. W. Ovitt, D.B. Van Wyck, M.H. Witte, less, the potential benefit of defining critical R.E. O'Mara , J.M. Wolfenden: Ischemic therapy splenic mass, relating it to vascular supply, ar­ in thrombocytopenia from hypersplenism. Arch. chitecture, and cell populations, and determin­ Surg. 111 (1976) 1115 ing the best way to attain and maintain this 12 Spigos, D.G., 0 . Jonasson, M. Mosez, V. Capek: Partial splenic embolization in the treatment of mass, is great, especially for young children, hypersplenism. Am. J. Radio!. 132 (1979) 777 immunosuppressed patients such as renal trans­ 13 Witte, C.L., D.B. Van Wyck, M.H. Witte , J.J. Cor­ plant recipients, and those with blood dyscra­ rigan , C.F. Zukoski, G.D. Pond, JM. Wolfenden: sias, where asplenism carries a particularly Ischemia and partial resection for control of splen­ high risk of OPSI (see Overwhelming Postsplen­ ic hyperfunction. Brit. J. Surg. 69 (1982) 531 14 Kamel, R. , M.A. Dunn: Segmental splenectomy in ectomy Infection). Titering splenic function Schistosomiasis. Brit. J. Surg. 69 (1982) 311 upward and downward to attain the ideal of 15 Crosby, W.H.: Hyposplenism: an inquiry into nor­ eusplenism - the optimal balance of the mal functions of the spleen. Ann. Rev. Med. 14 spleen's many and complex functions - re­ (1963) 349 16 Benjamin, J. T. , D.M. Komp, A . Shaw, C. W. Mc­ presents the real challenge of the future . In Millan: Alternatives to total splenectomy: two this context, "the salvaged spleen or splenic case reports. J. Ped. Surg. 13 (1978) 137 remnant is a far greater trophy . .. than the 17 Nielsen , J.L., F.H. Sorensen, P. Saksa, H.H. Han­ spleen in the pathologist's hands" ( 46). sen: Implantation of autologous splenic tissue af­ ter splenectomy for trauma. Brit. J. Surg. 69 (1982) 529 References 18 Dearth, J.C., G.S. Gilchrist, R.L. Telander, M.J. 0 'Connell, L.H. Weiland: Partial splenectomy for Warsaw , /.: Poet's Corner: Inside Story. JAMA staging Hodgkin's disease. Risk of false negative 230 (1974) 463 results. New Eng. J. Med. 299 (1978) 345 2 Morgenstern, L., S.J. Shapiro: Techniques of 19 Comas, F. V., G.A. Andrews, B. Nelson: Spleen splenic conservation. Arch. Surg. 114 (1979) irradiation in secondary hypersplenism: Am. J. 449 Roentgenol. 104 (1968) 668 3 Christo, M.C. : Segmental resections of the spleen: 20 Ahn, Y.S. , J.J. Byrnes, W.J. Harrington et al. : report on the first eight cases operated on. Hospi­ The treatment of idiopathic thrombocytopenia tal (Rio de Janeiro) 62 (1962) 575 with vinblastine-loaded platelets. New Engl. J. 4 Sherman, R. : Perspectives in management of trau­ Med. 298 (1978) 1101 ma to the spleen: 1979 Presidential Address, Am. 21 Ahn, Y.S., J.J. Byrnes, D.E. Brunskill et al.: Se­ Assoc. Surg. Trauma. J. Trauma 20 (1980) lective injury to macrophages: a new treatment 5 Aigner, K. , J. Dobraschke, E.G. Webber et al.: for idiopathic autoimmune hemolytic anemia. Successful reirnplantation of splenic tissue after Clin. Res. 26 (1978) 340 neonatal abdominal trauma. Lancet 1 (1980) 360 22 Lynch, W.E., G. Sartiano, A. Ghaffar: Erythro-

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cytes as carriers of chemotherapeutic agents for 35 Jacob , H.S., RA. MacDonald, J.H. Jand/: Regu­ targeting the reticuloendothelial system. Am. J. lation of spleen growth and sequestering function. Hemat. 9 (1980) 249 J. Clin. Invest. 42 (1963) 1476 23 Ariel, I., G. Padula: Irradiation of the spleen by 36 Perla, P. , J. Marmoston-Gottesman: Studies on the intraarterial administration of 90 yttrium mi­ Bartonella muris anemia of albino rats. III. The crospheres in patients with malignant lymphomas. protective effect of autoplastic splenic transplants Cancer 31 (1973) 90 on the Bartonella muris anemia of splenectomized 24 Fehr, J., V. Hofmann, U. Kappeler: Transient re­ rats. J. Exp. Med. 52 (1930) 131 versal of thrombocytopenia in idopathic throm­ 37 Likhite, V. V. : Evidence of immunologic activity bocytopenic purpura by high-dose intravenous and heterotopic autotransplanted splenic tissue gamma globulin. New Eng. J. Med. 306 (1982) and DBA/2 mice. Cell. Immun. 12 (1974) 382 1254 38 Bowman, CA., D.B. Van Wyck, M.H. Witte, C.L. 25 Stuart, A.E.: Chemical splenectomy. Lancet 1 Witte: Antibody formation by subcutaneous and (1960) 896 omental splenic autotransplants in rats. JAMWA 26 Pearson, H.A. , D.T. Johnston, KA. Smith, R.J. 32 (1977) 409 Toulukian: The born again spleen. Return of 39 Van Wyck, D.B., M.H. Witte, C.L. Witte, R. Strunk: splenic function after splenectomy for trauma. Humoral immunity in experimental hyposplenism. New Eng. J. Med. 298 (1978) 1389 Surg. 84 (1978) 134 27 Jacob, H.S.: Born again to work again. New Eng. 40 Van Wyck, D.B. , M.H. Witte, C.L. Witte, A.C. Thies: J. Med. 298 (1978) 1415 Critical splenic mass for survival from experimental 28 Pearson, H.A .: Splenectomy: its risks and its pneumococcemia. J. Surg. Res. 28 (1980) 14 roles. Hosp. Prac. (1980) p. 85-94 41 Van Wyck, D.B. , M.H. Witte, C.L. Witte: Synergism 29 Case records of the Massachusetts General Hos­ between the spleen and serum complement in ex­ pital (Case 36- 1975), ed. by. R.F. Scully, J.J. perimental pneumococcemia. J. lnf. Dis. 145 Galdabine, B.U. McNeely. New Eng. J. Med. 293 (1982) 514 (1975) 547 42 Van Wyck, D. , T. Moon, M.H. Witte, C.L. Witte: 30 Rice, H.M. , P.D. James: Ectopic splenic tissue A mathematical model to assess splenic remnant failed to prevent fatal pneumococcal septicemia protective function. Clin. Res. 30 (1982) 380A after splenectomy for trauma. Lancet (1980) 565 43 Crosby, W.H.: Current concepts: splenectomy in 31 Likhite, V. V.: Protection against fulminant sepsis hematologic disorders. New Eng. J. Med. 286 in splenectomized mice by implantation of auto­ (1972) 1252 chthonous splenic tissue. Exp. Hemat. 6 (1978) 44 Verheyden, C.N. , R. W. Be art, M.D. Clifton, R.L. 433 Phy/iky: Accessory splenectomy in management 32 Cooney, D.R., S.E. Swanson, J.C. Dearth, M.K. of recurrent idiopathic thrombocytopenic purpura. Dewanjee, R.L. Telander: Heterotopic splenic Mayo Clin. Proc. 53 (1978) 442 autotransplantation in prevention of overwhelm­ 45 Cummins, C.S., D.M. Linn: Reticulostimulating ing postsplenectomy infection. J. Ped. Surg. 14 properties of killed vaccines of anerobic coryne­ (1979) 336 forms and other organisms. J. Nat'!. Cancer lnst. 33 Dickerman, J.D. , S.R. Homer, JA. Coil, et al.: 59 (1977) 1697 The protective effect of intraperitoneal splenic 46 Morgenstern, L.: ln discussion of 8. Ann. Surg. autotransplants in mice exposed to an aerosol­ 194 (1981) 268 ized suspension of type 111 streptococcus pneu­ moniae. Blood 54 (1979) 354 34 Schwartz, A.D., J.F. Goldthorn, JA. Winkelstein, A.J. Swist: Lack of protective effect of autotrans­ planted splenic tissue to pneumococcal challenge. Blood 51 (1978) 475

Marlys H. Witte, M.D. , Departments of Surgery and Medicine, University of Arizona College of Medicine, Tucson , Arizona 85724

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