UEU-co logo

AccessSurgery – Print

  Print  |  Close Window

Note: Large images and tables on this page may necessitate printing in landscape mode.

Skandalakis’ Surgical Anatomy > Chapter 22. Spleen >


The anatomic and surgical history of the spleen is shown in Table 22-1.

Table 22-1. Anatomic and Surgical History of the Spleen

Hua To (115-205 A.D.)   Performed possible splenectomies in China
Jewish Talmud (2nd – 6th Centuries) 
  Described the spleen (“techol”) as the seat of laughter while providing analysis of its associated pathologies
Maimonides (1135-1204)   Described the blood-purifying properties of the spleen
Zaccarelli 1549 Performed one of the earliest splenectomies (many have argued that it was an ovariectomy instead)
Ballonii 1578 Told of a splenectomy performed by an unknown barber surgeon. In his report he asked, “Este igiture splenatam necessarius” (Is the spleen so necessary for life).
Rosetti 1590 First successful partial splenectomy
van Leeuwenhoeck (1632-1723)   Studied the spleen arguing that it played a role in the purification of the blood
Read 1638 Reported on a splenectomized dog with a six-week survival period. In his paper he argued, “. . .the spleen may be excised without harm.”
Clark 1673 Removed a portion of the spleen after his patient’s unsuccessful suicide attempt
Matthias 1678 Performed the first successful splenectomy for trauma
Fantoni of Turin ca. 1700 As reported by Grebezius he operated on the exposed spleen of a girl abused by her mother
Ferguson 1734 Performed a partial splenectomy
Hewson 1777 Cautiously speculated that the spleen formed erythrocytes
Assolant 1802 Ligated branches of the terminal division of the splenic artery in dogs, noting the segmental distribution of the splenic blood supply
O’Brien 1816 Performed the first splenectomy for trauma (knife wound) in the United States
Quittenbaum 1826 Deliberately performed splenectomy. His patient died six hours later from shock.
deGray 1844 Provided a case report of splenectomy to the French Academy of Surgeons. He noted that the patient recovered as expected but died thirteen years later of pneumonia (possibly the earliest reported case of Overwhelming Post-Splenectomy Infection [OPSI]).
Bryant 1866 Performed a splenectomy on a 20-year-old leukemia patient
Evans 1866 Reported delayed rupture of the spleen
Péan 1867 Performed the first segmental resection of the spleen on a 20-year-old woman suffering from a splenic tumor (she was originally thought to have an ovarian cyst)
Deeble 1889 Removed ¾ of the spleen to treat a gunshot wound
Billroth 1891 Reported an incidental autopsy finding of the spleen where, “[f]rom the appearance of the rent and the small quantity of blood effused, we conclude that the injury might have healed completely.” In this statement he ushered in the possibility of non-surgical management of splenic trauma.
James 1892 Sutured both the spleen and the diaphragm to treat a gunshot wound
Riegner 1892 Successfully removed a transected spleen for blunt trauma in a 14-year-old construction worker who had fallen off a scaffold and hit a board. On the justification of splenectomy for trauma he argued: “If the situation is so desperate and bleeding so extensive that we cannot think about the possibility of saving the patient through compression . . .ligate the specific vessels and remove the spleen.”
Zikoff 1895 Successfully sutured a lacerated spleen
Pitts and Ballance 1896 Reported a delayed splenic rupture with a five-day latent period
Jordan 1898 Reported partial splenectomy in dogs
Funaioli 1901 Offered a description of partial splenectomy and splenic hemostasis using segmental arterial ligation in dogs
Berger 1902 Used tamponade of the spleen as an alternative to splenectomy
Baudet 1907 Provided detailed descriptions of delayed splenic rupture latency, known now as the latent period of Baudet
Gibbon 1908 Argued, “. . .if the spleen were not so easily removed, fewer splenectomies for rupture would be reported, since the majority of these cases of hemorrhage can be controlled by judicious packing.”
W. Mayo 1910 Reported on a splenectomized patient treated for severe pneumonia
Pearce 1918 Published his classic book The Spleen and Anaemia stating that splenectomy was indicated for Banti’s diseases, pernicious anemia, hemolytic jaundice, Gaucher’s disease, trauma, cysts, tuberculosis, syphilis, and wandering spleen 
Morris and Bullock 1919 Performed classic experiments observing an 80% mortality in splenectomized rats given plague bacillus. In the control group the mortality rate was 35%.
Volkmann 1923 Argued that partial splenectomy is feasible in humans
Henschen 1928 Confirmed the segmental anatomy of the spleen in a review of several studies
Dretzka 1930 Reported on a series of 27 patients with rupture of the spleen treated with splenorrhaphy
McIndoe 1932 Offered his classical study on the concept of delayed splenic rupture
Ballance, Baudet, McIndoe, Zabinski 1943 Reported that the incidence of delayed splenic rupture is between 15-30%, noting a two-year latency in some
Gruber, Redner, and Kogut 1951 Provided the first report of post-splenectomy sepsis in infants
King and Shumacker 1952 Observed severe sepsis in five patients with congenital spherocytosis
Smith 1957 Reported the first severe infections following splenectomy for traumatic rupture
Campos Christo 1962 Revived the partial splenectomy as a viable alternative to total splenectomy
Coler 1963 Provided the first reported deaths of splenectomized children succumbing to overwhelming post-splenectomy sepsis
Ellis and Smith 1966 Reviewed immunologic properties of spleen
Bodon and Verzosa 1967 Challenged the necessity for splenectomy in all cases of incidental splenic injury
Najjar et al. 1970 Discovered “tuftsin,” a splenic peptide associated with immunity
Douglas and Simpson 1971 Provided a scheme for observation and nonoperative treatment in children with suspected splenic injury
Simpson et al. 1977  
Dixon et al. 1980 Divided spleen anatomically into three-dimensional cones. Advocated conservative treatment of vascular injury to the most external zone, and segmental ligation for deeper injury.
Delany et al. 1982 Used enveloping mesh to tamponade parenchymal bleeding
Carroll et al. 1992 Reported successful laparoscopic splenectomy
Cuschieri et al.
Delaitre and Magignieu
Thibault et al.
Liu et al. 1996 Provided anatomic segmental classification based on arterial patterns

History table compiled by David A. McClusky III and John E. Skandalakis.


Coon WW. The spleen and splenectomy. Surg Gynecol Obstet 1991;173:403-414.

Justicz AG, Skandalakis PN, Skandalakis LJ. Management of splenic trauma in adults. Probl Gen Surg 1990;7:128-141.

McClusky DA III, Skandalakis LJ, Colborn GL, Skandalakis JE. Tribute to a triad: History of splenic anatomy, physiology, and surgery. Part 1. World J Surg 1999;23:311-325.

McClusky DA III, Skandalakis LJ, Colborn GL, Skandalakis JE. Tribute to a triad: History of splenic anatomy, physiology, and surgery. Part 2. World J Surg 1999;23:514-526.

McDermott WV. Liver, biliary tract, pancreas, and spleen. In: Warren R. Surgery. Philadelphia, WB Saunders, p. 867.

Morgenstern L. The surgical inviolability of the spleen: Historical evolution of a concept. In: International Congress of the History of Medicine, 23rd, 1972: Proceedings. London: Wellcome Institute of the History of Medicine, 1974.

Pearce RM, Krumbhaar EB, Frazier CH. The Spleen and Anaemia: Experimental and Clinical Studies. Philadelphia: JB Lippincott, 1918, pp. 3-10.

Sherman R. Perspectives in Management of Trauma to the Spleen: 1979 Presidential Address, American Association for the Surgery of Trauma. J Trauma 1980;20:1-13.

Embryogenesis of the Spleen

Normal Development

The mesoderm is responsible for the genesis of the spleen, the largest of the lymphatic organs. Around the fifth week of gestation, mesenchymal cells between the leaflets of the dorsal mesogastrium and the cells of the coelomic epithelium of the dorsal mesentery form the early spleen. The dorsal mesogastrium (Fig. 22-1), which supports the embryonic stomach, expands around the fifth to sixth weeks to form the greater omentum.

Fig. 22-1.

Development of the spleen. A. The splenic primordium as it appears on the left side of the dorsal mesogastrium at 6 weeks. B. At 2 months. C. At 4 months. D. Angiogenesis is beginning in the early splenic primordia. (A-C, Modified from: Arey LB. Developmental Anatomy [6th ed]. Philadelphia: WB Saunders, 1954; D, from Ivemark BI. Implications of agenesis of the spleen on the pathogenesis of cono-truncus anomalies in childhood. Acta Paediatr 1955; 44[suppl 104]:1-110; with permission.)

The spleen remains within the mesenteric expansion but does not follow the downward formation of the omentum. In other words, the spleen is located between the leaves of the dorsal mesogastrium, and occupies this location in adult life (Fig. 22-2). All these embryogenic mechanisms take place on the left side of the dorsal mesogastrium, at the left upper quadrant, which will be the permanent home of the spleen. The organ’s origin is neither midline nor bilateral.

Fig. 22-2.

Peritoneal reflections of the spleen develop from the primitive dorsal mesentery. A. Relationships during the primitive embryonic stage. B. Relationships in the adult. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

The left side of the dorsal mesogastrium gives rise to the splenic ligaments (Fig. 22-3). With the possible rotation of the stomach, the left surface of the mesogastrium becomes fused to the peritoneum over the left kidney. The splenic artery is found posterior to the lesser sac and anterior to the left kidney. It is enveloped by the splenorenal ligament, which is the posterior portion of the dorsal mesogastrium. Mesenchymal cells differentiate to form both the capsule and a connective tissue framework.

Fig. 22-3.

Development of the splenic ligaments. A. Gastric and splenic rotation. B. Formation of omental bursa and its relation to the spleen. C. Beginning of formation of the greater omentum and its relationship to spleen. D. Formation of two major splenic ligaments. (Modified from Allen KB, Gay BB Jr, Skandalakis JE. Wandering spleen: anatomic and radiologic considerations. South Med J 1992;85:976-984; with permission.)

At 10 to 20 days, differentiation to true epithelium with visible basement membrane is evident. Clefts of mesenchymal origin (sinusoids without endothelial lining) are present at 29 to 30 days; they show evidence of communication with the capillaries. The spleen assumes its characteristic shape in the early fetal period; fetal lobulation normally disappears late in the prenatal period.

Around the 13th week, surface immunoglobulin-bearing B cells and erythrocyte rosette-forming T cells emerge. Immunoglobulins A and, perhaps, E are not synthesized during fetal life, but IgM and IgG antibodies are synthesized during the third trimester. The spleen cannot be considered a giant lymph node, since there is no connection of the splenic lymphatics with other lymph vessels.

Splenic lobules form around the central arteries in the first weeks of the second trimester. The red pulp develops at the periphery of the lobules. There is also an accumulation of lymphocytes, monocytes, and macrophages during the second trimester; this is the white pulp, which forms around the central arteries.

Congenital Anomalies


Asplenia may be associated with several other congenital anomalies. Asplenia is autosomal recessive, while splenic hypoplasia is autosomal dominant.


Polysplenia may be associated with several other congenital anomalies. It is distinct from accessory spleen, in which the normal spleen is present but is joined by one, two, or more splenic nodules of small size that are completely separated from the main organ.

Wandering Spleen

Although the etiology of wandering spleen may be multifactorial, the most compelling evidence points toward an error in the embryologic development of the spleen’s primary supporting ligaments (Fig. 22-4). The ligaments may be abnormal (too long, too short, too wide, too narrow, abnormally fused) or absent. Laxity of these ligaments and abnormal length of the splenic vessels can result in excessive splenic mobility and therefore, in the phenomenon of ptotic (wandering) spleen.

Fig 22-4.

Peritoneal attachments of the spleen. Inset: Hilum of the spleen, showing the short gastric and gastroepiploic vessels in the gastrosplenic ligament. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Six ligaments (gastrosplenic, splenorenal, splenophrenic, splenocolic, and pancreatosplenic ligaments, and presplenic fold) are directly associated with the spleen. Two others (pancreaticocolic and phrenicocolic) are indirectly associated with the spleen. Most of the literature holds the gastrosplenic, splenorenal, and phrenicocolic ligaments responsible for ptosis of the spleen. Allen et al.2 suggested that from an anatomic standpoint, the other ligaments (especially the splenocolic ligament) also participate in the development of ptosis of the spleen (Fig. 22-5).

Fig 22-5.

Major and minor splenic ligaments. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

Due to its abnormal fixation, the wandering spleen is susceptible to infarction as a result of twisting about its elongated vascular pedicle.3 Clinically the wandering spleen, whether infarcted or not, can present as either an acute or a chronic process: it can appear as an asymptomatic mass, a mass with pain, or an acute abdomen.4 In the pediatric population, Desai et al.3 recommend surgical splenopexy as definitive treatment except in cases of infarction. However, splenectomy should be done if there is no evidence of blood flow to the spleen.3

Wandering spleen is a rare clinical diagnosis, particularly in the pediatric population.5 In a review of 97 cases of wandering spleen with torsion of the pedicle, Abell6 found only one patient under 10 years of age. A review of the literature by Allen and Andrews7 yielded only 35 cases in children younger than 10. Wandering spleen that produced small-bowel obstruction in a neonate was reported by Gosselin and Chou.8 Spector and Chappell9 reported wandering spleen associated with gastric volvulus in a 5-year-old, in whom “normal ligamentous connections between the stomach, spleen, and posterior abdominal wall were absent. Developmental anomalies that result in wandering spleen may lead to hypermobility of the stomach and a predisposition to gastric volvulus. In such patients, prophylactic gastropexy should be considered.”

Splenogonadal Fusion

Splenic tissue is known to fuse with male and female gonads, as well as with the pancreas and liver. The latter two organs are derived from the caudal foregut, with which the development of the spleen is physically closely related although it is not a foregut derivative. In males splenogonadal fusion is indicated by the presence of splenic tissue in the left scrotum. As rare as the condition is, it is occasionally associated with two other rare defects: ectromelia and micrognathia. Splenogonadal fusion with limb deficiency and micrognathia was reported by Moore et al.10

The literature contains differing classifications of splenogonadal fusion. Putschar and Manion11 termed the condition continuous when there is a cord of splenic tissue or a fibrous formation between the main spleen and the gonadal-mesonephric structures, and discontinuous when discrete masses of splenic tissue are found fused to these structures. Le Roux and Heddle12 proposed that “continuous splenogonadal fusion with or without limb defects and micrognathia constitutes one syndrome… discontinuous splenogonadal fusion amounts to no more than a rare variant of an accessory spleen.” The authors of this chapter agree.

To correct splenogonadal fusion, surgery is the treatment of choice and is performed as follows in males:


1. Sever the band connecting the spleen with the left scrotum if obstruction is present

2. Remove the nodule with or without orchidectomy

3. Repair coexisting left indirect hernia

Splenogonadal fusion is far less common in women than in men. According to Gouw et al.,13 of 84 reported cases of splenogonadal fusion only 6 were females. Nonetheless, the phenomenon of splenic pregnancy has been reported. Alcaly et al.14 believes that primary splenic pregnancy is the rarest form of extrauterine pregnancy. There are fewer than 10 cases in the literature.15-17

Can mesonephric tissue produce splenic tissue (a very bizarre ectopia)? The authors do not know.

Splenic Cysts

Congenital splenic cysts are lined with epithelium. In 1970 Talerman and Hart18 reported several hundred epithelial cysts. Most of these cases involved children and young adults. Panossian et al.19 reported an epidermoid cyst of the spleen as a generalized peritonitis. The authors reviewed 159 cases, adding one of their own and advising splenectomy and an antibiotic regimen, including coverage for Salmonella infection.

Accessory Spleens

Accessory spleens are found in one fifth to one third of autopsies.20 Seventy-five percent of accessory spleens are located at the hilum (splenic porta). Although it may be possible for several accessory spleens to be found at the hilum, rarely is accessory splenic tissue found in more than two locations.21

The following is an analysis of 602 males whose accessory spleens were discovered at autopsy22,23:

  Number of cases
One accessory spleen 519
Two accessory spleens 65
Three accessory spleens 13
Four accessory spleens 3
Five accessory spleens 2

Curtis and Movitz21 reported a case with 10 accessory spleens. Abu-Hijleh24 reported 11 accessory spleens in a cadaver, with diameters from 0.5 cm to 6.0 cm. The locations of the accessory spleens in the splenic area were as follows: 2 at the hilum, 5 at the gastrosplenic ligament, and 4 at the splenorenal ligament.

We quote from Habib et al.25:

Accessory spleens are not infrequent and occur in 11 to 44 per cent of the population with a greater incidence in those with hematological disease. They may remain clinically silent or result in a number of pathologic processes. Abscess of an accessory spleen is rare but must be considered in the differential diagnosis of fever of unknown origin or sepsis in select groups of patients. Computerized tomography is the imaging modality of choice and may also be used in the percutaneous drainage of select cases. Laparoscopic splenectomy in the hands of the experienced laparoendoscopic surgeon is a viable treatment option.

Wekerle et al.26 reported intrahepatic splenic tissue in a patient with recurrent idiopathic thrombocytopenic purpura.


Splenic tissue in the peritoneal cavity may be produced by autotransplantation secondary to injury. Although the majority of cases are asymptomatic, there have been isolated reports in the literature of splenosis producing intestinal obstruction from adhesions, pain resulting from torsion, and stomach masses simulating carcinoma.27 Metwally and Ravo28 stated that the theory that splenosis is beneficial for a patient with an infection is controversial.

Surgical Anatomy of the Spleen

Topography and Relations

The spleen is located in the left upper quadrant of the abdomen in a niche formed by the diaphragm above it (posterolateral). The stomach is located medially (anteromedial), the left kidney and left adrenal gland posteriorly (posteromedial), the phrenicocolic ligament below, and the chest wall (the ninth to eleventh left ribs) laterally. The tail of the pancreas in most cases is related to the splenic hilum. The spleen is concealed at the left hypochondrium. It is not palpable under normal conditions.

The spleen is associated with the posterior portions of the left ninth, tenth, and eleventh ribs. It is separated from them by the diaphragm and the costodiaphragmatic recess (Fig. 22-6). The spleen is oriented obliquely. Its upper end is situated some 5 cm from the dorsal midline, approximating the level of the spinous processes of the tenth and eleventh thoracic vertebrae. The lower end lies just behind the midaxillary line. The long axis of the organ roughly parallels the course of the tenth rib. On roentgenograms, the spleen is typically about 5 cm wide and 14 cm long. The spleen descends about 2 to 5 cm with deep inspiration.29

Fig 22-6.

Location of the spleen. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

If one divides the spleen into three parts, the upper third is related to the lower lobe of the left lung, the middle third to the left costodiaphragmatic recess, and the lower third to the left pleura and costal origin of the diaphragm.

Size of the Spleen

The spleen can be very small or very large. The extremes are 1 ounce and 20 pounds, as reported by Gould and Pyle.30 Spleens of extreme size may be healthy or diseased.

The size of the spleen can change readily, enlarging with increases in blood pressure. The size increases after meals; conversely, its size decreases during exercise or immediately postmortem. The lymphoid tissue of the spleen, like lymphoid tissue elsewhere in the body, undergoes diminution sometime after the patient reaches the age of 10 years.31 There is some involution of the organ as a whole after the age of 60 years.

Under normal conditions, the long axis of the organ runs parallel to the tenth rib. With splenomegaly, the spleen is palpable below the left costal margin, with its long axis extending down and forward along the tenth rib.32,33

Harris’s odd numbers 1, 3, 5, 7, 9, and 11 (as reported by Last33) help one memorize certain average dimensions of the spleen:


The spleen measures 1 x 3 x 5 inches (2.5 x 7.5 x 12.5 cm)

The spleen weighs 7 oz (220 g)

The spleen relates to left ribs 9 through 11

Shape of the Spleen

According to Michels,34 the spleen has three forms. It is wedge-shaped in 44% of specimens, tetrahedral in 42%, and triangular in 14% (Fig. 22-7).

Fig 22-7.

Shapes of the spleen. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

A more useful system, also suggested by Michels,34 notes two forms of the spleen (Fig. 22-8). The first (30%) is a compact type of spleen with almost even borders and a narrow hilum in which the arterial branches are few and large. The second (70%) is a distributed type, with notched borders and a large hilum, in which the arterial branches are small and numerous.

Fig 22-8.

Classification of spleen shape based on general arterial distribution. (Adapted and modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

In an enlarged spleen the notched anterior border, when present, can be palpated. Michels34 advised surgeons that spleens with notched borders have multiple (more than two) arteries entering the medial surface. Polar arteries are common in this type of spleen. Consequently, a spleen with a notched anterior border is difficult to remove. However, in our small number of dissections in the laboratory and in our splenectomies in the operating room, we have observed these differences of vascular distribution on both notched and unnotched spleens. Therefore, an unnotched spleen does not necessarily indicate a limited vascular distribution.

Surfaces and Borders of the Spleen

For all practical purposes, the spleen has two surfaces: parietal and visceral. The convex parietal surface is related to the diaphragm; the concave visceral surface is related to the surfaces of the stomach, kidney, colon, and tail of the pancreas. On the concave hilar surface, the entrance and exit of the splenic vessels at the splenic portas in most specimens form the letter S, which is evident if one connects the upper polar, hilar, and lower polar vessels.

The spleen has two borders (Fig. 22-9): the superior (anterior) and the inferior (posterior). The superior border separates the gastric area from the diaphragmatic area, and the inferior border separates the renal area from the diaphragmatic area.

Fig 22-9.

Splenic borders. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

Surgical Applications


A patient with fractures of the left ninth to eleventh ribs should be observed closely. Such a patient is a candidate for an underlying splenic rupture. In a child, however, the spleen may rupture without rib fractures. We have seen spontaneous rupture of the pediatric spleen in the presence of diseases such as malaria, kala azar, and mononucleosis.

Morrell et al.35 reported a thirty-year trend in the growth of splenorrhaphy and observation instead of splenectomy for splenic injury treatment. In a study of trauma patients with blunt splenic injury, Goodley et al.36 found that nonoperative management was ineffective for older patients.

In a patient with empyema, a thoracic surgeon inadvertently placed a left thoracotomy tube through the left hemidiaphragm and into the upper pole of the spleen. Bleeding and a left subdiaphragmatic abscess ensued. With splenectomy, drainage, and large doses of antibiotics, the patient survived (JES, unpublished results).

In a series of articles, Moody37 and Moody et al.38,39 stated that the lower splenic pole is variable in position. It can relate to the upper half of the first lumbar vertebra or, more inferiorly, to the upper half of the fifth lumbar vertebra. Most frequently, it is related to the upper third of the third lumbar vertebra.

In splenomegaly, the spleen is always located in front of the splenic flexure of the colon. Adhesions are almost always present and are sometimes vascular. Often, an enlarged spleen has extensive adhesions to the colon. In elective splenectomies, intestinal preparation is essential if splenomegaly is present. The size of the spleen will dictate the type of incision (see “Incisions” in this chapter). Remember what Arthur H. Keeney40 stated: “Pray before surgery, but remember God will not alter a faulty incision.”

 Read an Editorial Comment


A notched spleen has multiple arteries that should be carefully ligated, one-by-one, close to the splenic porta (hilum). But remember, an unnotched spleen could also have an extreme vascular distribution.

The concave visceral surface should be handled with care. The small, short gastric veins retract instantly and therefore, require meticulous individual ligation. The tail of the pancreas should be separated from the spleen with great care to avoid pancreatic injury. If present, the pancreaticosplenic ligament should be ligated.

The posterior splenic border is related to the renal and diaphragmatic areas; separation of tissues should be toward the diaphragm to avoid injury to the renal capsule.

The convex parietal surface of the spleen is related to the diaphragm. It is avascular in most cases, but it would be wise to ligate the splenophrenic ligament, whether it is short or long.

By applying knowledge of the simple guidelines to the surgical anatomy of the spleen as described above, the surgeon can examine the shape, surfaces, and borders of the spleen and perhaps better anticipate potential troubles that may arise during splenectomy. If the surgeon is careful and proceeds slowly, he or she can avoid bleeding from the spleen, from the greater curvature of the stomach, and perhaps from the capsule of the left kidney.

Segmental Anatomy

Knowledge of the anatomic phenomenon of splenic segmentation is imperative for segmental resection. Kyber41 may have been the first to suggest splenic segmentation. Skandalakis et al.42 reported, however, that there is no consistent segmental arterial anatomy. Furthermore, the existence of arterial collaterals prevents standardized anatomic partial splenectomy based on blood supply. Remember that the segmentation of the spleen can be explained embryologically: the organ is formed by the fusion of vascularized, isolated mesenchymal aggregates.

Segmentation of the spleen appears to be variable (as is its description in the literature). Gupta et al.43 reported that the spleens examined had two lobes (superior and inferior) or three lobes (superior, middle, and inferior). In a study of 66 full-term newborn infants, Mandarim-Lacerda et al.44 found two lobar branches in a majority of splenic specimens (Fig. 22-10); the other specimens had either three or four lobar branches. In a study of 850 spleens Liu et al.45 found that there are two lobar arteries in most splenic specimens; the other specimens had three, one, or four lobar arteries (Fig. 22-11). These data are compiled into a single table for the purposes of comparison (Table 22-2). (See “Branches of the Splenic Artery” below for more discussion of this topic.)

Table 22-2. Distribution of “Lobes,” “Lobar Branches,” and “Lobar Arteries” in Splenic Specimens from Three Studies

  1 2 3 4
Gupta et al. (“lobes”)   84% 16%  
Mandarim-Lacerda et al. (“lobar branches”)*   68.2% 10.6% 4.5%
Liu et al. (“lobar arteries”) 0.8% 86% 12.2% 1%

*Remaining 16.7% of specimens had intersegmental anastomoses


Gupta CD, Gupta SC, Aorara AK, Singh P. Vascular segments in the human spleen. J Anat 1976; 121:613-616.

Mandarim-Lacerda CA, Sampaio FJ, Passos MA. Segmentation vasculaire de la rate chez le nouveau-ne: support anatomique pour la resection partielle. J Chir (Paris) 1983; 120:471.

Liu DL, Xia S, Xu W, Qifa Y, Gao Y, Qian J. Anatomy of vasculature of 850 spleen specimens and its application in partial splenectomy. Surgery 1996; 119:27-33.

Fig 22-10.

Cast of the spleen with a bifurcated splenic artery. 1, superior segment, 2, inferior segment. (From Mandarim-Lacerda CA, Sampaio FJB, Passos MARF. Segmentation vasculaire de la rate chez le nouveau-ne. J Chir (Paris) 1983; 120:471-73; with permission.)

Fig 22-11.

Vasculature of splenic hilum and intraspleen. 1. Common splenic artery; 2. Lobar arteries; 3. Segmental arteries; 4. Submental arteries. Relatively avascular planes between lobes or segments are observed. (From Liu DL, Xia S, Xu W, Qifa Y, Gao Y, Qian J. Anatomy of vasculature of 850 spleen specimens and its application in partial splenectomy. Surgery 1996;119:27-33; with permission.)

The number of segments or segmental arteries varies considerably also (Fig. 22-12, Fig. 22-13). Liu and colleagues45 reported finding three to eight segmental arteries in a subgroup of specimens. In the same study, 83% of the spleens examined had polar arteries (Table 22-3). Redmond et al.46 found three to seven segments among their specimens (Fig. 22-14), and Voboril47 reported finding as many as 10 splenic segments. The vasculature of each segment appears to be largely independent of that of its neighboring segments.

Table 22-3. Distribution of Polar Arteries in 280 Splenic Specimens

No. of Spleen Specimens SPA (%) IPA (%) SIPA (%)
280 31.3 38.8 13.3

SPA, Superior polar artery; IPA, inferior polar artery; SIPA, superior and inferior polar arteries.

Source: Liu DL, Xia S, Xu W, Qifa Y, Gao Y, Qian J. Anatomy of vasculature of 850 spleen specimens and its application in partial splenectomy. Surgery 1996; 119:27-33; with permission.

Fig 22-12.

Arrangement of intrasplenic vasculature manifests transverse pattern of arterial supply to lobes or segments. Spleen is defined as having three to five segments. Anatomically, they are named in sequence of segment 1 to segment 5 from superior pole to inferior pole (S1-S5). (Modified from Liu DL, Xia S, Xu W, Qifa Y, Gao Y, Qian J. Anatomy of vasculature of 850 spleen specimens and its application in partial splenectomy. Surgery 1996;119:27-33; with permission.)

Fig 22-13.

Diagram illustrating segments and subsegments. 1, polar subsegment; 2, central subsegment; 3, central segment; 4 polar segment. (Modified from Redmond HP, Redmond JM, Rooney BP, Duignan JP, Bouchier-Hayes DJ. Surgical anatomy of the human spleen. Br J Surg 1989, 76:198-201; with permission.)

Fig 22-14.

Cast of a spleen containing five segments. Blue and yellow, polar; white, green and red, central. Note the avascular planes between the segments. (From Redmond HP, Redmond JM, Rooney BP, Duignan JP, Bouchier-Hayes DJ. Surgical anatomy of the human spleen. Br J Surg 1989, 76:198-201; with permission.)

There is confusion in the literature about the terms splenic lobe, pole, and segment. Extrasplenic bifurcation of the splenic artery will produce two lobes, superior and inferior. However, further bifurcation or trifurcation often occurs and this gives rise to the vasculature of segments and poles. We propose that the term segments be used when referring to splenic parts separated by avascular planes, elsewhere called lobes. In surgery we speak of splenic segmentectomy and not about lobectomy or polectomy.

The planes separating segments or subsegments are usually obliquely situated with respect to the long axis, and often do not traverse the full thickness of the spleen from the visceral to the parietal surface.48

Segmentation can also be observed with respect to the venous drainage of the spleen. Dreyer and Budtz-Olson49 reported venous segmentation of the spleen. Dawson et al.48 found that 71% of spleens had two lobes and 29% had three. In half of the specimens the lobes were further subdivided into two segments. The avascular lines of separation of the lobes followed those of the arteries. In more than half of the specimens, the lines of lobar separation could be equated with marginal notching of the splenic border. The veins emanating from the lobes were individually accessible at the hilum. Examination of doubly injected (arterial and venous vessels) specimens confirmed that neither the arterial nor the venous supply to the lobes or segments crossed to adjacent parenchyma.

Garcia-Porrero and Lemes,50 using radiopaque injection media, found anastomoses between splenic arterial branches, especially between secondary branches, in about 30.5% of specimens. This low frequency of intrasplenic anastomoses was noted also by Mandarim-Lacerda et al.,44 who reported that 16.7% of specimens from full-term infants had intersegmental anastomoses (Fig. 22-15). They concluded that segmental splenic resection is possible in infants as well as adults.

Fig 22-15.

Cast of a spleen containing anastomoses between the inferior and superior segments. (From Mandarim-Lacerda CA, Sampaio FJB, Passos MARF. Segmentation vasculaire de la rate chez le nouveau-ne. J Chir (Paris) 1983; 120:471-73; with permission.)

Dixon et al.51 stated that intrasplenic vessels are lobar, segmented, and generally without intersegmental communication (Fig. 22-16). They conceived of the spleen as being divided into three-dimensional zones referred to as hilar, intermediate, and peripheral. Each zone requires a special technique for hemostasis. They advised conservative treatment such as the application of microfibrillar collagen to the exposed surface for the peripheral zone (arteriole and venous injury), and ligation for the intermediate and hilar zones (to take care of trabecular and segmental vessels).

Fig 22-16.

Regions indicated are shaped as a three-dimensional cone described by the length of a radius originating at the point of entrance of the major artery into the spleen. All regions contain penicilli, venules, and sinuses with addition of larger vessels as the hilum is approached. (Modified from Dixon JA, Miller F, McCloskey D, Siddoway J. Anatomy and techniques in segmental splenectomy. Surg Gynecol Obstet 1980;150:518; with permission.)

Spaces of the Left Upper Quadrant

The left suprahepatic space is bounded medially by the falciform ligament and superiorly by the left anterior coronary ligament and the left triangular ligament. Inferiorly, the space opens into the general peritoneal cavity.

The left infrahepatic space is subdivided into anterior and posterior spaces by the hepatogastric ligament, the stomach, and the gastrocolic ligament. The anterior space is the perigastric space; the posterior space is the lesser sac. The healthy spleen is closely related to the lesser sac, which is almost closed by the splenorenal and gastrosplenic ligaments.

In splenomegaly, the long axis of the spleen is directed down and forward, following the orientation of the tenth rib. It is parallel with the greater curvature of the stomach, and extends toward the umbilicus, in front of the left transverse colon and the splenic flexure. This oblique splenic axis is usual. Rarely, the axis is vertical or even transverse. These patterns further complicate the understanding of the perisplenic space.

The surfaces, borders, and topographic anatomy of the spleen all help radiologists to more accurately view and interpret the anatomy and condition of the spleen.

Peritoneum and Ligaments of the Spleen

The right and left layers of the greater omentum separate to enclose the spleen almost completely, except at the hilum, providing its serosal covering, or capsule (see Figs. 22-2, 22-3 and 22-17). The capsule formed by the visceral peritoneum is as friable as the spleen itself and as easily injured (see Fig. 22-4).

Fig 22-17.

Sagittal view of peritoneum covering the spleen. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

The peritoneal layers that enclose and suspend the spleen form the two chief ligaments of the spleen, the gastrosplenic ligament and the splenorenal ligament. These are portions of the embryonic dorsal mesentery, or mesogastrium, the leaves of which separate to surround the spleen. These two ligaments form the splenic pedicle (Fig. 22-18).

Fig 22-18.

The splenic pedicle. A. Long pedicle with a presplenic fold. B. Short pedicle. (Modified from Skandalakis JE, Gray SW, Rowe JS. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; 178; with permission.)

In addition to the two chief ligaments, there are several minor splenic ligaments and other topographically related ligaments, the names of which indicate their connections. These are the splenophrenic ligament, splenocolic ligament, pancreaticosplenic ligament, presplenic fold, phrenicocolic ligament, and pancreaticocolic ligament (see Fig. 22-5).

Gastrosplenic Ligament

The portion of the dorsal mesentery between the stomach and the spleen is the gastrosplenic ligament. Whitesell52 suggested that the ligament is best thought of as a triangle (Fig. 22-19). The two sides are the upper portion of the greater curvature of the stomach and the medial border of the spleen. At the apex of this triangle, the superior pole of the spleen lies close to the stomach and may be fixed to it. At the base of the triangle, the inferior pole of the spleen lies 5 to 7 cm from the stomach. The more cranial part of the gastrosplenic ligament contains the short gastric arteries, and the more caudal part contains the left gastroepiploic vessels.

Fig 22-19.

The gastrosplenic ligament connects the stomach and spleen. The two organs may be in contact superiorly, and the ligament is short. Inferiorly, the two organs are 5 to 7 cm apart and the ligament is longer. (Modified from Skandalakis JE, Gray SW, Rowe JS. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; 177; with permission.)

At the apex of the triangle just described, the leaves of the mesentery are reflected to the posterior body wall and the inferior surface of the diaphragm as the splenophrenic ligament. Perhaps the splenophrenic ligament is a reflection of the gastrosplenic ligament to the diaphragm. Remember the presence of this entity during surgery of the spleen. In 80% of bodies examined, Whitesell52 found smooth muscle fibers within the gastrosplenic ligament in its passage from the cardia of the stomach to the superior pole of the spleen. The muscle was well developed in some specimens and attenuated in others. Division of these muscle fibers mobilizes the superior pole of the spleen.

Splenorenal Ligament

The splenorenal ligament is the posterior portion of the primitive dorsal mesogastrium. It envelops the splenic vessels and the tail of the pancreas. Incision of the peritoneal layer of this ligament, together with mobilization of the tail of the pancreas, reestablishes the primitive condition. It is curious that the existence of the splenorenal ligament is often overlooked. In ten operating room reports selected at random, there was no mention made of the ligament, even though it obviously was encountered in the course of surgery.53

The outer layer of the gastrosplenic ligament forms the posterior layer of the splenorenal ligament. Therefore, careless division of the former can injure the short gastric vessels. Bleeding from these vessels may be the result of too-enthusiastic deep posterior excavation by the index and middle fingers of an operator seeking to mobilize and retract the spleen to the right.

The splenic pedicle can be narrow or wide, depending on the extent to which the primitive dorsal mesogastrium was absorbed into the body wall (see Fig. 22-18). The degree of effective mobilization of the spleen depends not on the splenorenal ligament, but on the length of the splenic vessels after incision of the ligament. A short splenic artery can make it impossible to deliver the spleen out of the abdomen. Gently pushing the tail of the pancreas away from the hilum of the spleen can increase splenic mobility.

Rosen et al.54 reported that the length of the splenorenal ligament ranges from 2.5 to 5.5 cm. The relations between the pancreatic tail and the splenic porta (hilum) are as follows:


24.0% tail did not penetrate the ligament

32.0% tail was within the ligament and did not reach the porta

29.7% tail reached the porta

13.0% tail passed over the hilum and penetrated the gastrosplenic ligament

The above authors classified the variations of the splenorenal ligament and the tail of the pancreas into four groups:


Type I: short ligament enveloped the tail

Type II: short ligament not penetrated by the tail

Type III: long ligament enveloped the tail

Type IV: long ligament not penetrated by the tail.

Splenophrenic Ligament

The splenophrenic ligament (see Fig. 22-5) may be said to be the reflection of the leaves of the mesentery to both the posterior body wall and to the inferior surface of the diaphragm at the area of the upper pole of the spleen close to the stomach. According to O’Rahilly,55 it is not known if the splenophrenic ligament gives rise to the splenorenal ligament from its lower part. It may be that the splenophrenic ligament is a reflection of the gastrosplenic ligament to the diaphragm.

Seufert and Mitrou56 suggest that the splenophrenic ligament contains the tail of the pancreas and all the splenic vessels. We believe that normally the splenorenal ligament is their home. If, however, the splenophrenic ligament reaches the hilum, then it may contain the tail of the pancreas and all the splenic vessels, including the root of the left gastroepiploic artery. The surgeon should remember the splenophrenic ligament during splenic surgery. It is usually avascular, but it should be inspected for possible bleeding after section.

Splenocolic Ligament

The splenocolic ligament (see Fig. 22-5, Fig. 22-20) is a remnant of the extreme left end of the transverse mesocolon. The mesocolon develops a secondary attachment to the spleen during embryonic fixation of the colon to the body wall. Because it is a secondary attachment, one would expect it to contain no large blood vessels. However, tortuous or aberrant inferior polar vessels of the spleen or a left gastroepiploic artery can lie close enough to be injured by careless incision of the ligament, possibly resulting in massive bleeding.34

Fig 22-20.

Relation of the pancreaticocolic, phrenicocolic, and splenocolic ligaments to the spleen. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

Pancreaticosplenic Ligament

The pancreaticosplenic ligament (see Fig. 22-5, Fig. 22-20) is said to be present when the tail of the pancreas does not touch the spleen. This cordlike formation is usually thin.

Presplenic Fold

Henry57 called attention to a peritoneal fold anterior to the gastrosplenic ligament (see Figs. 22-5, 22-18). The fold is usually free on its lateral border, but in a large, diseased spleen, it may be attached. Such a fold may be derived from the anterior limb of the inverted-Y arrangement of some hili.58 The presplenic fold often contains the left gastroepiploic vessels. Excessive traction during upper abdominal operations can result in a tear in the splenic capsule, which will require conservative procedures for splenic salvage.

Phrenicocolic Ligament

The phrenicocolic ligament (see Figs. 22-5, 22-20) develops at the region of the junction of the midgut and the hindgut, after the descending colon has become retroperitoneal. It is the rudimentary left end of the transverse mesocolon. Smooth muscle cells migrate into the ligament from the mesocolic taeniae. The ligament fixes the splenic flexure in place. Moreover, the development of the upper abdominal organs results in a descent of the spleen and contact of the caudal pole of the spleen with the ligament. As the spleen continues to grow, the phrenicocolic ligament is deformed, forming a pocket for the spleen.59

The phrenicocolic ligament extends between the splenic flexure and the diaphragm. It is not an intrinsic ligament of the spleen, but the spleen rests upon it. It is the “splenic floor,” but it is not connected to the spleen.

The surgeon should remember that the phrenicocolic ligament acts as a barricade at the left paracolic gutter. It is responsible, in most instances, for prohibiting blood from a ruptured splenic artery, or from the spleen itself, from traveling downward. Such blood collects at the anterior pararenal space retroperitoneally, or around the spleen at the left upper quadrant by displacing the colon laterally.

It is a mistake to call the phrenicocolic ligament the left phrenicocolic ligament because there is no right phrenicocolic ligament. There is but one phrenicocolic ligament, and it is on the left side.60

Pancreaticocolic Ligament

The pancreaticocolic ligament (see Figs. 22-5, 22-20) is the upper extension of the transverse mesocolon.

There is a degree of ambiguity about the three “colic” ligaments: the pancreaticocolic, the splenocolic, and the phrenicocolic. Do these peritoneal folds belong to the transverse mesocolon? Most likely, the answer is yes.

Other Peritoneal Folds

One of the authors of this chapter, John Skandalakis, has seen several unnamed peritoneal folds in the laboratory as well as in the operating room. Morgenstern61 was right when he stated that clear descriptions of these are absent from anatomic textbooks. The fold that is most constant and that Skandalakis observed several times is an avascular peritoneal fold from the left upper portion of the omentum to the medial part of the lower segment of the spleen, and especially to the lower pole of the spleen (Fig 22-21). Morgenstern called this the “criminal fold,” since careless traction may traumatize the spleen. Skandalakis calls this the spleno-omental “criminal” fold of Morgenstern. Rarely, Skandalakis has observed separate ligamentous bands interconnecting the summit of the convex surface of the spleen with the diaphragm. Obviously, rough handling of such an organ could lead readily to rupture of the capsule.

Fig 22-21.

Highly diagrammatic presentation of the spleno-omental “criminal” fold of Morgenstern from the left upper quadrant (LUQ) of the omentum to the medial part (MP) of the lower splenic segment and lower pole (P).

There has been controversy as to whether another avascular fold, the sustentaculum lienis (Fig. 22-22), supports the spleen. It is rarely seen in open surgery, but Poulin and Thibault62 wrote that it is readily seen through the laparoscope, and they described it as follows:

The phrenicocolic ligament courses from the diaphragm to the splenic flexure of the colon; its superior end is referred to as the phrenosplenic ligament.63 The attachment of the lower pole on the internal side is called the splenocolic ligament. Between these two, a horizontal shelf is formed on which rests the inferior pole of the spleen. It is often moulded into a sac that opens cranially and is called the sustentaculum lienis, acting as a brassière to the inferior pole of the spleen.

Fig 22-22.

Suspensory ligaments of the spleen. (Modified from Poulin EC, Thibault C. The anatomic basis for laparoscopic splenectomy. Can J Surg 1993;36:484; with permission.)

Surgical Applications


The short gastric vessels and the left gastroepiploic vessels should be ligated individually. The gastrosplenic ligament should be incised between clamps.

The splenorenal ligament is itself avascular, but it envelops the splenic vessels and the tail of the pancreas. Incision and finger excavation to mobilize the organ should be done with care.

Traction upon the splenophrenic ligament, if the ligament is short, can result in bleeding of the spleen, due to a tear of the capsule. Do not apply more traction than is necessary.

The splenocolic ligament, in close relation to the lower polar vessels of the spleen and the left gastroepiploic vessels, should be incised between clamps.

The presplenic fold is close to the left gastroepiploic vessels. Excessive traction can result in bleeding.

The pancreaticosplenic ligament, if present and long enough, should be incised between clamps. If this ligament is absent or short, careful separation of the pancreatic tail from the spleen is necessary to avoid pancreatic or splenic injury.

If the phrenicocolic ligament is short or fused, injury of the lower pole of the spleen or the splenic flexure of the colon is unlikely, but possible.

Careless traction of a short or fused pancreaticocolic ligament can also lead to colonic or pancreatic injury.

Remember that the Morgenstern fold should be divided carefully to avoid splenic capsular avulsion.

Splenic Mobility

Key Structures Affecting Splenic Mobility

The mobility of the spleen depends on the degree of laxity of both the splenic ligaments and the splenic blood vessels. We believe that only four of the ligaments can affect the position of the spleen in most cases. These are the gastrosplenic, splenorenal, splenocolic, and phrenicocolic ligaments (Fig. 22-22).

The limitation of movement of the spleen due to the gastrosplenic ligament depends on the mobility of the stomach. If the left kidney is fixed in its normal position without other abnormalities, the splenorenal ligament may play a small role. It is well known to radiologists that the left transverse colon and the splenic flexure are not displaced by renal tumors, and it is well known to clinicians that colonic resonance is present in that area. It appears that the restraint to the spleen provided by the splenocolic ligament depends on the mobility of the transverse colon and the splenic flexure. A low splenic flexure contributes to mobility of the spleen. The phrenicocolic ligament limits the downward movement of the spleen. The remaining ligaments appear to have little effect on the movement of the spleen.

Adkins64 stated that splenoptosis (wandering spleen) can be congenital or acquired. The congenital type is the result of a long splenic pedicle, and the acquired type is a sequela to splenomegaly and a relaxed abdominal wall.

The following questions arise regarding the mobility of the spleen:


When does ptosis become ectopia (i.e., displacement or malposition)?

Is ptosis a normal variation?

Is ectopia a pathologic entity involving several organs secondary to a named pathologic condition?

Radiologists suggest that the following conditions affect the position and movement of abdominal organs:29


Posture (gravity)

Respiratory movements

Tonus of the abdominal wall and the diaphragm

Degree of distention of the viscera

Tonus of the organ

Intrinsic movements of the viscera

Pressure of adjacent viscera

If one compares the liver with the spleen, one finds that hepatoptosis does not exist. The liver is fixed by the inferior vena cava and hepatic veins, the upper porta, and the falciform and coronary ligaments. The fixation of the spleen to the left upper quadrant is most likely the result of the combined tethering action of several ligaments, not the result of vessels passing into or leaving the spleen.64

Taveras65 wrote (Fig. 22-23):

[T]he spine, aorta, and the vena cava are probably the only structures which do not shift with change in position of the body. From the viewpoint of the cephalic end of the subject, all of the movable organs rotate in a counterclockwise direction when the body is turned on its left side, and vice versa when it is turned on its right side. Gravity tends to displace movable structures towards the earth.

Fig 22-23.

Schematic drawing of horizontal sections viewed from the head illustrates Taveras’65 concept of the mobility of organs caused by change in position. A. With the patient in the supine position, the liver and spleen remain in a posterior position. B. With the patient in the left lateral decubitus position, the right kidney and descending duodenum drop forward and the left lobe of the liver extends anteriorly toward the stomach, causing a prominent indentation on the anterior surface of the stomach. C. With the patient in the right lateral decubitus position, the left kidney and spleen and tail of the pancreas extend forward. The descending duodenum drops laterally and posteriorly, effacing the inferior vena cava. The left lobe of the liver does not indent the anterior surface of the stomach as prominently as in the left decubitus position. (Modified from Whalen JP. Radiology of the Abdomen. Baltimore: Lea & Febiger, 1976; with permission.)

Complications Resulting from Adjacent Visceral Pathology

The reader should remember that the peritoneal covering of the splenic vessels, which is in continuity with the splenic capsule, can be violated by pancreatic fluid during acute pancreatitis. It can also produce an intrasplenic pancreatic pseudocyst with splenic rupture and hemorrhage. McMahon et al.66 reported one instance of such an event and collected 19 others that had been reported previously.

The route and sequelae of pancreatic pseudocyst complicated by splenic involvement may be described as follows:


Secretion by the pancreas

Violation of the peritoneal coverage of the splenic vessels and the splenic portas

Intrasplenic collection of pancreatic fluid

Rupture of the splenic capsule


Collection of blood and pancreatic fluid in the left upper quadrant

Pancreatic bloody ascites if there is no left upper quadrant localization

Possible involvement of the perirenal and pararenal spaces with the aggregation of bloody fluid

Vascular System

Arterial Supply

Splenic Artery

In most people, the splenic artery is a branch of the celiac trunk, arising together with the common hepatic and left gastric arteries. The most common form of the celiac trunk is tripodal. According to Michels,67 the tripodal form occurs in 82% of individuals. Van Damme and Bonte68 report that this form occurs in 86% of individuals. When the above-mentioned arteries or other upper abdominal arteries arise from atypical sources, the tripodal arrangement may be replaced by a dipodal or a tetrapodal pattern of branching.

Course and Form of the Splenic Artery

In the majority of cases, subsequent to its origin from the celiac trunk the splenic artery courses leftward in close relation to the upper border of the pancreas (Fig. 22-24). Occasionally its course may be in front of or completely behind the pancreas. Very rarely it may be partially or totally within the pancreatic parenchyma. The splenic artery’s termination in the splenic porta is unpredictable owing to its number of branches to the spleen or neighboring organs, such as the left kidney, stomach, and omentum.

Fig 22-24.

Relation of splenic artery and splenic vein. A. Vein posterior to artery (this is the usual pattern). B. Vein both anterior and posterior to artery. C. Vein anterior to artery (this is the least common configuration). (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

The splenic artery varies in length from 8 to 32 cm and in diameter from 0.5 to 1.2 cm. It is noteworthy that the distance from the aorta to the spleen is only about 10 cm yet, in the extreme, the splenic artery can attain a length of 50 cm.

No definitive answer has been found to explain the peculiar degree of tortuosity present in the splenic artery that is seen in most individuals. Its amount of tortuosity does seem to be related to the age of individuals, but not to the presence of vascular disease affecting the vessel.69

The convolution characteristic of the splenic artery is not seen in animals such as the dog or the pig. However, this feature has been noted in infrahuman primates, including rhesus monkeys and baboons, although to a lesser degree than in humans.70

Waizer et al.71 reported that in nine out of 26 cadavers, the splenic artery made a loop to the right immediately after its origin from the celiac trunk. It appeared at the border of the lesser omentum. Therefore, it was vulnerable to iatrogenic injury during procedures on supracolic organs.

On its way to the spleen, the splenic artery forms the splenic peritoneal fold. It then ends in the splenorenal ligament, forming a peculiar tree whose pattern of branching seems different in every case. Thereafter, its branches reach and enter the splenic porta.

Branches of the Splenic Artery

Skandalakis et al.53 studied the splenic artery and its branches in toto, paying the most attention to the two distal segments – the prepancreatic and prehilar. Michels’67 four-part segmental arterial anatomy (suprapancreatic, pancreatic, prepancreatic, and prehilar) classification system was used. Angiography revealed unpredictable variations, with differences in the number and pattern of origin of arterial branches, and in the length, width, tortuosity, and course of the splenic artery with regard to the pancreas (above the upper border, in front or behind, or partially or totally within the pancreatic parenchyma).

There is considerable agreement that the splenic artery most commonly divides into two major branches (80-94% of the time72) and less commonly into three principal branches. Subsequent branching of these primary vessels three or more times results in a widely varying number of branches, which ultimately gain access to the hilum of the spleen. Garcia-Porrero and Lemes50 observed that the number of branches varied from 5 to 20, with an average of 11. Michels67 determined the extremes in numbers of terminal branches to be between 3 and 38.43,50,73,74

Differences in interpretation of the data related to numbers of branches of the splenic artery are the result of a number of factors, including the way in which one chooses to describe or number polar branches. There also seems to be a difference between male and female patients in the branching pattern of the splenic artery. In a study of 181 spleens from victims of accidental death, Garcia-Porrero and Lemes50 noted trifurcation of the splenic artery in 16.7% of female patients but only about 4% in male patients. They also observed a superior polar artery in 29.3% of specimens, in comparison with an inferior polar segmental artery in 44.8% of specimens. These terminal branches arise from the pancreatic, the prepancreatic, or the prehilar segments of the splenic artery.67 In contrast, Michels67 found a superior polar artery 65% of the time, and an inferior polar artery or arteries 82% of the time. The segmental origin of splenic arterial branches, according to Michels, is presented in Table 22-4.

Table 22-4. Segmental Origin of Splenic Arterial Branches

The suprapancreatic segment (The atypical branches are shown in italics.) 
  Left inferior phrenic a. 
  Dorsal pancreatic a.
  Superior polar a.
  Posterior cardioesophageal a. 
  Accessory gastric or hepatic a. 
  Inferior mesenteric a. 
  Posterior (dorsal) gastric a.
The pancreatic segment
  Great pancreatic a. (frequent)
  Superior polar a. (infrequent)
  Left gastroepiploic a. (rare)
  Posterior cardioesophageal a. (rare)
  One or more short gastric aa.
    Accessory left gastric a.
    Posterior gastric a.
The prepancreatic segment
  70% of the time, the terminal divisions begin here
  Inconstant branching patterns with several combinations, such as:
    Upper arterial trunk
    Middle arterial trunk
    Lower arterial trunk
    Left gastroepiploic a.
    Caudal pancreatic a.
    Superior polar a.
    Inferior polar a.
The prehilar segment
  More branching if the branching started in the pancreatic segment
  30% of the time, terminal branching starts here, not in the pancreatic segment
    In the 30%, the branches enter the spleen into a limited hilum

Source: Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis TN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Prob Gen Surg 7(1):1-17, 1990; with permission.


Michels NA. The variational anatomy of the spleen and the splenic artery. Am J Anat 1942; 70:21.

Skandalakis et al.53 dissected the splenic artery to learn about common patterns of the distal branches – those related to splenectomies. After dissecting 29 cadavers, no consistent pattern of branching could be observed. They found that 27 arteries arose from a hepatosplenogastric trunk (the normal form of the celiac artery), one arose from the common hepatic artery (hepatosplenic trunk), and one took origin from the left gastric artery (gastrosplenic trunk). Michels67 was correct when he stated that the patterns are never the same.

The splenic artery passes retroperitoneally under the posterior wall of the omental bursa, close to the upper posterior surface of the body and tail of the pancreas. In its course, it loops like a snake above and below the superior margin of the organ. According to Michels,67 the splenic artery appears more tortuous with the increasing age of the individual, there being little tortuosity in the artery of infants. Michels also called attention to the paradox of a large splenic artery supplying a relatively small organ, the spleen, in contrast to the narrower hepatic artery, which serves an organ five times larger. Sylvester et al.69 cautiously agreed with Michels in analyzing cadaveric and angiographic data of splenic artery tortuosity.

We strongly advise the interested student to study the work of Van Damme and Bonte.73

Short Gastric Arteries

In 29 cadaveric dissections,53 all the short gastric arteries arose from the proper splenic branches of the splenic artery. Helm75 wrote that their common origin is from the left gastroepiploic artery or from proper splenic branches. Michels67 found an average range of between two and four short gastric arteries and as many as nine such branches. Four to six short gastric arteries were found in each of our specimens, and they were considered to be end arteries, not anastomosing at the greater curvature of the stomach. In the series by Skandalakis et al.,53 there was a total of 145 short gastric arteries in 29 cadavers.

Because the left gastroepiploic artery does not reach the greater curvature of the stomach until the approximate midpoint of that curvature, the short gastric arteries are of special importance in supplying the more proximal part. The short gastric arteries anastomose with the cardiac branches of the left gastric artery. According to Keramidas,76 the short gastric arteries provide the collateral circulation of the spleen. Farag et al.77 stated that the short gastric arteries provide sufficient circulation to sustain just the upper third of a normal-sized spleen following removal of the lower two-thirds of the spleen.

Left Gastroepiploic Artery

According to Michels,67 the left gastroepiploic artery arises from the splenic trunk 72% of the time, from the inferior terminal splenic branch or its branches 22% of the time, and, rarely, from the middle splenic trunk or the superior terminal branch. In the series of Skandalakis et al.,53 the left gastroepiploic arose from the distal splenic trunk in 18 cadavers and from terminal branches entering the lower part of the hilum (including the lower polar artery) in ten cadavers. In one specimen, the left gastroepiploic artery originated from the caudal pancreatic artery (or, conversely, the caudal pancreatic artery originated from the left gastroepiploic artery); nonetheless, the arteries were branches of the pancreatic part of the splenic artery.

Other Branches of the Splenic Artery

There are named and small unnamed branches of the splenic artery. Among the named branches to the pancreas are the posterior gastric artery, dorsal pancreatic artery, transverse pancreatic artery, great pancreatic artery (pancreatica magna), and caudal pancreatic artery.

Posterior Gastric Artery

The posterior gastric (dorsal gastric) artery is a branch to the dorsum of the fundus of the stomach and the upper part of the body of the stomach. The reported incidence of the posterior gastric artery ranges from 4% to 99%, according to a table by Berens et al.78 that included studies from 1729 to 1991 (Table 22-5). This artery arises from the main stem of the splenic artery before its terminal bi- or trifurcation at the splenic hilum. Often, it appears nearly at the midpoint of the length of the splenic artery, ascending nearly vertically to reach the deep side of the proximal part of the stomach.

Table 22-5. Reported Incidence of Posterior Gastric Artery

Year Authors Incidence Breakdown
1729 Walther N/A N/A
1745 Haller N/A Origin-Midportion
1796 Sommerring “Sometimes” N/A
1873 Hyrtl “Inconsistent” N/A
1901 Haberer “In most cases” N/A
1904 Rossi and Cova 65.8% 2.5 cm from celiac
1907 Leriche and Villemin 12.7% Origin-Distal
1910 Piquand 99.0% Origin-Distal
1912 Rio-Branco 50.0% Origin-Proximal
1915 Helm 16.0% Origin-Proximal
1928 Adachi 21.6% 3-5 cm from celiac
1931 Testut and Latarjet N/A N/A
1932 Versari 66.0% N/A
1952 Franchi and Stuart N/A N/A
1955 Michels N/A N/A
1957 Weisz and Bianco 48.0% N/A
1959 Chiarugi 66.0% 2.5 cm from celiac
1962 Aboltin 77.1% N/A
1963 Tanigawa Adults 36.0% 2.2-13.1 cm from celiac axis
Fetuses 67.8%
1963 Couinaud N/A N/A
1967 Delteil et al. 64.3% N/A
1967 Kupic et al. 36.8% N/A
1968 Levasseur & Couinaud 50.0% N/A
1972 Laude et al. 4.0% N/A
1977 Ruzicka and Rankin N/A N/A
1978 Suzuki et al. 62.3% 18.4% Proximal third
47.8% Middle third
34.2% Distal third
1980 DiDio et al. 46.0% N/A
1983 Wald and Polk 88.0% N/A
1985 Trubel et al. 37.5% 33% had splenic branch
1986 Van Damme and Bonte 36% N/A
1988 Trubel et al. 27.7% (stomachial supply only)  
1990 Yu and Whang 84.0% 13% Proximal third
78% Middle third
9% Distal third
1990 Kaneko Fetuses 16.0% N/A
1991 Berens 48% Proximal third (3 cm)

Source: Modified from Berens AS, Aluisio FV, Colborn GL, Gray SW, Skandalakis JE. The incidence and significance of the posterior gastric artery in human anatomy. J Med Assoc Ga 80(8):425-428, 1991; with permission.

The posterior gastric artery is, characteristically, the sole branch to arise from the splenic artery and passes in a cephalic direction before the appearance of the hilar or polar branches. It may create a slight fold in the peritoneum of the posterior wall of the lesser omental bursa as it passes upward toward the stomach. Van Damme and Bonte68 pointed out that this artery can be confused with a gastric artery originating from a posterior polar branch of the splenic artery. They cited the incidence of the posterior gastric artery as 36%,79 similar to the 1985 findings of Trubel et al.80

Dorsal Pancreatic Artery

The dorsal pancreatic artery is the “supreme pancreatic artery” described by Kirk.81 It lies posterior to the splenic vein and is about 1.5 mm in diameter. Michels67 considered it the most variable of the celiacomesenteric vessels. According to Lippert and Pabst,82 the dorsal pancreatic artery (Fig. 22-25) originates from the splenic artery in 40% of specimens, but it may arise from other arteries including the celiac trunk (28%), common hepatic artery (17%), superior mesenteric artery (15%), or an aberrant hepatic artery (<1%). Occasionally it can be derived from the middle colic, accessory middle colic, or gastroduodenal artery. Details can be found in the chapter on the pancreas.

Fig 22-25.

Possible sites of origin of the dorsal pancreatic artery (percentages from Lippert and Pabst82). More than half of these arteries arise from the proximal splenic artery or the celiac trunk. (Modified from Lippert H, Pabst R. Arterial Variations in Man. Munich: J.F. Bergmann Verlag, 1985, pp. 41-45; with permission).

The dorsal pancreatic artery provides origin to the transverse pancreatic artery (also known as the inferior pancreatic artery) to the left. It commonly has a branch to the right, which anastomoses with arteries on the ventral surface of the head of the pancreas. Such a branch provides supply to the head and uncinate process. When the dorsal pancreatic artery arises from a branch to the colon, the main stem continues in the transverse mesocolon. In some cases, a dorsal pancreatic artery may give off an epiploic branch. Arteriography is essential for determining the origin and course of the dorsal pancreatic artery.

Transverse Pancreatic Artery

The transverse (inferior) pancreatic artery (Fig. 22-26) is the left branch of the dorsal pancreatic artery supplying the body and tail of the pancreas. The artery may be single, double, or absent; it may anastomose with the splenic arteries or not.83 If it does not, thrombosis of the artery can produce infarction and limited necrosis of the body and tail of the pancreas.84 The transverse pancreatic artery may be large enough that it could be mistaken for the splenic artery; however, the fact that it normally lies in a groove on the inferior border of the pancreas should preclude this mistake in identification.

Fig 22-26.

Possible configurations of the blood supply to the distal pancreas. Type I, blood supply from the splenic artery only. Type II, blood supply from the splenic and transverse pancreatic arteries with anastomosis in the tail of the pancreas. Type III, blood supply from splenic and transverse pancreatic arteries without distal anastomoses. This type is susceptible to infarction from emboli in the transverse artery. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Prob Gen Surg 1990; 7:1-17; with permission.)

Great Pancreatic Artery

One of the largest branches of the splenic artery, the great pancreatic artery (arteria pancreatica magna of Von Haller) (Fig. 22-27), is the chief blood supply of the distal body and tail of the pancreas. If this artery is singular, it usually arises from the midportion of the splenic artery.67 Van Damme and Bonte68 described in detail the confusion involved in the naming of the arteries which supply the body of the pancreas.

Fig 22-27.

Highly diagrammatic illustration of two variations of the great pancreatic artery. (Modified from Gray SW, Skandalakis JE, McClusky DA. Atlas of Surgical Anatomy for General Surgeons. Baltimore: Williams & Wilkins, 1985; with permission.)

Caudal Pancreatic Artery

According to Van Damme and Bonte,68 one (32%), two (46%), or more (22%) caudal pancreatic arteries arise from the terminal part of the splenic artery, or, variably, from the left gastroepiploic artery or a splenic branch at the hilum of the spleen. The caudate branch anastomoses with branches of the great pancreatic and transverse pancreatic arteries. When it is present at the hilum of the spleen, the caudal pancreatic artery can supply blood to accessory splenic tissue. It often courses within the pancreaticosplenic ligament to reach the pancreatic tail or spleen.

Collateral Circulation

The splenic artery is not the only artery to supply the spleen with blood. The additional blood supply comes from the inferior or transverse pancreatic artery (especially when it arises from the gastroduodenal), other pancreatic arteries, the short gastric arteries, or the left gastroepiploic artery. In 50 patients with schistosomal portal hypertension who were candidates for partial or total splenectomy, Petroianu and Petroianu85 observed that the number of splenogastric (short gastric) arteries varied from one to as many as 13. In 32 cases, the upper splenic pole remained viable even after division of both the splenic artery and the splenic vein, presumably because of the anastomoses present between the gastric and splenic parenchymal vessels.

Romero-Torres86 stated that the true blood supply of the spleen consists of the splenic artery, the short gastric vessels, and the left gastroepiploic artery. Because of the organization and anastomoses of the several arteries, he recommended that a distal pancreatectomy be performed without splenectomy and that ligation of the splenic artery is not necessary in portal hypertension if “disconnection” (ligation) of the portal-azygous system takes place (Fig. 22-28). Romero-Torres also ligates the left gastric artery and vein and the vasa brevia.

Fig 22-28.

Simple portal-azygous “disconnection.” A, Ligature of the left gastric vessels. B, Coagulation (or clipping) and cutting of the vasa brevia. C, Continuous locking suture of the anterior and posterior walls of the stomach. (With permission of R. Romero-Torres; modified.)

Venous Drainage

The splenic vein (Fig. 22-29) originates from several veins that leave the hilum of the spleen and join to form the major vessel at variable distances from the hilum. Polar tributaries are not uncommon. The splenic vein is of large caliber, but does not possess the tortuosity of the splenic artery. The vein passes through the splenorenal ligament with the artery and the tail of the pancreas, deep to the pancreas. The splenic vein receives tributaries from the pancreas, often indenting its dorsal surface, in a position inferior to the splenic artery. Deep to the region of the neck of the pancreas, the splenic vein joins the superior mesenteric vein to form the portal vein (see Fig. 22-24). Woodburne87 stated that in 60% of cases the splenic vein receives the inferior mesenteric vein before the formation of the portal vein.

Fig 22-29.

Anatomy of the splenic vein. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

Skandalakis et al.53 studied the splenic vein in 27 dissections and found that the vein was formed by three trunks in 16 cases, and four trunks in eight cases. In the remaining three cases, three trunks plus the left gastroepiploic vein formed the splenic vein. Douglass et al.88 also studied the anatomy of the splenic vein. Their findings can be summarized in Figure 22-29. The patterns are highly variable, and, as with the arteries, no one arrangement of veins duplicated the next. Considerable variation was found in the points of exit of the veins from the spleen, their point of confluence for the formation of the main splenic vein, and their entrance into other veins at the hilum or outside it.

The student of splenic anatomy should remember that very rarely do the short gastric veins enter the upper part of the spleen directly from the greater curvature of the stomach. More commonly, the short gastric veins cross the gastrosplenic ligament en route to the splenic vein or one of its tributaries.89

The relationship of the splenic vein to the splenic artery in their course together is subject to some variations (see Fig. 22-24). In 75 consecutive autopsies, Gerber et al.90 found three anatomic arrangements:


The vein lay entirely posterior to the artery in 54% of individuals

The vein was wrapped around the artery, in part posterior to it and in part anterior to it in 44% of individuals

The vein lay entirely anterior to the artery in 2% of individuals

Surgical Applications


If the spleen has not been mobilized, ligation of the splenic arteries is permissible. The spleen remains viable if the collateral circulation is intact (polar arteries, short gastric arteries, and left gastroepiploic arteries). If the color of the spleen is changed, however, and there is evidence of ischemia, a splenectomy should be performed. In general, ligation of the splenic artery should be done only if absolutely necessary (i.e., during splenectomy).

Proximal double and distal ligation of the artery is advisable.

Ligation of the splenic vein alone should be avoided.

Total splenectomy is indicated with splenic vein thrombosis.

As a rule, ligation of the artery should precede ligation of the vein.

The tortuous splenic artery should be ligated with care, avoiding pancreatic and splenic vein injury. The elevated segments of the splenic artery facilitate ligation of the artery without anatomic complications.

The terminal arterial and venous branches should be isolated and ligated close to the splenic portas to avoid bleeding, because the origin and ultimate termination of these vessels are unpredictable.

Because the origins of the splenic branches also are unpredictable, the use of a preoperative arteriogram is essential in determining the point of ligation of the splenic artery. Because collateral circulation is available, there is no question that the spleen can tolerate ligation of the splenic artery. Therefore, the spleen can be saved if necessary. Surgeons should remember that ligation of the splenic artery near its origin can produce hyperamylasemia resulting from deterioration of the pancreatic blood supply.56 Preoperative splenic arterial occlusion as an adjunct to high-risk splenectomy has been advised by Fujitani et al.91 According to Gray’s Anatomy,89 there are no anastomoses between the smaller branches of the splenic arteries, so that obstruction leads to infarction of the spleen. Dumont and Lefleur92 suggested that there is increased splenic arterial flow in patients with isolated obstruction of the splenic vein.

For all practical purposes, the main splenic arteries are the terminal branches of the splenic artery. They are responsible for the arterial blood supply of the organ. They originate either from the superior and inferior terminal arteries or from other terminal branches. The superior and inferior polar arteries should be considered part of the main splenic artery. They penetrate the splenic parenchyma above and below the portas and usually originate from the prehilar segment. The superior polar artery is almost always present.

According to Guyton and Hall,93 60 percent of all the blood in the circulatory system is usually within the veins, making the venous system the blood reservoir for the circulatory system. When necessary, the spleen can release as much as 100 ml of blood into the circulation from both of its storage areas (venous sinuses and pulp).

Lankisch94 found a 95 percent incidence of splenic vein thrombosis in patients whose pancreatitis was complicated by splenomegaly in association with gastric and esophageal varices.

Partial splenectomy is now feasible due to increased understanding of the arterial and venous segmentation of the organ. The arteries and veins serve essentially as end vessels. Because of the immunologic importance of the spleen, awareness of this aspect of surgical anatomy has been an important development. Dawson et al.48 verified the segmentation of the spleen. They demonstrated that the spleen is divided most commonly into two or three lobes, each of which possesses one or two segments. The avascular planes between lobes pass perpendicularly to the long axis of the organ, although the intersegmental avascular planes are more variable. Dawson et al. emphasized that the venous segmentation is as predictable as the arterial segmentation. In more than half of their cases, the intersegmental planes of the spleen were indicated by notches in the margin of the organ.

In addition to the two or three hilar branches of the splenic artery, a separate superior polar branch (in about 30% of spleens) and an inferior polar branch (in about 45%) were observed by Garcia-Porrero and Lemes.50 They demonstrated the segmental nature of the vascular supply in most spleens, and observed anastomotic bridges between segmental branches and between these and polar branches in about 20% of cases.

Orozco et al.95 reported that splenectomy is not routinely necessary in devascularization procedures for bleeding esophageal or gastric varices.

Firstenberg et al.96 reported successful treatment of delayed splenic rupture by embolization of the splenic artery.

Lymphatic Drainage

The lymphatic vessels of the spleen arise from the splenic capsule and some of the larger splenic trabeculae. One of the peculiarities of this enigmatic organ is the lack of provision for lymphatics for the splenic pulp. In the classification of the various groups of lymph nodes and lymphatic vessels draining the spleen, as described by Rouviere,97 the splenic chain (Fig. 22-30) includes suprapancreatic nodes, infrapancreatic nodes, and afferent and efferent lymph vessels. Weiss et al.98 reported that pancreatic tumors divide the splenic nodes into two groups: the nodes of the splenic hilum and the nodes of the tail of the pancreas. The lymph nodes described above just happen to be located in the splenic neighborhood. Their primary function is that of draining the lymph of the stomach rather than that of the spleen.

Fig 22-30.

Lymphatic drainage of the spleen. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

The splenopancreatic lymph glands are located along the splenic artery. This is the largest group of splenic lymph nodes. However, a small number can be found in the area of the short gastric vessels. The local lymph nodes that receive lymph from the spleen also receive lymphatic drainage from the stomach and the pancreas.



The spleen comprises one quarter of the lymphoid mass of the body.

The sum of the body’s lymphoid tissue and the lymphocytes in the bone marrow correspond to 1 percent of the weight of the body. As a mass, it is approximately one-half the weight of the liver.99

The dilemma often facing the surgeon is whether the spleen ought to be removed when the splenic lymph nodes are involved in disease. We do not yet have a definitive answer. Boles et al.100 advised partial splenectomy for staging Hodgkin’s disease. Dearth et al.101 indicated that although “occult splenic involvement by Hodgkin’s disease cannot be confidently excluded by . . .partial splenectomy,” retaining a splenic remnant offers some protection against postoperative sepsis, which is often fatal in children. In the event that total splenectomy is performed, antibiotics and active immunization against pneumococci definitely lessen the risk of postsplenectomy sepsis.

Splenic Innervation

The nerve supply to the spleen arises from the more medial and anterior portions of the celiac plexus (Fig. 22-31). Visceral nerve fibers from this plexus accompany the splenic vessels into the hilum. Allen31 stated that fibers from the right vagus nerve or the posterior vagal trunk also pass to the spleen. However, this configuration has been questioned by others, based on the results of nerve degeneration studies after vagotomy performed on cats.102 Some myelinated fibers, few and probably sensory in function, can be identified histologically in a ratio of about 1:20 to unmyelinated autonomic fibers. These sensory fibers terminate in the spinal cord at the level of the sixth to eighth thoracic vertebrae. From these same levels, preganglionic sympathetic neurons arise in the intermediolateral cell column, passing within the greater thoracic splanchnic nerve to the celiac ganglion and to extensions of the ganglion along the splenic artery. In some mammals, the postganglionic sympathetic autonomic fibers terminate upon smooth muscle of the capsule, trabeculae, arteries, and veins.103 In humans, however, the autonomic fibers appear to travel together with the branches of the splenic arteries.89

Fig 22-31.

Splenic innervation. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

Histology and Physiology

The spleen is composed of 75-85 percent red pulp and approximately 20 percent white pulp. Some arterioles apparently open directly into sinusoids as a closed circulation; others open into meshwork as part of an open circulation. In open circulation, which processes 80-90 percent of splenic blood flow, the blood passes through splenic capillaries into the splenic red pulp. Splenic macrophages in the intercellular gaps of the red pulp phagocytize damaged red blood cells and particulate matter. In closed circulation, blood cells pass through the capillaries directly into venous sinusoids.

The spleen is relatively small in size, but it is the largest lymphatic organ in the body. According to Seufert and Mitrou,56 it comprises about 0.1% of the body’s weight and receives 300 mL/min of blood (approximately 6% of the cardiac output) per minute, which corresponds to approximately 3 mL/min per gram of splenic tissue. The spleen contains only 1% of the total red blood cell mass, which corresponds to 25 ml of red blood cells. As each red blood cell passes through the spleen, its destruction, if it is old or defective, is assured. Even the escape of a normal red blood cell is occasionally difficult.

We quote from Chadburn104:

[T]he spleen is able to maintain the integrity of the blood and respond to circulating antigens. However, this can be a double-edged sword in the case of patients suffering from autoimmune diseases such as immune thrombocytopenic purpura since the spleen can be the site of both antibody production and circulating cell destruction.

The spleen serves four functions: blood storage, hematopoiesis, filtration, and immunologic response. We have not found a more complete and elegant description of the filtration process than that of Wolf and Neiman105 (Table 22-6).

Table 22-6. Splenic Functions

A. Culling—erythrocyte (or other blood cell) destruction
  1. Physiologic (as red blood cells age)
  2. Pathologic
    a. Associated with blood cell abnormalities
    b. Associated with primary splenic changes
  B. Pitting (“facelifting” of erythrocytes)
    1. Removal of cytoplasmic inclusions*
    2. Remodeling of cell membranes
  C. Erythroclasis—destruction of abnormal red blood cells with liberation into circulation of erythrocyte fragments*
  D. Removal of other particulate material (e.g., bacteria, colloidal particles)*

*Editorial note: These functions were mentioned by Galen.

Source: Modified from: Wolf BC, Neiman RS. Disorders of the Spleen. Philadelphia: Saunders, 1989 (Table 2-1); with permission.

In addition to the four known functions, the spleen probably has other unknown roles. In contemplating this unfathomable organ, one of the authors of this chapter (JES) is reminded of Winston Churchill’s106 characterization of Russia: “…a riddle wrapped in a mystery inside an enigma.”

Surgery of the Spleen

Twelve Principles of Splenic Surgery

The surgical procedures of the spleen include total open splenectomy, partial splenectomy, laparoscopic splenectomy, splenic repair, splenic fixation, splenic detorsion and splenopexy, distal pancreatectomy with splenic preservation, treatment of splenic artery aneurysm, staging laparotomy, transplantation, incision and draining of parasitic or nonparasitic cysts, and removal of accessory spleens.

Surgery of the spleen is the surgery of its ligaments, vessels, and segments. Twelve principles of splenic surgery should be followed strictly, without deviation. We do not claim that the collection of rules presented here is complete, but we believe that if a surgeon follows these procedures, anatomic complications will be avoided and treatment will be successful.


1. Know surgical anatomy. A surgeon should know not only the unpredictable vascular supply of the spleen but also the various ligaments associated with the spleen and its neighboring organs, as well as their relations to the vessels that they envelop. The ligaments may or may not be avascular, but routine clamping and ligation of them are signs of good and sound surgical judgment.

Knowledge of the segmental anatomy of the spleen and its relation to the vascular system helps a surgeon perform a partial splenectomy.

It is important to know, for example, that the splenic lymph nodes are above and below the pancreatic tail. In metastatic disease, the lymph nodes should be removed, and splenectomy may be required as well.

2. Know clinical and surgical pathology. Cooperation with a hematologist and a pathologist is essential. The anatomy of the peripheral blood, normal or abnormal, and the surgical pathologic characteristics of the specimen or specimens help the surgeon, and later the oncologist and radiation therapist, treat the patient.

3. Know surgical procedures. No one procedure is adequate for all patients. The surgeon should be knowledgeable about all surgical techniques.

4. Perform a physical examination. A physical examination should include the detection of metabolic problems, tests for collagen deficiency disease, tests for allergic reactions and susceptibility to anesthesia, and a hematologic consultation.

5. Assess the diseased spleen. The key person here is the internist or the hematologist. The surgeon performs the procedure requested by the hematologist.

6. Know how to treat a ruptured spleen. The Luna and Dellinger107 flow-chart is helpful (Fig. 22-32).

7. Perform adequate preoperative preparations. Polk108 proposed a simple preoperative checklist (Table 22-7). We consider this to be one of the best of such lists available.

8. Adhere to operating room rules. One should not break dress code or fail to use sterile techniques. Good hemostasis should be obtained and kept. The surgeon should make a well-informed decision about a drain and select appropriate suture and wrapping material in case of ruptured spleen.

9. Place the patient in a convenient position.

10. Choose an incision. The type of incision is up to the surgeon, who must know the anatomy pertinent to opening and closing an incision.

11. Assess congenital anomalies and variations.

12. Provide optimal postoperative care.

Fig 22-32.

Flow chart for decisions in the management of splenic injuries. Asterisk (*) indicates transfusions required for abdominal injury. DPL, diagnostic peritoneal lavage; RBC, red blood cell count; CT, computed tomography; US, ultrasonography. (Modified by DV Feliciano from Luna GK, Dellinger EP. Nonoperative observation therapy for splenic injuries: a safe therapeutic option? Am J Surg 1987;153:463; with permission.)

Table 22-7. Sample Preoperative Checklist

Operative permit—appropriately signed and witnessed
Dietary considerations
  For abdominal operation, liquid diet and laxatives to ensure clean, collapsed bowel 
  Nothing by mouth at least 6 hr. before operation
Review of life-support systems
  Vital signs recorded often enough to establish normal
  Pulmonary system—chest films; other studies as indicated
  Cardiac function—electrocardiogram; other studies as indicated
  Renal function—urinalysis; blood urea nitrogen and possibly creatinine determinations
Adequate hydration up to time of operation—especially to compensate for laxatives and fasting 
Area of operation washed with appropriate germicidal detergent and shaved, clipped, or cleansed with depilatory agent
Blood transfusions prepared as anticipated
Order that patient should void on call to operating room
Preoperative medications—vagolytic and sedative drugs
Special medications—digitalis, insulin, and so forth

Source: Polk HC Jr. Principles of preoperative preparation of the surgical patient. In: Sabiston DC Jr (ed). Textbook of Surgery (15th ed). Philadelphia: WB Saunders, 1997, p. 116. Modified from Houston MC, Ratcliff DG, Hays JT, Gluck FW. Preoperative medical consultation and evaluation of surgical risk. South Med J 80:1385, 1987; with permission.

 Read an Editorial Comment


Total Open Splenectomy

Total open splenectomy (the removal of the spleen in toto) can be performed by an anterior approach or a posterior approach (Fig. 22-33). In the anterior approach, the surgeon first incises the gastrocolic ligament, allowing entry to the lesser sac, and then ligates the splenic artery. In the posterior approach, the surgeon ligates the splenic artery after incising the posterior layer of the splenorenal ligament and mobilizing the spleen to the right, thereby working within the greater peritoneal cavity. The aim of both approaches is the ligation of the splenic pedicle.

Fig 22-33.

The anterior and posterior approaches to total splenectomy. (Modified from Pemberton LB, Skandalakis LJ. Indications for and technique of total splenectomy. Probl Gen Surg 1990;7:85-102; with permission.)

A mass ligation of the splenic pedicle after incision of the posterior part of the splenorenal ligament includes the following structures: the presplenic fold, gastrosplenic ligament, splenic artery, and the incised portion of the splenorenal ligament.109

 Read an Editorial Comment

In an anterior approach to the splenic artery at the pedicle (Fig. 22-34), if there is a well-developed presplenic fold, six sheets of peritoneum, fat, lymph nodes, and pancreas fused into a single mass may be encountered.57 The lesser sac, as well as the space between the presplenic fold and the gastrosplenic ligament, may be obliterated. In the anterior approach, the surgeon incises three peritoneal layers (two layers of the gastrosplenic ligament and the one layer comprising the anterior leaflet of the splenorenal ligament) (Fig. 22-35A). Ligation of the splenic artery and short gastric vessels by the anterior approach is indicated in Figure 22-35B and ligation of the splenic vein and its branches is shown in Figure 22-35C. In the posterior approach (see Fig. 22-34), only one layer, the anterior layer of the splenorenal ligament, is incised (Fig. 22-36).

Fig 22-34.

Diagrammatic section through the splenic pedicle containing presplenic fold, gastrosplenic ligament, and splenorenal ligament. Vessels, fat, lymph nodes, accessory spleens, and the tail of the pancreas are all present. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983, p.182; with permission.)

Fig 22-35.

Splenectomy by the anterior approach. A, Anterior approach and access to the lesser sac. B, Ligation of the splenic artery and the short gastric arteries and vein. C, Ligation of the splenic vein. (Modified from Pemberton LB, Skandalakis LJ. Indications for and technique of total splenectomy. Probl Gen Surg 1990;7:85-102; with permission.)

Fig 22-36.

Splenectomy by the posterior approach. (Modified from Pemberton LB, Skandalakis LJ. Indications for and technique of total splenectomy. Probl Gen Surg 1990;7:85-102; with permission.)

Selection of an anterior or posterior approach is up to the surgeon, who should have a good understanding of the indications for splenectomy, the nature of the particular disease of the spleen, and thorough knowledge of splenic anatomy.

Partial Open Splenectomy

The following information about partial splenectomy comes from a personal communication to John E. Skandalakis from Steven R. Shackford, M.D., on November 21, 1997.

Partial splenectomy (as opposed to total splenectomy) requires a mature judgment and technical skill. Judgment must be exercised in knowing when to preserve the spleen and when to excise it. Generally, this decision is based upon the age of the patient, the condition of the patient, and the condition of the spleen.

With regard to the age of the patient, every attempt should be made to preserve the spleen in the pediatric population, in whom exposure to encapsulated organisms may be quite limited. In the older population (greater than age 30) splenic preservation becomes less necessary and less important. In those cases, splenic preservation will be determined primarily by the condition of the spleen (grade of injury) and the condition of the patient (hemodynamic and metabolic stability).

Two points deserve emphasis. First, complete mobilization of the spleen is absolutely necessary. This means freeing the spleen of all retroperitoneal, diaphragmatic, and colonic attachments. In addition, all of the short gastrics should be divided. This will allow complete mobilization of the spleen and allow the surgeon to completely examine the spleen for all types of injury. Second, in the pediatric population the splenic capsule is relatively thick compared to the splenic capsule found in older patients. This is because, in children, the myoepithelial capsule is retained. As the spleen enlarges and matures, the myoepithelial elements “thin out.” As a result, the capsule in the pediatric patient is more “forgiving” and holds sutures much better than that of the older population.

Morgenstern110 stated:

Partial splenectomy is a feasible method of preserving immunologic function in the traumatized spleen. At least one-third and preferably one-half of viable spleen should be preserved in suitable patients. Essential steps in the technique include an adequate incision, temporary splenic artery occlusion, atraumatic mobilization of the spleen, selective ligation of segmental vasculature, and controlled intrasplenic dissection, with individual ligation or clipping of the intraparenchymal vessels. Variations on this technique include the use of an absorbable mesh for coaptation of multiple fragments and the use of an ultrasonic surgical aspirator for dissection of the intrasplenic vessels. Drains are not recommended unless there is concomitant pancreatic injury. The technique is also feasible for resection of splenic cysts and may be applicable to disorders such as Gaucher’s disease and schistosomiasis.

Morgenstern advised the following:110


Administration of polyvalent antipneumococcal vaccine before surgery, plus a broad-spectrum antibiotic administered in three doses — one prior to surgery and two after

For a segmental (partial) splenectomy, the best incision is left upper quadrant (LUQ). However, a midline incision is acceptable if there is a possibility of multiple intraabdominal injuries.

Temporary occlusion of the splenic artery

Preparation and isolation of segmental splenic arteries and veins and ligation of the vessels that supply the segment to be removed

A check of the color, size, and consistency of the segment to be preserved

Separation by noncircumferential incision of the viable segment from the splenic part to be removed. The surgeon should proceed with careful intrasplenic dissection and ligation of bleeding vessels, using miniclips or regular hemoclips.

If there are deep lacerations in the splenic remnant, an absorbable polyglycolic mesh should be used as a wrap

Replacement of the splenic segment in the LUQ

Observation of the segment for 5 to 10 minutes for color and bleeding

Usage of drains is required if pancreatic injury is suspected; in other cases drains are used at the discretion of the surgeon

Laparoscopic Splenectomy

Poulin and Thibault62 advised that the surgeon acquire thorough knowledge of the standard anatomy and possible variations of the following anatomic entities before performing laparoscopic splenectomy:


Length of the splenic artery

Number of arterial branches entering the medial splenic surface (see Fig. 22-8, Fig. 22-37)

Ligaments of the spleen (Fig. 22-5)

Relation of the pancreatic tail and the spleen (Fig 22-38).

Fig 22-37.

General scheme of splenic artery branches. Asterisk (*) indicates present in only 20 percent of cases. (From Poulin EC, Thibault C. The anatomic basis for laparoscopic splenectomy. Can J Surg 1993;36:484; with permission.)

Fig 22-38.

Relations of the tail of the pancreas to the spleen. (Modified from Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990; 7:1-17; with permission.)

Brunt et al.111 suggested that laparoscopic splenectomy should become the procedure of choice for the removal of a normal or near-normal sized spleen. They stated that the laparoscopic operation is not only safe, but also has advantages when compared to open procedures. Waldhausen and Tapper112 found that laparoscopic splenectomy can be performed safely in children, and advocated it because it permits faster return to normal activities. Decker et al.113 stated, based on a small study sample, that laparoscopic splenectomy may be as beneficial for patients with malignant processes as for those with benign hematologic conditions. According to Katkhouda et al.,114 “laparoscopic splenectomy is feasible for the surgeon, teachable for the resident, and beneficial to the patient.”

Park et al.115 stated that “[c]ompared with OS (open splenectomy), the lateral approach to LS (laparoscopic splenectomy) takes longer to perform but results in reduced blood loss, shorter postoperative stay, and fewer complications. Mean weighted cost of LS is lower than OS at the study institutions.”

We highly recommended that the interested student read the beautiful description of laparoscopic splenectomy by Phillips et al.116

Considerations in Splenectomy

In at least three diseases — sickle-cell anemia, cold antibody immune hemolytic anemia, and glucose-6-phosphate deficiency — splenectomy is of little or no benefit to the patient, and therefore rarely indicated.

Al-Salem117 reported that splenectomy in children with massive splenomegaly is a safe and effective procedure if the perioperative management is good.

Because performing a splenectomy or adding it to another abdominal operation has a high operative morbidity (15-50%) and mortality (6-27%), surgeons have tried to devise operative methods to minimize or prevent complications.118,119 The operative anatomy of splenectomy is summarized in Table 22-8.

Table 22-8. The Technical Steps in Performing a Splenectomy

For Trauma For Hematologic Disorders Staging Procedure
Incision Incision Incision
Mobilizing the spleen Arterial ligation Detailed exploratory laparotomy (lymph nodes)
Vascular ligation Mobilizing the spleen Wedge and needle biopsies of both lobes of liver
Dividing the hilum Dividing the hilum Total splenectomy
Hemostasis Hemostasis Retroperitoneal exploration
Drains Accessory spleen Biopsy of iliac crest marrow
Closure Drains Search for accessory spleens
  Closure Translocation of ovaries
    Application of metal clips

Source: Pemberton LB, Skandalakis LJ. Indications for the technique of total splenectomy. Probl Gen Surg 7(1):85-102, 1990; with permission.

The main goal of performing a splenectomy, regardless of the size of the spleen, is to remove the spleen rapidly and safely. This part of the operation should result in minimal blood loss, clean removal of the entire spleen, and minimal injury to the adjacent structures. In addition, the surgeon wants to try to avoid the most common complications of splenectomy: atelectasis, subphrenic abscess, and postoperative hemorrhage from the splenic bed.

After rupture of the spleen, the surgeon should evaluate the organ and decide if it is salvageable. Consideration should be given to partial splenectomy or splenorrhaphy (Fig. 22-39). One should also evaluate the possibility of applying topical items, hemostatic agents, or splenic mesh wrap (Fig. 22-40). Autotransplantation should also be contemplated to preserve the spleen and retain immunological function (Fig. 22-41).

Fig 22-39.

A, Splenic rupture with hematoma. B, Splenorrhaphy with omental fixation. C, Partial splenectomy with omental fixation. (Modified from Pemberton LB, Skandalakis LJ. Indications for and technique of total splenectomy. Probl Gen Surg 1990;7:85-102; with permission.)

Fig 22-40.

Splenic mesh wrap. Top left, Passage of injured spleen through hole in center of mesh. Top right, Wrapping spleen in mesh. Bottom, Sewing opposite edges of mesh to each other to create tamponade. (Modified from Lange DA, Zaret P, Merlotti GJ, Robin AP, Sheaff C, Barrett JA. The use of absorbable mesh in splenic trauma. J Trauma 1988;28:269-275; with permission.)

Fig 22-41.

Autotransplantation. (Modified from Pemberton LB, Skandalakis LJ. Indications for and technique of total splenectomy. Probl Gen Surg 1990; 7:85-102; with permission.)

 Read an Editorial Comment

Powell et al.120 stated that successful nonoperative treatment of blunt splenic trauma in children can be accomplished in more than 90% of patients, though it has not been as successful with adults. This is because in addition to different splenic anatomy, the mechanism of injury also differs in children.

Autotransplantation of splenic tissue within the peritoneal cavity can also follow injury. Multiple splenic fragments of small size produce splenosis. Splenosis can be an asymptomatic benign process, although it is occasionally symptomatic. Metwally and Ravo28 stated that it is generally agreed that patients who have undergone partial splenectomy survive bacterial challenge better than those receiving autotransplantation of much larger volumes of spleen.

Studies by Weber et al.121 showed that when in situ preservation of the spleen is not possible by other techniques, splenic autotransplantation into the greater omentum should be considered, especially in the pediatric patient.

There are three different types of splenectomy. The first type is the rapid, safe excision of a normal- or almost normal-sized spleen. This type of operation includes most splenectomies done for such diagnoses as external trauma and intraoperative trauma, and many hematologic diseases.

The second type of splenectomy is excision of a massively enlarged spleen. These spleens frequently extend down to the iliac crest and occasionally to the pelvic cavity. Their sheer weight and size make them difficult to move or lift without rupturing the capsule or the attachments. This type of splenectomy requires patience and some special technical maneuvers.

The third type of splenectomy is staging splenectomy for Hodgkin’s disease. The operation for staging has many different components and represents a special type of splenectomy. The components of the operation for the staging of Hodgkin’s disease are presented in the last part of this section.


The midline incision (Fig. 22-42) is the incision of choice for most indications, such as trauma, hypersplenism with coagulation problems, staging laparotomy for Hodgkin’s disease, and massive splenomegaly. The midline incision has several important advantages in splenectomy. First, with a large enough incision and adequate exposure of the left upper quadrant, the surgeon can safely remove the spleen, no matter what size it is. Second, the incision is quick and easy to make, and results in little loss of blood. Third, this incision allows the surgeon to explore the entire abdomen and to deal with any other associated problems, such as gallstones, lacerated liver, and splenosis, and to perform multiple biopsies, if necessary.

Fig 22-42.

Incision for total splenectomy. (Modified from Pemberton LB, Skandalakis LJ. Indications for and technique of total splenectomy. Probl Gen Surg 1990;7:85-102; with permission.)

The left subcostal incision, also, can give adequate exposure for a splenectomy. It is appropriate for a mass in a normal-sized spleen or even a spleen that is twice the normal size, or when no other abdominal procedures are contemplated.122 But because these indications occur infrequently, most splenectomies are performed through a midline incision.

No difference in postoperative complications has been observed between midline and subcostal incisions, so the surgeon should choose the incision that gives the best exposure for the operation planned123 and with which he or she is most familiar.

Occasionally, a thoracoabdominal incision may make removal of a massive spleen with many adhesions safe and easy.124 The risks of increased morbidity and mortality from this incision must be compared with the benefits of improved exposure and control. The thoracoabdominal incision is an operation that can be considered for use in splenectomy in a few selected patients.


The use of drains is controversial. Advice ranges from always using drains to never using drains.118,125 Drains are used in patients having splenectomy to prevent a left subphrenic collection and an abscess formation. The risk of a subphrenic infection developing is greatly increased when the gastrointestinal tract is opened, the indication for splenectomy is hypersplenism, or the patient has a pancreatic injury or a malignant disease. When one of these conditions is present, the patient may be a candidate for a drain. Carmichael et al.126 supported selective splenic bed drainage.

Although some are better than others, most drains accomplish their purpose of removing an accumulation of blood, lymph, or pancreatic fluid from the subphrenic space. The main problem with placing drains in the splenic bed is the possibility of an ascending infection inoculating the splenic bed and producing an abscess. Thus, the drain could cause, rather than prevent, a subphrenic abscess.

The three main types of drains available are the Penrose, the open sump suction, and the closed suction drains. The advantage of the Penrose is that it provides very good drainage. Its disadvantage is that there is no way to apply suction to the drain, so bacteria and fluid can ascend as well as descend. The advantage of open and closed suction drains is decreased risk of infection, but their disadvantage is that the lumina of the drainage tubes can become occluded with coagulated blood and other matter, thus limiting drainage.

Ellison and Fabri127 reported a 4.2% incidence of subphrenic abscesses in 1,944 splenectomies. They reviewed five studies of the use of drains (Penrose or open suction) after splenectomy and found an incidence of 6.5% to 48% of subphrenic infections in patients with drains compared with 0.4% to 12% in patients without drains. These authors concluded that drains should be avoided when possible; if drainage is needed, a closed-suction system should be used and removed as soon as feasible.

Two studies investigated the efficacy of using closed-suction drains to prevent subphrenic collection and infection. In a prospective, randomized, controlled study, Pachter et al.128 compared 23 patients with no drains and 30 patients with Jackson-Pratt closed-suction drains. All drains were removed within 48 hours, except for those in two patients with persistent drainage who had 48 more hours (4 days total) of the drainage. Neither drained nor undrained patients developed subphrenic infection.

The duration of the use of drains is an important part of their safe implementation after splenectomy. Ugochukwu and Irving125 reported the use of closed-suction drains in 282 consecutive splenectomies in which the drains were removed in 3 to 5 days. The incidence of subphrenic infection in this large group of patients with drains was 0.71%.

Scanlon129 wrote that intraabdominal dead space following splenectomy “usually is filled by the small intestine, and, to a certain extent, by the colon and the stomach.” He indicated that when residual air persists it is replaced by serum, which can become infected. He suggested that the presence of fluid in the dead space posed a greater risk of infection than did a drain.

 Read an Editorial Comment

Olsen and Beaudoin130 reported that prophylactic drainage increases the incidence of subphrenic abscess. Jordan131 did not recommend routine drainage. Maingot132 believed that drainage is unnecessary. McNair133 avoided the use of drains. Fabri et al.134 did a retrospective study of splenectomy, citing authors who drained the splenic bed along with others who believed that drainage has become a matter of election; Fabri and colleagues used no drainage. Chassin135 advises drainage if there is injury to the pancreas or if there is incomplete hemostasis.

Surgery for Splenic Artery Aneurysms

The most common visceral artery aneurysms are those of the splenic artery;136 they may be multiple.137,138 They occur most frequently in the distal splenic artery.139 Multiparous women constitute a well-recognized risk group; the mechanism of this association is uncertain.140 Portal hypertension is reportedly also associated with an increased risk of aneurysm formation140-142 (probably secondary to increased splenic flow).143 Since most splenic aneurysms are asymptomatic, they are often identified only at the discovery of a calcified lesion in the left upper quadrant.141 Majeski144 advised that if calcifications are present in the left upper quadrant, diagnostic imaging procedures will help differentiate the diagnosis of splenic artery aneurysm from a calcified tortuous splenic artery.

Sometimes splenic aneurysms present with left upper quadrant pain; a small percentage proceed to rupture. Of those that rupture, 25 percent exhibit a double-rupture phenomenon: bleeding occurs first in the lesser sac (where it is temporarily contained) before free rupture into the peritoneal cavity.139,142,145 According to Lumsden et al.,136 patients with symptomatic or expanding aneurysms should undergo resection.

Pregnant women are at particular risk of aneurysm rupture.146 They should have resection, ideally in midtrimester. Those planning pregnancy should have aneurysm repair before their pregnancy. Patients with small aneurysms (<2.5 cm) may be observed carefully.147 Should intervention be necessary, there are a variety of options. Surgically, the best option is aneurysm resection. However, if it is fixed to the pancreas, ligation alone may suffice. For distal aneurysms, splenectomy or distal pancreatectomy and splenectomy may be necessary. Splenic artery embolization is feasible, particularly if surgery is contraindicated.

De Perrot et al.148 reported that of 8 patients presenting with rupture of splenic artery aneurysm between 1977 and 1996, 7 survived. They stated that an aneurysm of the splenic artery may rupture at any age, and aggressive surgery is the procedure of choice.

The true incidence of splenic artery aneurysms is difficult to ascertain; estimates range from 0.098% to 10.4% of the population.147,149,150 However, splenic artery aneurysms are more common than generally suspected. Autopsy studies have demonstrated that 10% of elderly patients have a splenic artery aneurysm.149,150 Other researchers, using postmortem injection of the splenic artery, observed a 7.5% incidence of aneurysm formation.151 Retrospective reviews of patients who had celiac angiography demonstrated an incidence of 5 to 13%.143,151 Splenic artery aneurysms were found to occur in 9% of patients with portal hypertension having splenic arteriography.152 However, in an unselected series of 28,500 autopsies, a 0.16% incidence of splenic artery aneurysms was observed;141 this latter figure probably most accurately reflects the incidence in the general population.

The type of procedure to be performed in treating a splenic arterial aneurysm is largely dictated by the site of the aneurysm (Fig. 22-43). Those situated away from the celiac axis, not embedded in the pancreas, and not at the splenic hilum, should be excised, and the splenic artery ligated doubly (proximal and distal ligation). For aneurysms deeply embedded within the pancreas, the feeding vessels should be ligated and the devascularized aneurysmal sac left in situ. Aneurysms occurring in the splenic hilum require a concomitant splenectomy. Occasionally, when an aneurysm is partially embedded in the distal pancreas, a distal pancreatectomy and splenectomy may be warranted.

Fig 22-43.

Type of procedure performed is dictated largely by the site of the aneurysm. Top left, When feasible, the aneurysm should be excised and the splenic artery ligated. Bottom left, If the aneurysmal sac is embedded within the pancreas, then proximal and distal ligation of the artery should be performed. Right. Distal aneurysms may be treated by excision with either the spleen or a concomitant distal pancreatectomy. (Modified from Lumsden AB, Riley JD, Skandalakis JE. Splenic artery aneurysms. Probl Gen Surg 1990;7:113-121; with permission.)

With an increased awareness of postsplenectomy sepsis, some authors strongly advocate splenic conservation, with proximal and distal ligation of the splenic artery, when technically feasible.153 Although this approach is appealing, there is good evidence that interruption of the splenic artery with preservation of the spleen may still compromise splenic function. Consequently, the risk of postsplenectomy sepsis may persist.154 Excision of an aneurysm with reanastomosis of the splenic artery has also been reported in a patient in whom the aneurysm developed after a distal splenorenal shunt.155

Embolization (Fig. 22-44) has been proposed for patients at high risk. This technique is in fairly widespread use for the treatment of bleeding pseudoaneurysms.156,157

Fig 22-44.

Selected aneurysms may be successfully embolized with Gianturco coils. (From Lumsden AB, Riley JD, Skandalakis JE. Splenic artery aneurysms. Probl Gen Surg 1990;7:113-121; with permission.)

Indications for Splenic Surgery

One of a surgeon’s primary responsibilities is to know the reasons for operating, meaning that the surgeon must understand the benefits a patient will derive from a splenectomy. The four main indications or reasons for performing a splenectomy are hemorrhage, hypersplenism, Hodgkin’s disease staging, and hodgepodge (this word was chosen for lack of a better word beginning with “h” to complete the mnemonic device). When a surgeon decides to operate, these items are the determining factors in making that decision. Thus surgeons do not operate on diseases of the spleen but on special circumstances during those diseases that appear to be best treated by an operation.124,158,159


The primary disorder that causes splenic hemorrhage is trauma. Trauma can be classified into two main categories: external and internal (Table 22-9).

Table 22-9. The Traumatic Indications for Splenectomy in Hemorrhage

External trauma
Internal trauma

Source: Pemberton LB, Skandalakis LJ. Indications for and technique of total splenectomy. Probl Gen Surg 7(1):85-102, 1990; with permission.

External trauma is the most common disorder of the spleen, and is divided into either blunt or penetrating injuries. The spleen is more commonly injured by blunt trauma than any other abdominal organ.160 Usually, the blunt trauma causes a left upper quadrant injury with rib fractures or contusions of the left flank or lower left chest. A chest roentgenogram may show these injuries as an elevated diaphragm, rib fractures, or pleural effusion.161 The well-protected posterior position of the spleen causes blunt trauma with high energy to split or fragment the solid spleen.

One useful diagnostic test for hemorrhage is peritoneal lavage, which reveals intraabdominal blood. Other tests involve detection of the injured spleen itself. They include computed tomography (CT), ultrasonography, or arteriography. Andrews162 found ultrasound useful for noninvasive examination of the spleen and identification of splenic injury, hemangioma, accessory spleens, splenomegaly, focal solid or cystic masses, calcifications, thickening of the cystic wall, and splenic infarction. Penetrating trauma injures the spleen much less frequently because of the small size of the organ and its protected location.

Nonoperative management of blunt splenic injury has emerged as the most common method of splenic conservation. According to Krause et al.,163 hemodynamically stable patients age 55 years and older who do not require significant blood transfusion and have no other associated abdominal injuries meet the criteria for nonoperative management. Velmahos et al.164 found that patients who required a transfusion of more than one unit of blood or sustained a severe blunt injury were likely to need surgery after a period of nonoperative management, and recommended that they be closely monitored.

Using a large database from 27 trauma centers, Peitzman et al.165 reported that “38.5% of adults with blunt splenic injury went directly to laparotomy. Ultimately, 54.8% of patients were successfully managed nonoperatively; the failure rate of planned observation was 10.8%, with 60.9% of failures occurring in the first 24 hours. Successful nonoperative management was associated with higher blood pressure and hematocrit, and less severe injury based on the Injury Severity Score, Glasgow Coma Scale, grade of splenic injury, and quantity of hemoperitoneum.”

Nonoperative management is also the treatment of choice for traumatic injury of the spleen in newborns, a rare condition.166

Splenic injury can occur from a knife or gunshot wound of the left upper quadrant, the left flank, or the left lower chest. Any penetrating injury below the level of the nipple anteriorly, or the tip of the scapula posteriorly, can injure the spleen. Penetrating splenic trauma usually injures one or more adjacent organs, such as the stomach, colon, kidney, diaphragm, or pancreas.167 Because almost all of these penetrating injuries are explored, the surgeon is the one responsible for identifying other associated injuries and treating them in the operating room.

Internal trauma accounts for 10% to 30% of splenic injuries and splenectomies. It is caused most often by intraoperative splenic injury, or, infrequently, by spontaneous rupture of an enlarged spleen.127,168 Although intraoperative splenic injury complicates 2% of abdominal operations, it occurs mostly during operations on abdominal organs of the left upper quadrant.127

The most common form of left upper quadrant intraoperative splenic injury comes from traction on the greater omentum and avulsion of its attachment to the inferior pole of the spleen. One can avoid this intraoperative complication either by ligating and dividing this attachment, or by retracting only the omentum and the stomach or the left transverse colon toward the patient’s left foot.

The other form of internal trauma is spontaneous rupture of the spleen, which is quite unlikely with a normal spleen. Patients with spontaneous rupture have abnormal spleens and no history of trauma. The two most common causes are malaria and infectious mononucleosis.124 Some other diagnoses that have accompanied spontaneous splenic rupture are sarcoidosis, leukemia, and congestive splenomegaly. Celebrezze et al.169 reported spontaneous splenic rupture secondary to splenic peliosis (blood-filled cystic structures).

Splenosis develops frequently following traumatic splenic rupture, and should be considered in the differential diagnosis of previously splenectomized patients who present with occult gastrointestinal bleeding or unexplained masses.170

De Vuysere et al.171 reported a case of intrahepatic splenosis:

[T]he diagnosis of intrahepatic splenosis occurring after previous splenic trauma and splenectomy was suggested by a constellation of MRI findings. The diagnosis was confirmed by histologic examination. Knowledge of these MRI characteristics may avoid the use of surgical interventions to arrive at the correct diagnosis of these rare liver lesions.

The nontraumatic indications for splenectomy are shown in Table 22-10.

Table 22-10. The Nontraumatic Indications for Splenectomy

  Congenital anemias
  Hemolytic anemias
  Leukemia or lymphoma
  Other nonspecific diseases
Hodgkin staging
  Diagnostic laparotomy
Hodgepodge (1-2% of operations)

Source: Pemberton LB, Skandalakis LJ. Indications for and technique of total splenectomy. Probl Gen Surg 7(1):85-102, 1990; with permission.


One of the main functions of the spleen is to remove the damaged blood elements, and diseases of the spleen can cause an acceleration in this removal.124 If rapid destruction and removal involves one of the three elements — red blood cells, white blood cells, or platelets — the result is anemia, leukopenia, or thrombocytopenia, respectively. If this accelerated destruction involves all three blood elements, the process results in pancytopenia.

Hypersplenism is, in effect, an exaggeration of the normal splenic physiologic state. The syndrome is characterized by splenic enlargement, a decrease in circulating levels of one or more of the blood lines, and a compensatory increase in bone marrow activity in response to the deficiency in the circulating blood elements. As a result of these defects there is increased cell turnover of the affected cell lines. In order for the diagnosis of hypersplenism to be considered correct there must be some degree of improvement following splenectomy.

Hypersplenism is classified as either primary or secondary. Primary hypersplenism is a diagnosis of exclusion, where identification of exaggerated splenic function is made without an apparent etiology. It is important to note that true primary hypersplenism is an exceedingly rare entity usually found in women. Diagnosis can be made only after an extensive search for other causes. Secondary hypersplenism refers to cases in which the disorder is found in association with a specific disease process. Diseases commonly associated with secondary hypersplenism are listed in Table 22-11.

Table 22-11. Diseases Associated with Secondary Hypersplenism

Congestive splenomegaly
  Splenic vein thrombosis
  Portal hypertension
  Metastatic carcinoma
Chronic inflammatory
  Systemic lupus erythematosus
  Felty’s syndrome
  Gaucher’s disease
  Niemann-Pick disease
Chronic hemolytic diseases
Myeloproliferative disorders
  Myelofibrosis with myeloid metaplasia

Source: Modified from Way LW. Current Surgical Diagnosis and Treatment, 11th ed. Norwalk, Conn: Appleton & Lange, 1994; with permission.

Splenomegaly is sometimes confused with hypersplenism. Splenomegaly simply refers to the enlargement of the spleen from any cause. Hypersplenism refers to an excessive removal of the blood elements resulting in some form of cytopenia. Furthermore, these two splenic disorders usually occur separately. Most patients with hypersplenism do not have splenomegaly (more than 90%). Fewer than 10% of patients with splenomegaly have hypersplenism.124

Some patients with massive splenomegaly have hypersplenism as part of the indication for splenectomy.172 Almost all patients with splenomegaly who require surgery have either hypersplenism, splenic infarction, or splenic rupture as the precipitating indication for a splenectomy. Splenomegaly by itself seldom appears to be an appropriate indication for splenectomy.

Cytopenia (hyperfunction of the spleen’s removal of any of the blood elements) is an indication for splenectomy. The four main categories of diseases that cause these cytopenias are the congenital anemias, the hemolytic anemias, white blood cell malignancies, and miscellaneous disorders.

Spherocytosis and elliptocytosis are congenital diseases that produce round and ovoid red blood cells, respectively. The shape of these cells makes it difficult for them to pass through the splenic filter. Because the red blood cells pass through the spleen about 1,000 times per day, the splenic cords and sinuses have many opportunities to trap and destroy the cells with these abnormal shapes.124 Splenectomy removes the splenic filter that destroys the cells, and improves the red blood cell survival rate.

Idiopathic thrombocytopenic purpura (ITP) is thought to involve an immune mechanism that causes premature platelet destruction and low platelet counts.124 Its signs are bleeding into the skin, such as purpura or ecchymosis, and bleeding into the gastrointestinal, urinary, or genital tract. ITP occurs mostly in women, and may follow an upper respiratory infection. Initial treatment is with steroids. If steroids fail or the disease recurs, a splenectomy is indicated and produces a favorable response 85% to 95% of the time.124 Removal of accessory spleens must also be done. ITP accounts for about 20% of the hematologic diseases treated by splenectomy.119,173

Schwartz174 evaluated the role of splenectomy in hematologic disorders. He stated that for hereditary spherocytosis, splenectomy is curative; for ITP, splenectomy is therapeutic. Winde et al.175 emphasized that splenectomy is the treatment of choice for idiopathic thrombocytopenic purpura. In contrast, Bussel176 reviewed splenectomy-sparing treatment for chronic ITP, and suggested a measured tolerance for lower platelet counts before recommending intervention. Bell177 added further cautions:

[S]plenectomy as a treatment for ITP has a fairly favorable initial response rate of 60% to 80%. Few studies that have followed such patients for extended periods, however, show a durable response, and there is no question that the longer the follow-up period for ITP patients who have undergone splenectomy, the lower the success rate.

White blood cell malignancies, namely lymphoma and leukemia, can produce hypersplenism in the course of these chronic diseases. Patients with lymphocytic lymphoma and chronic lymphocytic leukemia have splenic infiltration that causes splenomegaly, slow transit time of blood elements, and pancytopenia.124 Positive chromium-labeled red blood cell studies confirm splenic sequestration. A splenectomy can ameliorate the pancytopenia in these patients.

Cusack et al.178 reported that if splenectomy in chronic lymphocytic leukemia is performed early in patients with Hb 10 g/dL or plt 50 x 109/L, the survival rate of these patients is significantly improved.

Hodgkin’s Disease Staging

Since 1971, laparotomy has been recommended for more accurate staging of Hodgkin’s lymphoma. This has allowed treatment to be optimized for early- as well as late-stage disease. Taylor et al.179 reported on 825 patients with Hodgkin’s disease who had a staging laparotomy. They found that 356 (43%) patients had a change in their clinical staging as a result of this operation: an increase in 296 patients (36%) and a decrease in 60 patients (7%). Even though the study was retrospective, they concluded that the improvements in survival and the freedom from progression that resulted from the accurate staging and more precise therapy justified the continued use of staging laparotomy. Furthermore, they concluded that splenectomy must remain an essential part of staging laparotomy because the spleen was the only tissue that contained Hodgkin’s disease in 50%, or 160, of the 321 patients who had positive findings.179

With the development of better imaging technology, reliance on the staging laparotomy has diminished. Although staging laparotomy is performed much less commonly, in select patients, such as those who are not candidates for chemotherapy, this procedure may still be quite useful. Baccarani et al.180 stated that laparoscopic staging of Hodgkin’s disease is, from an oncologic standpoint, equivalent and functionally superior to open staging laparotomy.

Recently, both Klasa et al.181 and Santoro et al.182 have reported complete remission in 95-98% of patients with stage I-II disease. Given the risks associated with splenectomy and the fact that it will be difficult to improve on these data, many are advocating that the treatment of Hodgkin’s disease be based on clinical staging, i.e., physical exam, CT and magnetic resonance imaging, and bone marrow aspiration.

If a staging laparotomy is to be performed, understanding the stages of Hodgkin’s disease is helpful in this exploratory surgery to define the anatomic sites of involvement. The four stages of Hodgkin’s disease and clinical modifiers are listed in Table 22-12.183 A staging laparotomy should be preceded by the following: history, physical examination, complete blood count, urinalysis, blood chemistries, bone marrow aspiration, chest roentgenogram, CT or magnetic resonance imaging of the abdomen, and sometimes lymphangiography.

Table 22-12. Ann Arbor Staging System for Hodgkin’s Disease

Stage I Single lymph node region or extralymphoid site
Stage II Two or more lymph node areas or one extralymphoid site with one lymph node area; but all are on one side of the diaphragm
Stage III Multiple lymph node sites on both sides of the diaphragm. With localized extralymphoid sites, this is IIIE; with splenic involvement, IIIS; and with both, IIIES.
Stage IV Diffuse involvement of extralymphoid organs, with or without adenopathy
Clinical Modifiers 
A No systemic symptoms
B Temperature above 38°C, night sweats, or weight loss

Source: Meyer AA. Spleen. In: Greenfield LJ, Mulholland M, Oldham KT, Zelenock GB, Lillemoe KD (eds). Surgery: Scientific Principles and Practices, 2nd ed. Philadelphia: Lippincott-Raven, 1997, p. 1274; with permission).

Staging procedures for Hodgkin’s disease and limited non-Hodgkin’s lymphoma include the following (Fig. 22-45):

Fig 22-45.

The tissues to be removed or to undergo biopsy in a staging laparotomy for Hodgkin’s disease. Splenectomy, liver biopsy, and lymph node sampling in the specific sites are shown. Bone marrow biopsy can be done if necessary. (Modified from Meyer AA. Spleen. In: Greenfield LJ, Mulholland M, Oldham KT, Zelenock GB, Lillemoe KD (eds.) Surgery: Scientific Principles and Practices, 2nd ed. Philadelphia: Lippincott-Raven, 1997, p. 1275; with permission.)


Detailed exploratory laparotomy

Examination of nodes, and wedge and needle biopsies of both lobes of the liver

Total splenectomy with splenic lymph node biopsy

Retroperitoneal exploration of the celiac axis, hepatoduodenopancreatic lymph nodes, periaortic lymph nodes, inferior vena caval lymph nodes, iliac lymph nodes, and mesenteric lymph nodes of the small and large intestines for lymph node biopsies

Biopsy of iliac crest marrow

Search for accessory spleens

Oophoropexy (ovarian translocation) in young women

Placement of metal clips at the splenic pedicle, the areas where biopsies have been done on lymph nodes, the areas of lymph nodes on which biopsies have not been performed, and at the site of ovarian translocation

Because a staging laparotomy is done for diagnosis, the correct handling of these fresh specimens usually requires the presence of a pathologist in the operating room.184 Touch preparations of the lymph nodes and spleen should be made. Tissues should be placed in a special fixative solution for electron microscope examination. Slides of bone marrow specimens should be made. The pathologist can then choose any other tissue preparation for future examination. The proper handling of these tissues completes the staging laparotomy for Hodgkin’s disease.


This last category includes a miscellaneous group of disorders. Splenic abscesses, cysts, and tumors produce a mass within the spleen. Their removal and definitive treatment usually requires a splenectomy.

Splenic Abscesses

Isolated splenic abscess is a rare condition, with fewer than 400 cases being reported from the beginning of the century until 1986.185-187 However, over the last 15 years this uncommon clinical entity has been increasingly identified as the cause of intraabdominal sepsis in a wide variety of clinical situations, particularly in immunosuppressed patients. In a study of 287 cases reported in the literature between 1987 and 1995, Ooi and Leong187 found that immunosuppressed states were present in 33.5% of the cases. Acquired immune deficiency syndrome and intravenous drug use accounted for half of the immunosuppressed cases. The authors reported Staphylococcus, Salmonella, and Escherichia coli to be the organisms most commonly identified by culture.

Early diagnosis is the key to effective treatment of splenic abscesses. Ultrasonography and computerized tomography are diagnostic. Splenectomy is the treatment of choice. Percutaneous drainage, however, is a possible alternative in selected or debilitated patients.188,189 Ooi and Leong187 report that US- or CT-guided percutaneous aspiration and catheter drainage have demonstrated sufficient success rates (75%)190,191 to be considered first-line therapy in certain situations such as uncomplicated solitary lesions, critically ill patients, and pediatric patients in whom splenic conservation is important.

Phillips et al.192 advised that the diagnosis of splenic abscess should be considered in patients using intravenous drugs who are suffering fever and abdominal pain.

Splenic Cysts

Cysts of the spleen are rare, but more common than primary tumors. Worldwide, the most common splenic cysts are parasitic, the majority of which are echinococcal. Even in countries where echinococcus is endemic, however, hydatid disease of the spleen is a rare clinical entity.193 The spleen ranks third, behind the liver and the lung, as the most commonly involved organ in hydatid disease.193-196

In North America, nonparasitic cysts are found much more frequently than parasitic cysts. Sirinek and Evans184 reported that nonparasitic splenic cysts usually occur in persons between the ages of 10 and 40 years. These cysts include the following (in decreasing order of frequency): pseudocysts, hemangiomas, epidermoid cysts, and dermoid cysts. Because most splenic cysts are unilocular (80%), CT scan is the preferred method of detecting these rare lesions. With the exception of small nonparasitic cysts, for which observation may be sufficient, splenectomy is usually the treatment of choice for all types of splenic cysts, parasitic or nonparasitic.

Atraumatic rupture of the spleen due to ceroid histiocytosis was reported by Wilson et al.197

Splenic Tumors

Primary tumors of the spleen are very rare entities.122 The treatment of choice for splenic tumors is splenectomy.

The most common splenic tumors are not from lymphoid tissue but are vascular neoplasms: hemangioma, hemangioendothelioma, lymphangioma, and hamartoma. The other primary tumors are various malignant tumors (Table 22-13). Although the majority of primary splenic tumors are vascular in origin, primary splenic lymphoma and primary tumors of other origin have been reported. Salgado et al.198 reported cases of B-type large-cell primary splenic lymphoma with massive involvement of the red pulp. Rosso et al.199 reported three cases of splenic marginal zone cell lymphoma arising from the white pulp of the spleen, but without splenomegaly or bone marrow and lymph node involvement. Usually this disease produces massive splenomegaly with bone marrow and lymph node involvement. Westra et al.200 reported a malignant mixed (epithelial and stromal elements) primary tumor of the spleen, perhaps of extrauterine mullerian origin. Brune et al.201 reported splenic lymphoma with villous lymphocytes. This is a distinct entity, separate from other B-cell lymphoproliferative disorders.

Table 22-13. Malignant Splenic Lesions

I. Lymphoproliferative disorders
  Non-Hodgkin’s lymphoma
  Hodgkin’s disease
  Chronic lymphocytic leukemia
  Hairy cell leukemia
  Acute lymphoblastic leukemia
  Waldenström’s macroglobulinemia
II. Myeloproliferative disorders
  Chronic myelogenous leukemia
  Myelofibrosis (agnogenic myeloid metaplasia)
  Polycythemia vera
  Essential thrombocythemia
III. Vascular tumors
IV. Metastatic tumors
  Breast, lung, melanoma, cervix, etc.
V. Others
  Malignant fibrous histiocytoma
  Malignant teratoma
  Kaposi’s sarcoma

Source: Giles FJ, Lim SW. Malignant splenic lesions. In: Hiatt JR, Phillips EH, Morgenstern L (eds). Surgical Diseases of the Spleen. Berlin: Springer, 1997; with permission.

Clinically, metastasis to the spleen is a rare phenomenon even though it is found fairly frequently by careful examination at autopsy.202 If, indeed, metastasis occurs, it is probably hematogenous or resulting from invasion of the spleen by neighboring organs such as the stomach, pancreas, colon, left kidney, or by malignant tumors of the retroperitoneal space. We have seen only one instance of metastatic carcinoma to the spleen in patients hospitalized with carcinoma. The subject of metastasis to the spleen will be addressed in depth later in this chapter.

Specific Notes on Surgical Anatomy


The splenorenal ligament has small veins that can cause problems.

The perisplenic adhesions are vascular.

The terminal splenic vessels are fragile and easily torn or perforated.

The splenic capsule, also, is friable.

Dissection of the splenic artery close to the celiac artery, through the gastrocolic omentum, can be done if the spleen is large or has moderate splenomegaly and adhesions. However, one must not forget the superfragile splenic vein; it can coil around the artery and produce a sudden large loss of blood.

With huge spleens (such as those secondary to malaria or kala azar) with heavy and vascular multiple adhesions, the artery can be ligated along the upper pancreatic border after the gastrocolic ligament is opened.

A healthy ruptured spleen can be delivered easily from the abdomen.

A large, diseased spleen requires careful dissection of the prehilar area and ligation of the vessels.

In thrombocytopenic purpura, the abdomen should be explored after the spleen is removed.

In ITP, the splenic artery should be ligated as soon as possible.

In the presence of hemolytic anemia, transfusions should not be given before the operation. Platelets should be transfused after splenic artery ligation.

Short gastric arteries and veins should be transfixed, and the greater curvature of the stomach should be inverted to avoid bleeding and gastric necrosis. In the period immediately after splenectomy, a roentgenographic gastrointestinal series should be taken, and the image of the deformity of the greater curvature should be saved for future comparison.

 Read an Editorial Comment


If the splenic artery requires ligation proximally, it should also be ligated distally, as close to the hilum as feasible.

The pancreatic tail should be handled gently, particularly where it is usually vulnerable: at the hilum, posterior to the pedicle.

The renocolosplenic area should be handled gently to avoid renal or colonic injury or bleeding from the spleen.

If the splenic pedicle is ligated en masse, the hilar vessels should be religated. The pedicle should be ligated twice.

An autologous splenic capsule should be used over the raw splenic surface; the graft should be secured with fine sutures.203

The pancreas should be separated from the spleen by division of the splenic artery and the splenic vein distal to the tip of the pancreas. The spleen can survive on the short gastric vessels, which should be carefully preserved. Warshaw204 applied the technique successfully in 22 of 25 consecutive patients.

The technique selected for ligation of the splenic vessels for splenectomy depends on the length of the splenic pedicle, the close relation of the pedicle and the hilum of the spleen to the tail of the pancreas, the presence of splenic adhesions, and the size of the spleen.

Because the splenic pedicle is formed by the splenorenal ligament, gastrosplenic ligament, and presplenic fold, the length of the pedicle depends on the length of these anatomic entities, including the distal branches of the splenic artery (see Fig. 22-5). Also, the splenic pedicle may be narrow or wide, depending on the extent to which the primitive dorsal mesogastrium was absorbed into the body wall. The degree of effective mobilization of the spleen depends ultimately not on the splenorenal ligament, but on the length of the splenic vessels after incision of the ligament. Short splenic vessels may make it impossible to deliver the spleen out of the abdomen. Gently pushing the tail of the pancreas away from the hilum of the spleen may increase splenic mobility. Occasionally, the tail of the pancreas does not touch the spleen, but the tail and the spleen are bridged by the pancreatosplenic ligament. Careful division of this ligament in splenectomy avoids intraoperative bleeding or postoperative pancreatitis.

The hilum of the spleen and the tail of the pancreas touch one another in about one-third of individuals,63 and are within 1 cm of each other in about half of the population.52 In 50% of individuals, the closest approach of the pancreas is at the middle of the spleen.52 In 42%, the closest approach is near the inferior pole.52

The major artery limiting mobilization of the pancreas away from the spleen is the great pancreatic artery, which usually arises from the second or third segment of the splenic artery. In addition, if there are caudal pancreatic arteries arising from terminal branches of the splenic artery, they can be ruptured if the tail of the pancreas is too vigorously mobilized. Whitesell52 stated that the tail of the pancreas can be dissected back 3.5 to 5.0 cm. Phelan et al.205 suggested 2 to 3 cm as the limit to be expected.


When there is splenomegaly, heavy adhesions may be present between the spleen and the diaphragm (above and laterally), the stomach (medially), and the splenic flexure (below). In many cases, the spleen is fixed with the anterolateral peritoneum of the abdominal wall. These adhesions can contain large neoplastic vessels, which can produce tremendous bleeding if not ligated and secured before their division.

If a patient has a hemorrhagic disorder, a nasogastric tube should not be passed until the patient is in the operating room. Then the anesthesiologist should pass it under direct vision.

In elective splenectomy with a large spleen, intravenous preoperative antibiotics and occlusion of the splenic artery are advisable. The latter should be performed by a radiologist just before the incision is made. With such a procedure, the surgeon is committing to a total splenectomy.

 Read an Editorial Comment


If a blood transfusion becomes necessary for a successful splenorrhaphy, then splenectomy without transfusion is the safer treatment.206

Otsuji and colleagues207 reported that splenectomy during total gastrectomy for gastric cancer did not have an effect on the survival rate. The simultaneous splenectomy itself was correlated with postoperative complications.

Cocanour et al.208 reported that significant numbers of delayed (>48 hours) complications occur with nonoperative management of adult splenic injury. Without attempting to define the controversial management of blunt splenic injury, these authors advised very close followup of patients with splenic trauma.

Anatomic Complications of Splenic Surgery

The anatomic complications of splenic surgery are summarized in Table 22-14.

Table 22-14. Summary of Anatomic Complications of Some Splenic Procedures

Procedure Vascular Injury Organ Injury Inadequate Procedure
Total splenectomy Hemorrhage from polar arteries; retrograde from branch of splenic artery. Ischemia to greater curvature. Diaphragm, tail of pancreas, stomach, transverse colon, left kidney, etc. Preservation of accessory spleen in splenectomy for hemolytic disease
Partial splenectomy As above; hemorrhage from splenic remnant As above; rupture of splenic capsule Unlikely
Laparoscopic splenectomy As above As above As in total and partial
Splenic repair Bleeding As above but very rare Unlikely
Splenopexy Bleeding As above but very rare Ptosis after repair
Splenic detorsion and splenopexy Total or partial infarction As above but very rare Unlikely if viability of spleen is obvious
Distal pancreatectomy with splenic preservation Bleeding and splenic infarction Pancreas Unlikely
Splenic artery aneurysm Bleeding Pancreas Not ligating the feeding artery after proximal and distal ligation
Staging laparotomy Bleeding   By not performing multiple biopsies, oophoropexy, etc.
Transplantation Infarction and necrosis None Unlikely
Incision and drainage Bleeding None Contamination of the abdominal cavity

Total Splenectomy

Vascular Injury

Hemorrhage and Ischemia

Hemorrhage following splenectomy results from either surgical error or the presence of hemolytic disease that produces pathologic bleeding. Martin and Cooper209 found hemorrhage to have been mentioned in 2.8 percent of 777 splenectomies performed by 11 authors.

Vascularization of the several splenic ligaments increases with portal hypertension. Therefore, careful division and ligation between clamps is essential.

Surgical Considerations for Hemostasis

Based on the vascular anatomy described earlier, we can determine the origins of bleeding following ligation of the splenic artery and removal of the spleen. There are two major sources of such bleeding: (1) bleeding from polar arteries arising proximal to the ligation (a superior polar artery may arise from the third segment of the splenic artery), and (2) retrograde bleeding from splenic arteries distal to the ligation (short gastric, caudal pancreatic, and left gastroepiploic arteries may arise from terminal branches of the splenic artery beyond the point of ligation). Such vessels must be identified and ligated separately. Where possible, the ligation should be distal to the origin of the left gastroepiploic artery. The short gastric veins are another source of bleeding.

The splenic artery may be ligated without removing the spleen; the short gastric arteries are the collateral circulation of the spleen.76,210,211,212 If the splenic vein is injured, the spleen must be removed or the vein must be anastomosed to another vein.

Organ Injury


Martin and Cooper209 mentioned trauma to the diaphragm.

If diaphragmatic injury involves the entire thickness of the diaphragm, the defect should be repaired with through-and-through interrupted nonabsorble sutures.


The close proximity of the tail of the pancreas to the spleen may result in pancreatic injury during splenectomy. The insult may involve pancreatic ducts, pancreatic vessels, and severe injury to the tail of the pancreas. Injury of ducts and/or vessels should be treated by ligation. Resection of the pancreatic tail is necessary when it is severely injured. Closed drainage is recommended.

There were 14 injuries to the pancreas (2.2 percent) among 632 splenectomies in four series.213-216


Injury to the stomach or ischemia of the gastric remnant may accompany splenectomy and the sacrifice of the short gastric arteries.217 With gastric injury superficial to or through the total thickness of the gastric wall, gastrorrhaphy and inversion is the procedure of choice.

Harrison et al.218 reported 18 cases of gastrocutaneous fistula following splenectomy. They listed five conditions that predispose to the formation of gastric fistula after splenectomy:


Abrasions or denudation of the serosal covering of the greater curvature of the stomach, which often results from a technically difficult splenectomy

Interruption of a reflection of gastric muscle fibers into the gastrosplenic ligament at the attachment to the stomach wall52

Decreased vascularity, especially in elderly patients with arteriosclerosis of the gastric vessels

An organizing hematoma with inflammatory reaction in the gastrosplenic omentum adjacent to the gastric wall secondary to rupture of the spleen

Severe trauma with multiple injuries or any conditions predisposing to stress ulcerations


The distal transverse colon, the splenic flexure, and the proximal descending colon may be injured during splenic artery surgery. The segments related to the spleen via the splenocolic and phrenicocolic ligaments are the most vulnerable. There is occasional involvement of the pancreaticocolic ligament, dependent on the ligament’s width and the spleen’s size. Gentle treatment and ligation of these ligaments will avoid colon injury.

Colonic wall repair in two layers is the procedure of choice.

Kidney, Ureter, Adrenal, and Retroperitoneal Space

Occasionally, a megaspleen is heavily fixed to organs of the left retroperitoneal space, namely the left adrenal gland, the left kidney, and the left ureter. The ureteric part involved is again related to the size of the spleen. While these are very rare injuries, the wise surgeon will not forget their potential.

Bleeding must be controlled. If the ureter is injured, the surgeon should proceed with the anastomosis of his or her choice.

Splenectomy complicating nephrectomy was reported by Cooper et al.219 To our knowledge, nephrectomy complicating splenectomy has not been reported, but it is a possibility.

Other Organs

The authors have occasionally seen patients with severe adhesions of loops of small bowel as well as adhesions to the left ovary and tube from splenomegaly secondary to malaria and kala azar. In these cases, total splenectomy plus small bowel resection and left salpingo-oophorectomy were performed.

Partial Splenectomy

The anatomic complications of partial splenectomy are similar to those of total splenectomy. In addition, there is the possibility of bleeding from the preserved splenic remnant. Excessive traction on the presplenic fold containing the left gastroepiploic vessels may tear the splenic capsule. Infarction of the splenic remnant is possible. Partial splenectomy is preferable to total splenectomy when it is possible because it decreases the likelihood of postsplenectomy sepsis.

The authors witnessed a case of iatrogenic splenosis. This can occur with or without other complications such as intestinal obstruction or hematologic problems.

Laparoscopic Splenectomy

For all practical purposes, the anatomic complications of laparoscopic splenectomy are those of total and partial splenectomy. In view of its efficacy and reduction in morbidity and mortality, the laparoscopic approach to splenctomy is now regarded by many authors as being preferable to open splenectomy for hematologic disease.220,221 Glasgow and Mulvihill222 stated that laparoscopic splenectomy is evolving and may become the procedure of choice for the treatment of splenic disorders.

In a case-controlled study of patients undergoing elective splenectomies in immune thrombocytopenia purpura, hairy cell leukemia, and staging for Hodgkin’s disease, Diaz et al.221 reported that laparoscopic splenectomy resulted in shorter hospitalization (2.3 vs 8.8 days with open splenectomy) and fewer postoperative complications.

Targarona et al.223 stated that laparoscopic splenectomy is a promising procedure in the management of hematologic disorders, but it is absolutely essential to avoid parenchymal rupture and cell spillage as well as to avoid leaving accessory spleens, which can lead to the failure of surgical treatment.

Lozano-Salazar et al.224 reported that laparoscopic splenectomy in the treatment of immune thrombocytopenic purpura (ITP) is comparable to open splenectomy in terms of safety and efficacy, and is associated with a shorter hospital stay. Tanoue et al.,225 reported that for treatment of ITP, laparoscopic splenectomy is an alternative modality. Fass et al.226 concurred that it was a safe and effective treatment for elderly patients. Katkhouda and Mavor227 stated, “Laparoscopic splenectomy for selected hematologic disorders should replace open splenectomy as the technique of choice and prompt earlier consideration of surgery when it is indicated.”

A study by Rescorla et al.228 found that in comparison to open splenectomy in children with hematologic disorders, laparoscopic splenectomy resulted in longer operative times, less narcotic administration, shorter length of stay, and lower total hospital charge.

Based on a retrospective chart review, Terrosu et al.229 concluded that laparoscopic splenectomy by experienced laparoscopic surgeons is feasible, effective, safe, and offered several advantages over open surgery.

Splenic laceration may occur during laparoscopic surgery, with distortion and stretching of small vascular adhesions between the spleen and abdominal wall. Chang et al.230 reported a case of splenic laceration complicating salpingoplasty.

Metastasis and the Spleen

Various studies have shown that metastatic carcinoma of the spleen is a rare occurrence.231-233 In routine autopsy series, involvement has been found in 0.3 to 9% of patients with cancer.234,235 Berge202 studied 7,165 postmortem cases of primary carcinomatous tumors, of which 4,404 (61.5%) were found to have spread to one or more organs; only 312 cases (7.1%) metastasized to the spleen.

When splenic metastasis is found, it usually reflects late disseminated disease.235-237 Harmon and Dacorso237 found splenic metastases in 50% of postmortem patients with evidence of metastasis to organs in both the thoracic and abdominal cavities. Berge238 reported finding microscopic evidence of splenic metastasis in 70% of all subjects who had metastases in six or more organs.

Marymont and Gross236 reported that 30-67% of all splenic metastases arise from primary carcinoma of the breast and lungs. Breitbart and Harris239 reported metastatic breast carcinoma to the spleen. Reports of metastases from the skin (melanoma),202,240 ovary,202,235 and endometrium,241,242 and also in lymphoma,237,243 have been well documented in the literature. Murthy et al.244 reported a very unusual case of metastasis from esophageal carcinoma.

From postmortem examination on 312 patients with splenic involvement, Berge238 reported microscopic metastasis from adenocarcinoma of the colon and rectum in 4.4% and 1.6% of the cases, respectively. Interestingly, isolated splenic involvement (without visceral or nodal metastasis) with regard to colonic and rectal carcinoma is exceedingly rare. With the addition of one case report from our own experience,245 review of the English literature produced only seven proven cases of colorectal adenocarcinoma with metastatic disease limited to the spleen.233,243,245,246,247,248,249

An ileal carcinoid tumor with splenic metastasis was reported by Falk and Stutte.250 Sharpe et al.251 reported on a patient with hairy-cell leukemia found to have metastatic adenocarcinoma in the spleen.

One of the few tumors that will metastasize to the spleen is melanoma.252-254 Its most common diagnosis usually occurs as an incidental finding of a liver-spleen scan, an abdominal CT scan, or a laparotomy. Metastatic melanoma may be a rare cause of splenomegaly. Up to 88% of patients with splenic metastases have concomitant liver or pancreatic metastases.255

Hypotheses for Splenic Resistance to Metastasis

Splenic metastases from solid, nonreticular neoplasms are rare compared with the incidence of spread to the lymph nodes, liver, and lungs.256 Since the spleen represents one-fourth of the reticuloendothelial system, this apparent paradox warrants explanation. We agree with Hull et al.257 that the influence of a functional spleen on induction and growth of cancer remains unexplained. Nonetheless, anatomic, histologic, and functional explanations of this phenomenon have been proposed.258

Anatomic Basis for Splenic Resistance

In 1922, Sappington259 thought that the sharp angle that exists at the origin of the splenic artery from the celiac artery limits tumor metastasis. This sharp angle would theoretically impede larger tumor emboli from reaching the spleen.

Histologic Bases for Splenic Resistance

There are two histologic theories regarding the relationship between cancer and the spleen. The contraction theory advanced by Kettle,260 and later by Herbut and Gabriel,261 stated that the rhythmic contractions provided by the sinusoidal splenic architecture prevent implantation of malignant cells on vascular endothelial cells.

The second theory, presented by Warren and Davis,235 is that in addition to the limitations from the contractions, the scarcity of lymphatic vessels extending into the intrasplenic parenchyma also limits splenic metastases. They considered this scarcity to be of even greater significance than the contractions. This is an attractive argument because today we believe that the splenic parenchyma and capsule have a paucity of lymphatic vessels. The matter is still controversial. Sporadic metastases of epithelial and nonepithelial tumors to the spleen have been reported from time to time in the literature.

Functional Theory of Splenic Resistance

While anatomic and histologic theories offer intriguing possibilities, the spleen’s functional capacity with regard to its immunologic surveillance and antitumorigenic properties seems most likely to be responsible for the rarity of splenic metastases. Hull et al.257 attributed the ability of the spleen to protect rats from the induction of malignant colonic tumors induced by 1,2-dimethylhydrazine (DMH) to the preservation of immunologic surveillance in the host.

The possibility of production by the spleen of antineoplastic substances inhibiting tumor growth has been reported by Pollard262 and also by Woglam.263 Miller and Milton232 demonstrated experimentally that tumor cells implanted within mice grow at a significantly slower rate in the spleen than in the liver. Small and Trainin264 illustrated the antigenic response to splenic inoculation with tumor cells in mice. These specific tumor-inhibitory cells, identified as inhibitory T-cells, are thought to play a key role in the inhibition of splenic metastases.

The spleen’s inhibitory effect may simply prevent microscopic metastases from maturing into macroscopic metastases with clinical significance. In an autopsy series, Warren and Davis235 noted that only 42 of 1140 subjects studied without regard to tumor type had histologic evidence of splenic metastases; macroscopic tumor involvement was present in only 22 of those 42.

Numerous studies suggest that the spleen has an antitumorigenic effect on the host. Sato et al.265 found that growth of colonic tumors in mice was enhanced after splenectomy. Wanebo et al.266 recently reported their results from a study that reviewed and analyzed the effect of splenectomy on survival in patients having curative gastrectomy for stomach cancer. The authors found that the 5-year survival rate was 20.9% in patients having elective splenectomy versus 31% in patients who did not receive splenectomy (P <0.0001). Davis et al.267 suggested that splenectomy should be considered a probable factor in the decreased survival of patients operated on for regional colorectal cancer. Arwari, in a discussion of Davis’ findings,267 asked this question: “If colon cancer is metastatic to the splenic hilar nodes and invades the pancreatic capsule, should en bloc dissection including the pancreatic tail take place while leaving the spleen alone?” Davis’s answer was to “save the spleen, if possible.”267

There is some evidence that the spleen may not be protective against malignant tumor growth in animal models. Meyer et al.268 reported decreased tumor growth in rats whose spleens had been removed. Ferrer269 found the rate of growth of sarcoma to be reduced in rats without spleens.

Description of the natural history of carcinoma metastatic to the spleen is incomplete because the event is so rare. This rarity may be due to anatomic, histologic, and functional characteristics of the spleen. Although no long-term follow-up data are available, splenectomy for isolated metastasis is clearly indicated, especially when no other evidence of metastatic disease is detectable.

The spleen is an enigmatic organ that still does not unveil its secrets to us. The authors recommend that all primary or metastatic tumors of the spleen be reported, so that in the future, medical science may be able to answer some of today’s questions.

Skandalakis et al.258 posed the following questions about this spleen-cancer phenomenon. There are many other unanswered questions:


What is the relationship between cancer and the spleen?

Why is the spleen so rarely a primary or a metastatic site?

What is the survival rate among patients with cancer metastatic to other areas after splenectomy?

Is splenectomy itself carcinogenic?

Are all the effects of radiation and immunosuppression following splenectomy known?

Does normal splenic function influence the growth of malignant tumors?

Disease and the Spleen

Association of the Spleen with Diseases of the Liver

The liver and the spleen are fellow travelers in certain well-known diseases, and also in some extremely rare conditions.

There is a notable tendency for splenomegaly to be associated with hepatomegaly.258 This is not always the case, but enlargement of both organs is a common phenomenon in hepatosplenic disorders. The spleen is extremely sensitive to elevation of vascular pressure. Because of the anatomic vascular relations of the two organs, splenic changes such as splenomegaly can take place secondary to hepatic changes such as portal hypertension associated with certain pathologic processes of the liver. The involvement of the spleen with diseases of the liver, such as Budd-Chiari syndrome, is also well known. Diagnostic procedures such as venography and splenoportography, and therapeutic procedures such as placement of splenorenal shunts (Fig. 22-46), have been developed.

Fig 22-46.

Diagrammatic illustration of the selective distal splenorenal shunt. (Modified from Salam AA, Warren WD. Anatomic basis of the surgical treatment of portal hypertension. Surg Cllin North Am 1974;54:1247-1257; with permission.)

Thoracic transposition of the spleen, or splenopneumopexy, has been employed for the treatment of portal hypertension. Surgery consists of mobilization of the spleen, left diaphragmotomy, splenic displacement into the left thoracic cavity, partial removal of the splenic capsule, partial abrasion of the surface of the left lower lobe, and suturing the prepared areas of the spleen and lung. It is doubtful that this procedure produces neovascular venous connections between the two systems that are sufficiently large to decompress the liver.

Salvage of the spleen in splenomegaly resulting from cirrhosis has also been urged. In their studies of splenic conservation, Ying-jian et al.158 observed that the splenic artery divided into two major branches in 46 of 61 patients and three branches in 15. External lobulation of the spleen could be predicted on the basis of hilar branching patterns. Partial splenectomy was used to treat portal hypertension with associated splenomegaly. Drainage was maintained for 24 to 36 hours. The remaining portion of the spleen was effective in lessening the incidence of fever after splenectomy. The residual spleen was still within normal limits of size one year after the operation. Bleeding from the salvaged spleen was controlled with an omental graft.

Association of the Spleen with Diseases of the Pancreas

Pancreatitis and pancreatic carcinoma are the most common causes of occlusion of the splenic vessels. Ku et al.159 described three phases in the clinical course of the disease:


The splenic vein is partially occluded; gastric varices and splenomegaly are absent

The splenic vein is completely occluded; the splenic artery is patent; gastric varices and splenomegaly are present

In the vanishing phase, the effects of arterial occlusion are superimposed on those of venous occlusion; gastric varices disappear and the enlarged spleen shrinks

We quote from Mercie et al.270:

Splenic venous thrombosis is a frequent complication occurring in the course of pancreatic cancer. It is easily diagnosed using abdominal computerized tomography. Arterial thrombosis is rarely observed.

Chronic pancreatitis can lead to splenic rupture, which is secondary to peptic digestion of the splenic parenchyma with the formation of an intrasplenic pseudocyst.271,272 Hemorrhagic pleural effusion may follow such a catastrophe.273,274 How can this transdiaphragmatic voyage of blood from the spleen be explained? Perhaps the several openings of the diaphragm, which are weak areas, are responsible. These openings are the three large openings for the inferior vena cava, the esophagus, and the aorta and the nine small openings for structures such as the greater and lesser thoracic splanchnic nerves and the hemiazygous vein. The well-known communications by lymphatics between the peritoneal and pleural cavities may be responsible as well. Involvement of mediastinal lymph nodes from intraabdominal disease may also be a cause. Intrathoracic disease, such as pulmonary carcinoma or tuberculosis, may metastasize to the adrenal glands. We agree with Nath and Warshaw275 that the subject is open to speculation.

Extravascular inflammation of the splenic artery and its branches secondary to erosion from chronic pancreatitis with the formation of micropseudoaneurysms or macropseudoaneurysms was described by Frey et al.276 According to Frey and colleagues, splenic artery pseudoaneurysms resulting from pancreatitis constitute less than 5% of all splenic artery aneurysms, most of them located at vessel bifurcations. These pseudoaneurysms may cause bleeding by rupture (Fig. 22-47). The association of splenic and portal venous thrombosis (Fig. 22-48) with chronic pancreatitis, with or without the formation of pancreatic abscess, is also well known. Nishiyama et al.277 presented splenic vein thrombosis secondary to pancreatitis; one of his three cases had an abscess. Bradley278 reported on 11 cases of splenic thrombosis secondary to pancreatitis with bleeding but without abscess formation.

Fig 22-47.

Pseudoaneurysms resulting from pancreatitis may cause hemorrhage by rupture either into the pancreatic ductal system or directly into the stomach or duodenum. SA, splenic artery. (Modified from Frey CF, Eckhauser F, Stanley JC. Hemorrhage. In: Bradley EL (ed). Complications of Pancreatitis. Philadelphia: WB Saunders, 1982; with permission.)

Fig 22-48.

Diagrammatic representation of collateral circulation characteristic of isolated occlusion of the splenic vein. (Modified from Salam AA, Warren WD. Anatomic basis of the surgical treatment of portal hypertension. Surg Clin North Am 1974;54: 1252; with permission.)

Spleen and AIDS

In an excellent paper on human immunodeficiency virus-related immune thrombocytopenia, Ferguson279 reported the following:

Infection by human immunodeficiency virus (HIV) may result in immune thrombocytopenia. The etiology of this immune thrombocytopenia (ITP) is not entirely clear, but treatment is similar to that of classic ITP. However, response to steroids is unpredictable and short-lived. Splenectomy provides immediate resolution of thrombocytopenia in the majority of cases and does not appear to increase the incidence of opportunistic infections.

Tsoukas et al.280 stated that the absence of a spleen during the asymptomatic phase of HIV infection seems to have a beneficial effect on HIV disease progression.

Unusual Disease Processes

The following is a list of some very rare eponymous syndromes or diseases that we call splenic curiosities:


Magocchi’s syndrome: Symmetric skin hemangiomas with hemangiomas of spleen, liver, and other organs

Omenn’s disease: Familial reticuloendotheliosis with eosinophilia, splenomegaly, and hepatomegaly

Tangier disease (Tangier is an island in Chesapeake Bay): storage disease with splenomegaly, hepatomegaly, lymphadenopathy, and hypercholesterolemia

Savitsky, Hyman, and Hyman disease: a disease associated with unidentified reticuloendothelial cell storage with splenomegaly and hepatomegaly

Chediak-Higashi syndrome (Caesar syndrome): oculocutaneous albinism, anomaly of the granules of leukocytes, lipid metabolism, and splenohepatomegaly

Prasad syndrome: dwarfism, hypogonadism, iron-deficiency anemia, and splenohepatomegaly

Sicca syndrome: Hashimoto thyroiditis, generalized lymphadenopathy, splenohepatomegaly, nonthrombocytopenic purpura, leukopenia, lymphopenia, hypergammaglobulinemia, and circulating tissue antibodies all occuring together with enlargement of the salivary glands

Dacie syndrome: a congenital anomaly associated with pancytopenia and nontropical idiopathic splenomegaly.


1. Ogle W (translator). Aristotle on the Parts of Animals. London: Kegan Paul, Trench & Co, 1882, Book III, Chapter 7 (p. 77).

2. Allen KB, Gay BB Jr, Skandalakis JE. Wandering spleen: anatomic and radiologic considerations. South Med J 1992;85: 976-984. [PubMed: 1411739]

3. Desai DC, Hebra A, Davidoff AM, Schnaufer L. Wandering spleen: a challenging diagnosis. South Med J 90:439-443, 1997. [PubMed: 9114840]

4. Buchner M, Baker MS. The wandering spleen. Surg Gynecol Obstet 175:373-387, 1992.

5. Allen KB. Wandering spleen. Probl Gen Surg 1990;7:122-127.

6. Abell I. Wandering spleen with torsion of the pedicle. Ann Surg 1933;98:722-735.

7. Allen KB, Andrews G. Pediatric wandering spleen, the case for splenopexy: review of 35 reported cases in the literature. J Pediatr Surg 1989;24:432-435. [PubMed: 2661792]

8. Gosselin B, Chou S. Wandering spleen producing small-bowel obstruction in a neonate. Pediatr Surg Int 9:583-584, 1994.

9. Spector JM, Chappell J. Gastric volvulus associated with wandering spleen in a child. J Pediatr Surg 2000;35:641-642. [PubMed: 10770406]

10. Moore PJ, Hawkins EP, Galliani CA, Guerry-Force ML. Splenogonadal fusion with limb deficiency and micrognathia. South Med J 90(11):1152-1155, 1997.

11. Putschar WGJ, Manion WC. Splenic-gonadal fusion. Am J Pathol 1956;32:15-33. [PubMed: 13275562]

12. Le Roux PJ, Heddle RM. Splenogonadal fusion: is the accepted classification system accurate? BJU Int 2000;85:114-115.

13. Gouw AS, Elema JD, Bink-Boelkens MT, de Jongh HJ, ten Kate LP. The spectrum of splenogonadal fusion: case report and review of 84 reported cases. Eur J Pediatr 1985;144:316-323. [PubMed: 4076247]

14. Alcalay J, Reif RM, Bogokowsky H. Primary splenic pregnancy [Hebrew]. Harefuah 100(12):577, 1981.

15. Kushner DH, Dobrzynski FA. Abdominal pregnancy with placenta attached to the spleen. Am J Obstet Gynecol 52:160-161, 1946.

16. Repin AV. Abdominal pregnancy of 28 weeks with implantation of the fertilized ovum at the hilum of the spleen [Russian]. Akush Ginekol 2:107-108, 1962.

17. Caruso V, Hall WHJ. Primary abdominal pregnancy in the spleen: a case report. Pathology 16:93-94, 1984. [PubMed: 6538959]

18. Talerman A, Hart S. Epithelial cysts of the spleen. Br J Surg 1970; 57:201-204.

19. Panossian DH, Wang N, Reeves CD, Weeks DA. Epidermoid cyst of the spleen presenting as a generalized peritonitis. Am Surg 1990;56:295-298. [PubMed: 2185675]

20. Neiman RS, Orazi A. Disorders of the Spleen, 2nd Ed. Philadelphia: WB Saunders, 1999, p. 18.

21. Curtis GM, Movitz D. The surgical significance of the accessory spleen. Ann Surg 1946; 123:276-298.

22. Halpert B, Gyorkey F. Lesions observed in accessory spleens of 311 patients. Am J Clin Pathol 1959;32:165-168. [PubMed: 13670140]

23. Halpert B, Alden ZA. Accessory spleens in or at the tail of the pancreas. Arch Pathol 1964;77:652-654. [PubMed: 14130052]

24. Abu-Hijleh MF. Multiple accessory spleens: case report and literature review. Clin Anat 1993;6:232-239.

25. Habib FA, Kolachalam RB, Swason K. Abscess of an accessory spleen. Am Surg 2000;66:215-218. [PubMed: 10695757]

26. Wekerle T, Eichinger S, Maier A, Wrba F, Möschl P. Intrahepatic splenic tissue in a patient with recurrent idiopathic thrombocytopenic purpura. Surgery 123:596-599, 1998. [PubMed: 9591017]

27. Fleming CR, Dickson ER, Harrison EG. Splenosis: autotransplantation of splenic tissue. Am J Med 61:414, 1976. [PubMed: 961705]

28. Metwally N, Ravo B. Splenosis: a review. Contemp Surg 1991; 39:33.

29. Hamilton WJ, Simon G, Hamilton SGI. Surface and Radiological Anatomy. Baltimore: Williams and Wilkins Co, 1976.

30. Gould GM, Pyle WL. Anomalies and Curiosities of Medicine (2nd ed). New York: Bell Publishing Co, 1956, p. 657.

31. Allen L. The lymphatic system and the spleen. In: Anson BJ (ed). Morris’s Human Anatomy (12th ed). New York: McGraw-Hill, 1966, p. 907.

32. Healey JE Jr. A Synopsis of Clinical Anatomy. Philadelphia: WB Saunders, 1969, p. 162.

33. Last RJ. Anatomy: Regional and Applied (5th ed). Baltimore: Williams & Wilkins, 1972, p. 470.

34. Michels NA. Blood Supply and Anatomy of the Upper Abdominal Organs, with a Descriptive Atlas. Philadelphia: JB Lippincott, 1955.

35. Morrell DG, Chang FC, Helmer SD. Changing trends in the management of splenic injury. Am J Surg 1995;170:686-690. [PubMed: 7492027]

36. Goodley CD, Warren RL, Sheridan RL, McCabe CJ. Nonoperative management of blunt splenic injury in adults: age over 55 years as a powerful indicator for failure. J Am Coll Surg 1996;183: 133-139.

37. Moody RO. The position of the abdominal viscera in healthy young British and American adults. J Anat 1927;61:223.

38. Moody RO, Chamberlain WE, Van Nuys RG. Visceral anatomy of healthy adults. Am J Anat 1926;37:273.

39. Moody RO, Van Nuys RG. Some results of a study of roentgenograms of the abdominal viscera. AJR 1928;20:348.

40. Strauss MB (ed). Familiar Medical Quotations. Boston: Little, Brown and Co, 1968, p. 598.

41. Kyber E. Uber die Milz des Menschen und einiger Saugetiere. Arch Mikrosk Anat Entw Mech 1870;6:540-570.

42. Skandalakis PN, Colborn GL, Skandalakis LJ, Richardson DD, Mitchell WE Jr, Skandalakis JE. The surgical anatomy of the spleen. Surg Clin North Am 1993;73:747-768. [PubMed: 8378819]

43. Gupta CD, Gupta SC, Aorara AK, Singh P. Vascular segments in the human spleen. J Anat 1976; 121:613-616.

44. Mandarim-Lacerda CA, Sampaio FJ, Passos MA. Segmentation vasculaire de la rate chez le nouveau-ne: support anatomique pour la resection partielle. J Chir (Paris) 1983; 120:471. [PubMed: 6619226]

45. Liu DL, Xia S, Xu W, Qifa Y, Gao Y, Qian J. Anatomy of vasculature of 850 spleen specimens and its application in partial splenectomy. Surgery 1996;119:27-33. [PubMed: 8560382]

46. Redmond HP, Redmond JM, Rooney BP. Surgical anatomy of the human spleen. Br J Surg 1989; 76:198-201.

47. Voboril Z. On the question of segmentation of the human spleen. Folia Morphol 1982; 30:295-314.

48. Dawson DL, Molina JE, Scott-Conner CEH. Venous segmentation of the human spleen. Am Surg 1986;52:253. [PubMed: 3706915]

49. Dreyer B, Budtz-Olson OE. Splenic venography: demonstration of the portal circulation with diodone. Lancet 1952;1:530.

50. Garcia-Porrero JA, Lemes A. Arterial segmentation and subsegmentation in the human spleen. Acta Anat 1988;131:276. [PubMed: 3376732]

51. Dixon JA, Miller F, McCloskey D, Siddoway J. Anatomy and techniques in segmental splenectomy. Surg Gynecol Obstet 1980; 150:516. [PubMed: 7361237]

52. Whitesell FB. A clinical and surgical anatomic study of rupture of the spleen due to blunt trauma. Surg Gynecol Obstet 1960;110: 750. [PubMed: 13844448]

53. Skandalakis JE, Colborn GL, Pemberton LB, Skandalakis PN, Skandalakis LJ, Gray SW. The surgical anatomy of the spleen. Probl Gen Surg 1990;7:1-17.

54. Rosen A, Nathan H, Luciansky E, Sayfan J. The lienorenal ligament and the tail of the pancreas: a surgical anatomical study. Pancreas 1988;3:104-107. [PubMed: 3362836]

55. O’Rahilly R. Gardner-Gray-O’Rahilly Anatomy: A Regional Study of Human Structure (5th ed). Philadelphia: WB Saunders, 1986, pp. 414-415.

56. Seufert RM, Mitrou PS. Surgery of the spleen. Reber HA (trans). New York: Thieme, 1986.

57. Henry AK. The removal of large spleens. Br J Surg 1940;107:464.

58. Lord MD, Gourevitch A. The peritoneal anatomy of the spleen, with special references to the operation of partial gastrectomy. Br J Surg 1965;52:202. [PubMed: 14261128]

59. VanderZypen E, Revez E. Investigation of development, structure and function of the phrenicocolic and duodenal suspensory ligaments. Acta Anat (Basel) 1984;119:142.

60. Skandalakis JE, Colborn GL, Skandalakis LJ. Benign anatomical mistakes: myths or enigmas? Am Surg 15(1):88-89, 1999.

61. Morgenstern L. Splenic repair and partial splenectomy. In: Nyhus LM, Baker RJ (eds). Mastery of Surgery (2nd ed). Boston: Little, Brown, 1992, pp. 1102-1112.

62. Poulin EC, Thibault C. The anatomical basis for laparoscopic splenectomy. Can J Surg 1993;36:484. [PubMed: 8221408]

63. Baronofsky ID, Walton W, Noble JF. Occult injury to the pancreas following splenectomy. Surgery 1951;29:852. [PubMed: 14835182]

64. Adkins EH. Ptosed spleen with torsion of pedicle. Ann Surg 1938; 107:832.

65. Taveras JM. Golden’s Diagnostic Roentgenology. Baltimore, Williams & Wilkins, 1964.

66. McMahon WG, Norwood SH, Silva JS. Pancreatic pseudocyst with splenic involvement: an uncommon complication of pancreatitis. South Med J 1988;81:910. [PubMed: 3393950]

67. Michels NA. The variational anatomy of the spleen and the splenic artery. Am J Anat 1942;70:21.

68. Van Damme JPJ, Bonte J. The blood supply of the stomach. Acta Anat 1988;131:89-96.

69. Sylvester PA, Stewart R, Ellis H. Tortuosity of the human splenic artery. Clin Anat 1995;8:214-218. [PubMed: 7606595]

70. Borley NR, McFarlane JM, Ellis H. A comparative study of the tortuosity of the splenic artery. Clin Anat 1995;8:219-221. [PubMed: 7606596]

71. Waizer A, Baniel J, Zin Y, Dintsman M. Clinical implications of anatomic variations of the splenic artery. Surg Gynecol Obstet 1989; 168:57. [PubMed: 2909134]

72. Treutner KH, Klosterhalfen B, Winkeltau G, Moench S, Schumpelick V. Vascular anatomy of the spleen: the basis for organ-preserving surgery. Clin Anat 1993;6:1-8.

73. Van Damme JPJ, Bonte J. Systemization of the arteries in the splenic hilus. Acta Anat 1986;125:217.

74. Katritsis E, Parashos A, Papadopoulos N. Arterial segmentation of the human spleen by post-mortem angiograms and corrosion casts. Angiology 1982;33:720. [PubMed: 7137654]

75. Helm HM. The gastric vasa brevia. Anat Rec 1915;9:637.

76. Keramidas DC. The ligation of the splenic artery in the treatment of traumatic rupture of the spleen. Surgery 1979;85:530-533. [PubMed: 432814]

77. Farag A, Shoukry A, Nasr SE. A new option for splenic preservation in normal sized spleen based on preserved histology and phagocytic function of the upper pole using upper short gastric vessels. Am J Surg 1994;168:257-261. [PubMed: 8080064]

78. Berens AS, Aluisio FV, Colborn GL, Gray SW, Skandalakis JE. The incidence and significance of the posterior gastric artery in human anatomy. J Med Assoc Ga 1991;8:425-428.

79. Van Damme JPJ, Bonte J. Arteria splenica and the blood supply of the spleen. Probl Gen Surg 1990;7:18-27.

80. Trubel W, Turkof E, Rokitansky A, Firbas W. Incidence, anatomy and territories supplied by the posterior gastric artery. Acta Anat 1985;124:26-30. [PubMed: 4072606]

81. Kirk E. Untersuchungen uber die grossere und feinere topographische Verteilung der Arterien, Venen und Ausfuhrungsgange in der menschlichen Bauchspeicheldruse. Ztschr Ges Anat 1931; 94:822.

82. Lippert H, Pabst R. Arterial Variations in Man. Munich: J.F. Bergmann Verlag, 1985, pp. 41-45.

83. Mellière D. Variations des artères hépatiques et du carrefour pancréatique. J Chir (Paris) 98:5-42, 1968. [PubMed: 16303608]

84. Jonsell G, Boutelier P. Observations during treatment of acute necrotizing pancreatitis with surgical ablation. Surg Gynecol Obstet 148:385, 1979. [PubMed: 419439]

85. Petroianu A, Petroianu S. Anatomy of splenogastric vessels in patients with schistosomal portal hypertension. Clin Anat 1994; 7:80-83.

86. Romero-Torres R. The true splenic blood supply and its surgical applications. Hepato-Gastroenterology 45:885-888, 1998. [PubMed: 9684152]

87. Woodburne RT. Essentials of Human Anatomy. New York: Oxford University Press, 1969, p. 430.

88. Douglass BE, Baggenstoss AH, Hollinshead WH. The anatomy of the portal vein and its tributaries. Surg Gynecol Obstet 1950;91: 562. [PubMed: 14787850]

89. Williams PL (ed). Gray’s Anatomy (38th ed). New York: Churchill Livingstone, 1995, p. 1603.

90. Gerber AB, Lev M, Goldberg SL. The surgical anatomy of the splenic vein. Am J Surg 1951;82:339. [PubMed: 14868823]

91. Fujitani RM, Johs SM, Cobb SR, Mehringer CM, White RA, Klein SR. Preoperative splenic artery occlusion as an adjunct for high risk splenectomy. Am Surg 1988;54:602. [PubMed: 3178046]

92. Dumont AE, Lefleur RS. Significance of an enlarged splenic artery in patients with splenic vein thrombosis. Am Surg 1988;54: 613. [PubMed: 3178047]

93. Guyton AC. Textbook of Medical Physiology, Arthur C. Guyton, John E. Hall (9th ed). Philadelphia: WB Saunders, 1996.

94. Lankisch PG. The spleen in inflammatory pancreatic disease. Gastroenterology 1990;88:509.

95. Orozco H, Mercado MA, Martinez R, Tielve M, Chan C, Vasquez M, Zenteno-Guichard G, Pantoja JP. Is splenectomy necessary in devascularization procedures for treatment of bleeding portal hypertension? Arch Surg 133:36-38, 1998. [PubMed: 9438756]

96. Firstenberg MS, Plaisier B, Newman JS, Malangoni MA. Successful treatment of delayed splenic rupture with splenic artery embolization. Surgery 123:584-586, 1998. [PubMed: 9591013]

97. Rouviere H. Anatomy of the Human Lymphatic System. Ann Arbor MI: Edwards Brothers, 1938.

98. Weiss L, Gilbert HA, Ballon SC (eds). Lymphatic System Metastasis. Boston: GK Hall Medical Publishers, 1980.

99. Drinker CK, Yoffey JM. Lymphatics, Lymph, and Lymphatic Tissue. Cambridge, Mass: Harvard University Press, 1941, p 12.

100. Boles ET Jr, Haase GM, Hamoudi AB. Partial splenectomy in staging laparotomy for Hodgkin’s disease: an alternative approach. J Pediatr Surg 1978;13:581-586. [PubMed: 731356]

101. Dearth JC, Gilchrist GS, Telander RL. Partial splenectomy for staging Hodgkin’s disease: risk of false-negative results. N Engl J Med 1978;299:345-346. [PubMed: 683267]

102. Utterback RA. Innervation of the spleen. J Comp Neurol 1944; 81: 55.

103. Crosby ED, Humphrey T, Lauer EW. Correlative Anatomy of the Nervous System. New York: Macmillan and Co., 1962.

104. Chadburn A. The spleen: anatomy and anatomical function. Semin Hematol 2000;37 (Suppl 1) 13-21.

105. Wolf BC, Neiman RS. Disorders of the spleen. Philadelphia: WB Saunders, 1989.

106. Churchill W. Radio speech (October 1, 1939). Cited in Rawson H, Miner M. The New International Dictionary of Quotations. New York: EP Dutton, 1986, p. 188.

107. Luna GK, Dellinger EP. Nonoperative observation therapy for splenic injuries: a safe therapeutic option? Am J Surg 1987;153: 463.

108. Polk HC Jr. Principles of preoperative preparation of the surgical patient. In: Sabiston DC Jr (ed). Textbook of Surgery (13th ed). Philadelphia: WB Saunders, 1986, pp. 87-98.

109. Dunphy JE. Splenectomy for trauma. Am J Surg 1946;71:450.

110. Morgenstern L. Technique of partial splenectomy. Prob Gen Surg 1990;7:103-112.

111. Brunt LM, Langer JC, Quasebarth MA, Whitman ED. Comparative analysis of laparoscopic versus open splenectomy. Am J Surg 1996;172:596-601. [PubMed: 8942570]

112. Waldhausen JHT, Tapper D. Is pediatric splenectomy safe and cost-effective? Arch Surg 132:822-824, 1997. [PubMed: 9267264]

113. Decker G, Millat B, Guillon F, Atger J, Linon M. Laparoscopic splenectomy for benign and malignant hematologic diseases: 35 consecutive cases. World J Surg 22:62-68, 1998. [PubMed: 9465763]

114. Katkhouda N, Waldrep DJ, Feinstein D, Soliman H, Stain SC, Ortega AE, Mouiel J. Unresolved issues in laparoscopic splenectomy. Am J Surg 1996;172:585-590. [PubMed: 8942568]

115. Park A, Marcaccio M, Sternbach M, Witzke D, Fitzgerald P. Laparoscopic vs open splenectomy. Arch Surg 134:1263-1269, 1999. [PubMed: 10555644]

116. Phillips EH, Korman JE, Friedman R. Laparoscopic splenectomy. In: Hiatt JR, Phillips EH, Morgenstern L (eds). Surgical Diseases of the Spleen. New York: Springer-Verlag, 1997, pp. 211-232.

117. Al-Salem AH. Is splenectomy for massive splenomegaly safe in children? Am J Surg 178:42-45, 1999. [PubMed: 10456701]

118. Tractow WD, Fabri PJ, Carey LC. Changing indications for splenectomy: 30 years experience. Arch Surg 1980;115:447.

119. Musser G, Lazar G, Hocking W, Busuttil RW. Splenectomy for hematologic disease: the UCLA experience with 306 patients. Ann Surg 1984;200:40. [PubMed: 6732325]

120. Powell M, Courcoulas A, Gardner M, Lynch J, Harbrecht BG, Udekwu AO, Billiar TR, Federle M, Ferris J, Meza MP, Peitzman AB. Management of blunt splenic trauma: significant differences between adults and children. Surgery 122(4):654-660, 1997.

121. Weber T, Hanisch E, Baum RP, Seufert RM. Late results of heterotopic autotransplantation of splenic tissue into the greater omentum. World J Surg 22:883-889, 1998. [PubMed: 9673564]

122. Morgenstern L, Rosenberg BA, Geller SA. Tumors of the spleen. World J Surg 1985;9:468. [PubMed: 4040300]

123. Hiatt JR, Allins A, Kong LR. Open splenectomy. In: Hiatt JR, Phillips EH, Morgenstern L (eds.) Surgical Diseases of the Spleen. New York: Springer-Verlag, 1997, pp. 197-210.

124. Mitchell A, Morris PJ. Surgery of the spleen. Clin Haematol 1983; 12:565. [PubMed: 6413110]

125. Ugochukwu AI, Irving M. Intraperitoneal low pressure suction drainage following splenectomy. Br J Surg 1985;72:247. [PubMed: 2579704]

126. Carmichael J, Thomas WO, Dillard D, Luterman A, Ferrara JJ. Indications for placement of drains in the splenic fossa. Am Surg 1990;56:313-318. [PubMed: 2334074]

127. Ellison EC, Fabri DJ. Complications of splenectomy: etiology, prevention and management. Surg Clin North Am 1983;63:1313. [PubMed: 6417808]

128. Pachter HL, Hofstetter SR, Spencer FC. Evolving concepts in splenic surgery. Am Surg 1981;194:262. [PubMed: 7023394]

129. Scanlon EF. The intraabdominal dead space and abscess formation. Surg Gynecol Obstet 1978;146:789. [PubMed: 644438]

130. Olsen WR, Beaudoin DE. Wound drainage after splenectomy: indications and complications. Am J Surg 1969;117:615. [PubMed: 5791029]

131. Jordan GL Jr. Complications of splenectomy. In: Hardes JD (ed). Complications in Surgery and Their Management. Philadelphia: WB Saunders, 1981.

132. Maingot R. Abdominal Operations (6th ed). New York: Appleton-Century-Crofts, 1974.

133. McNair TJ (ed). Hamilton Bailey’s Emergency Surgery (9th ed). Baltimore: Williams & Wilkins, 1972.

134. Fabri PJ, Metz EN, Nick WV, Zollinger RM. A quarter century with splenectomy. Arch Surg 1974;108:569. [PubMed: 4815931]

135. Chassin JL. Operative Strategy in General Surgery: An Expositive Atlas. New York: Springer-Verlag, 1984.

136. Lumsden AB, Riley JD, Skandalakis JE. Splenic artery aneurysms. Probl Gen Surg 1990;7:113-121.

137. Rogers DM, Thompson JE, Garrett WV, Talkington CM, Patmen RD. Mesenteric vascular problems: a twenty six year experience. Ann Surg 195:554, 1982. [PubMed: 7073353]

138. Busuttil RW, Brin BJ. The diagnosis and management of visceral artery aneurysms. Surgery 88:619, 1980. [PubMed: 7434201]

139. Spittel JA, Fairbairn JF, Kincaid OW, Remine WH. Aneurysm of the splenic artery. JAMA 175:452, 1961.

140. Stanley JC, Fry WJ. Pathogenesis and clinical significance of splenic artery aneurysms. Surgery 76:898, 1974. [PubMed: 4428355]

141. DeVries JE, Schattenkerk ME, Malt RA. Complications of splenic artery aneurysm other than intraperitoneal rupture. Surgery 91: 200, 1980.

142. O’Grady JP, Day EJ, Toole AL, Paust JC. Splenic artery aneurysm rupture in pregnancy: a review and case report. Obstet Gynecol 50:627, 1977. [PubMed: 16456908]

143. Boijsen E, Efsing HO. Aneurysm of the splenic artery. Acta Radiol 8:29, 1969. [PubMed: 5800861]

144. Majeski J. Splenic artery tortuosity simulating a splenic artery aneurysm. South Med J 91(10):949-950, 1998.

145. McFarlane JR, Thorbjarnarson B. Rupture of the splenic artery during pregnancy. Am J Obstet Gynecol 95:1025, 1966.

146. Vassalotti SB, Schaller JA. Spontaneous rupture of splenic artery aneurysm in pregnancy: report of first known antepartum rupture with maternal and fetal survival. Obstet Gynecol 30:264, 1967. [PubMed: 5212337]

147. Stanley JC, Wakefield TW, Graham LM. Whitehouse WM, Zelenock GB, Lindenhauer SM. Clinical importance and management of splanchnic artery aneurysms. J Vasc Surg 3:836, 1986. [PubMed: 3701947]

148. de Perrot M, Bühler L, Deléaval J, Borisch B, Mentha G, Morel P. Management of true aneurysms of the splenic artery. Am J Surg 175:466-468, 1998.

149. Bedford PD, Lodge B. Aneurysm of the splenic artery. Gut 1960; 1:312. [PubMed: 13688586]

150. Ferrari L. The recognition and incidence of splenic artery aneurysms. Australas Radiol 1972;16:126

151. Kreel L. The recognition and incidence of splenic artery aneurysms. Australas Radiol 1974;18:415. [PubMed: 4462545]

152. Puttini M, Aseni P, Brambilla G, Belli L. Splenic artery aneurysms in portal hypertension. J Cardiovasc Surg 1982;23:490. [PubMed: 7153237]

153. Taylor JL, Woodward DAK. Splenic conservation and the management of splenic artery aneurysms. Ann R Coll Surg Engl 1987; 69:179. [PubMed: 3631876]

154. Horton J, Ogden ME, Williams S, Coln D. The importance of splenic blood flow in clearing pneumococcal organisms. Ann Surg 1982;95:172.

155. Gonzalez EM, Garcia-Blanch G, Blanco JMS, Garcia IG, Ocana AG. Treatment of splenic artery aneurysm after distal splenorenal shunt: a case report. Jpn J Surg 1981;11:377. [PubMed: 7311198]

156. Mandel SR, Jaques PF, Mauro MA, Sanofsky S. Nonoperative management of peripancreatic arterial aneurysms. Ann Surg 1987; 205:126. [PubMed: 3492972]

157. Baker KS, Tisnado J, Cho SR, Beachley MC. Splanchnic artery aneurysms and pseudoaneurysms: transcatheter embolization. Radiology 1987;163:135. [PubMed: 3823426]

158. Ying-jian A, Qing-you L. Subtotal splenectomy in cirrhotic patients. Chin Med 99:191, 1986.

159. Ku Y, Kawa Y, Fujiwara S, Nishiyama H, Tanaka Y, Okumura S, Ohyanagi H, Saitoh Y. Hemodynamic study of occlusion of the splenic vein caused by carcinoma of the pancreas. Surg Gynecol Obstet 168(1):17-24, 1989.

160. Miller TA, Rowlands BJ (eds). Physiologic Basis of Modern Surgical Care. St. Louis: CV Mosby, 1988.

161. Blaisdell FW, Trunkey DD (eds). Trauma Management. Vol 1: Abdominal trauma. New York: Thieme-Stratton, 1982.

162. Andrews MA. Ultrasound of the spleen. World J Surg 2000;24:183-187. [PubMed: 10633145]

163. Krause KR, Howells GA, Bair HA, Glover JL, Madrazo BL, Wasvary HJ, Bendick PJ. Nonoperative management of blunt splenic injury in adults 55 years and older: a twenty-year experience. Am Surg 2000;66:636-640. [PubMed: 10917473]

164. Velmahos GC, Chan LS, Kamel E, Murray JA, Yassa N, Kahaku D, Berne TV, Demetriades D. Nonoperative management of splenic injuries: have we gone too far? Arch Surg 2000;135:674-681. [PubMed: 10843363]

165. Peitzman AB, Heil B, Rivera L, Federle MB, Harbrecht BG, Clancy KD, Croce M, Enderson BL, Morris JA, Shatz D, Meredith JW, Ochoa JB, Fakhry SM, Cushman JG, Minei JP, McCarthy M, Luchette FA, Townsend R, Tinkoff G, Block EFJ, Ross S, Frykberg ER, Bell RM, Davis F III, Weireter L, Shapiro MB, Kealey GP, Rogers F, Jones LM, Cone JB, Dunham CM, McAuley CE. Blunt splenic injury in adults: multi-institutional study of the Eastern Association for the Surgery of Trauma. J Trauma 2000;4 9:177-189.

166. Bickler S, Ramachandran V, Gittes GK, Alonso M, Snyder CL. Nonoperative management of newborn splenic injury: a case report. J Pediatr Surg 2000;35:500-501. [PubMed: 10726697]

167. Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983.

168. Danforth DN, Thorbjarnarson B. Incidental splenectomy: a review of the literature and the New York hospital experience. Am Surg 1976;183:124. [PubMed: 1247309]

169. Celebrezze JP Jr, Cottrell DJ, Williams GB. Spontaneous splenic rupture due to isolated splenic peliosis. South Med J 91(8):763-764, 1998.

170. Sikov WM, Schiffman FJ, Weaver M, Dyckman J, Shulman R, Torgan P. Splenosis presenting as occult gastrointestinal bleeding. Am J Hematol 2000;65:56-61. [PubMed: 10936865]

171. De Vuysere S, Van Steenbergen W, Aerts R, Van Hauwaert H, Van Beckevoort D, Van Hoe L. Intrahepatic splenosis: imaging features. Abdom Imaging 2000:25:187-189.

172. Goldstone J. Splenectomy for massive splenomegaly. Am J Surg 1978;135:385. [PubMed: 626319]

173. Schwartz SJ. Splenectomy for thrombocytopenia. World J Surg 1985;9:416. [PubMed: 4040298]

174. Schwartz SI. Role of splenectomy in hematologic disorders. World J Surg 1996;20:1156-1159. [PubMed: 8864075]

175. Winde G, Schmid KW, Lügering N, Fischer R, Brandt B, Berns T, Bünte H. Results and prognostic factors of splenectomy in idiopathic thrombocytopenic purpura. J Am Coll Surg 183:565-574, 1996. [PubMed: 8957458]

176. Bussel JB. Splenectomy-sparing strategies for the treatment and long-term maintenance of chronic idiopathic (immune) thrombocytopenic purpura. Semin Hematol 2000;37(Suppl 1):1-4.

177. Bell WR Jr. Long-term outcome of splenectomy for idiopathic thrombocytopenic purpura. Semin Hematol 2000;37(Suppl 1):22-25.

178. Cusack JC, Seymour JF, Lerner S, Keating MJ, Pollock RE. Role of splenectomy in chronic lymphocytic leukemia. J Am Coll Surg 185:237-243, 1997. [PubMed: 9291400]

179. Taylor MA, Kaplan HS, Nelsen RS. Staging laparotomy with splenectomy for Hodgkin’s disease: the Stanford experience. World J Surg 1985;9:449. [PubMed: 4013359]

180. Baccarani U, Carroll BJ, Hiatt JR, Donini A, Terrosu G, Decker R, Chandra M, Bresadola F, Phillips EH. Comparison of laparoscopic and open staging in Hodgkin disease. Arch Surg 133: 517-522, 1998. [PubMed: 9605914]

181. Klasa RJ, Connors J, Hoskins P, et al. Early stage Hodgkin’s disease: impact of brief chemotherapy together with radiotherapy without staging laparotomy. Proc Am Soc Clin Oncol 13:372, 1994.

182. Santoro A, Bonfante V, Viviani S, et al. Subtotal nodal versus involved field irradiation after 4 cycles of ABVD in early stage Hodgkin’s disease. Proc Am Soc Clin Oncol 15:415, 1996.

183. Meyer AA. Spleen. In: Greenfield LJ, Mulholland MW, Oldham KT, Zelenock GB, Lillemoe KD (eds.). Surgery: Scientific Principles and Practice (2nd ed). Philadelphia: Lippincott-Raven, 1997, pp. 1262-81.

184. Sirinek KR, Evans WE. Non-parasitic splenic cysts: case report of an epidermoid cyst and review of the literature. Am J Surg 1973; 126:8. [PubMed: 4714784]

185. Chun CH, Raff MJ, Contreras L. Splenic abscess. Medicine 59: 50-65, 1980. [PubMed: 6986009]

186. Nelken N, Ignatius J, Skinner M, Christensen N. Changing clinical spectrum of splenic abscess. A mullticenter study and review of the literature. Am J Surg 154:27-34, 1987. [PubMed: 3300398]

187. Ooi LP, Leong SS. Splenic abscesses from 1987 to 1995. Am J Surg 174:87-93, 1997. [PubMed: 9240961]

188. Gadacz JR. Splenic abscess. World J Surg 1985;9:410. [PubMed: 3892934]

189. Lerner RM, Spataro RF. Splenic abscess: percutaneous drainage. Radiology 1984;153:643. [PubMed: 6494461]

190. Quinn SF, Van Sonnenberg E, Casola G. Interventional radiology in the spleen. Radiology 161:289-291, 1986. [PubMed: 3763890]

191. Gleich S, Wolin DA, Herbsman H. A review of percutaneous drainage in splenic abscess. Surg Gynecol Obstet 167:211-216, 1988. [PubMed: 3046013]

192. Phillips GS, Radosevich MD, Lipsett PA. Splenic abscess. Arch Surg 132:1331-1336, 1997. [PubMed: 9403539]

193. Safioleas M, Misiakos E, Manti C. Surgical treatment for splenic hydatidosis. World J Surg 21:374-378, 1997. [PubMed: 9143567]

194. Uriarte C, Pomares N, Martin M, et al. Splenic hydatidosis. Am J Trop Med Hyg 44:420, 1991. [PubMed: 2042707]

195. Moumen M, El Alaoui M, Mokhtari M, El Fares F. Pour un traitement conservateur du kyste hydatique de la rate. J Chir 128: 260, 1991. [PubMed: 1880184]

196. Berrada S, Ridai M, Mokhtari M. Kystes hydatiques de la rate: splenectomies ou chirurgie conservatrice? Ann Chir 45:434, 1991. [PubMed: 1859117]

197. Wilson CI, Cabello-Inchausti B, Sendzischew H, Robinson MJ. Ceroid histiocytosis: an unusual cause of splenic rupture. South Med J 2001;94:237-239. [PubMed: 11235042]

198. Salgado C, Feliu E, Monserrat E, Villamor N, Ordi J, Aguilar JL, Vives-Corrons JL, Rozman C. B-type large-cell primary splenic lymphoma with massive involvement of the red pulp. Acta Haematol 1993;89:46-49. [PubMed: 8480487]

199. Rosso R, Neiman RS, Paulli M, Boveri E, Kindl S, Magrini U, Barosi G. Splenic marginal zone cell lymphoma: report of an indolent variant without massive splenomegaly presumably representing an early phase of the disease. Human Pathol 1995;26: 39-46. [PubMed: 7821915]

200. Westra WH, Anderson BO, Klimstra DS. Carcinosarcoma of the spleen: an extragenital malignant mixed mullerian tumor? Am J Surg Pathol 1994;18:309-315. [PubMed: 8116800]

201. Brune MB, Cain DL, Cardwell EM, Janckila AJ. Splenic lymphoma with villous lymphocytes: diagnosis by flow cytometry and immunocytochemistry. South Med J 1995;88:1260-1263. [PubMed: 7502121]

202. Berge T. Splenic metastases. Frequencies and patterns. Acta Pathol Microbiol Scand (A) 82:499-506, 1974. [PubMed: 4854372]

203. Brown DA, Mukherjer D. Partial splenectomy with autologous capsule graft. Surg Gynecol Obstet 1988;166:555. [PubMed: 3375969]

204. Warshaw AL. Conservation of the spleen with distal pancreatectomy. Arch Surg 1988;123:550. [PubMed: 3358679]

205. Phelan JT, Grace JT, Wayne AL, Moore GE. A technique of splenectomy. Surg Gynecol Obstet 1963;116:501. [PubMed: 13943118]

206. Beal SL, Spisso JM. The risk of splenorrhaphy. Arch Surg 1988; 123:1158. [PubMed: 3415469]

207. Otsuji E, Yamaguchi T, Sawai K, Ohara M, Takahashi T. End results of simultaneous splenectomy in patients undergoing total gastrectomy for gastric carcinoma. Surgery 1996;120:40-44. [PubMed: 8693421]

208. Cocanour CS, Moore FA, Ware DN, Marvin RG, Clark JM, Duke JH. Delayed complications of nonoperative management of blunt adult splenic trauma. Arch Surg 133:619-625, 1998. [PubMed: 9637460]

209. Martin JC, Cooper MN. Complications of splenectomy. South Surg 1950;16:1047.

210. Shackleford RT. Surgery of the Abdominal Tract. Philadelphia: Saunders, 1955.

211. Dalton ML, West RL. Fate of dearterialized spleen. Arch Surg 1965;91:541. [PubMed: 14332424]

212. Piedad OH, Wels PB. Retrograde distal pancreatectomy. Am J Surg 1972;124:431. [PubMed: 4560388]

213. Schmeiden V, Sebening W. Surgery of the pancreas with especial consideration of acute pancreatic necrosis. Surg Gynecol Obstet 1928;46:735.

214. Daoud F, Fischer D, Hafner CD. Complications following splenectomy with special emphasis on drainage. Arch Surg 1966;92: 32. [PubMed: 5901259]

215. Hodam RP. The risk of splenectomy: a review of 10 cases. Am J Surg 1970;119:709. [PubMed: 5445994]

216. Kassum D, Thomas EJ. Morbidity and mortality of incidental splenectomy. Can J Surg 1977;20:209. [PubMed: 858095]

217. Graves HA, Nelson A, Byrd BF. Gastrocutaneous fistula as a postoperative complication. Ann Surg 1970;171:656. [PubMed: 5441361]

218. Harrison BF, Glanges E, Sparkman RS. Gastric fistula following splenectomy: its cause and prevention. Ann Surg 1977;185:210. [PubMed: 836094]

219. Cooper CS, Cohen MB, Donovan JF Jr. Splenectomy complicating left nephrectomy. J Urol 1996;155:30-36. [PubMed: 7490874]

220. Sabiston DC. Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 15th Ed. Philadelphia: WB Saunders Co, 1997.

221. Diaz J, Eisenstat M, Chung R. A case-controlled study of laparoscopic splenectomy. Am J Surg 173:348-350, 1997. [PubMed: 9136795]

222. Glasgow RE, Mulvihill SJ. Laparoscopic splenectomy. World J Surg 1999;23:384-88. [PubMed: 10030862]

223. Targarona EM, Espert JJ, Balaguè C, Sugrañes G, Ayuso C, Lomeña F, Bosch F, Trias M. Residual splenic function after laparoscopic splenectomy: a clinical concern. Arch Surg 133:56-60, 1998. [PubMed: 9438760]

224. Lozano-Salazar RR, Herrera MF, Vargas-Vorácková F, López-Karpovitch X. Laparoscopic versus open splenectomy for immune thrombocytopenic purpura. Am J Surg 176:366-369, 1998. [PubMed: 9817257]

225. Tanoue K, Makoto H, Morita M, Migoh S, Tsugawa K, Yagi S, Ohta M, Sugimachi K. Results of laparascopic splenectomy for immune thrombocytopenic purpura. Am J Surg 1999;177:222-226. [PubMed: 10219858]

226. Fass SM, Hui TT, Lefor A, Maestroni U, Phillips EH. Safety of laparoscopic splenectomy in elderly patients with idiopathic thrombocytopenic purpura. Am Surg 2000;66:844-847. [PubMed: 10993613]

227. Katkhouda N, Mavor E. Laparoscopic splenectomy. Surg Clin North Am 2000;80:1285-1297. [PubMed: 10987036]

228. Rescorla FJ, Breitfeld PP, West KW, Williams D, Engum SA, Grosfeld JL. A case controlled comparison of open and laparoscopic splenectomy in children. Surgery 124:670-676, 1998. [PubMed: 9780987]

229. Terrosu G, Donini A, Baccarani U, Vianello V, Anania G, Zala F, Pasgualucci A, Bresadola F. Laparoscopic versus open splenectomy in the management of splenomegaly: our preliminary experience. Surgery 124:839-843, 1998. [PubMed: 9823396]

230. Chang MY, Shiau CS, Chang CL, Hou HC, Chiang CH, Hsieh TT, Soong YK. Spleen laceration, a rare complication of laparoscopy. J Am Assn Gynecol Laparosc 2000;7:269-272. [PubMed: 10806277]

231. McWorter JE, Cloud JW. Malignant tumors and their metastasis. Ann Surg 1930;92:434-443.

232. Miller JN, Milton GW. An experimental comparison between tumor growth in the spleen and liver. J Pathol 1965;90:515-519. [PubMed: 5849609]

233. Slavin JD, Mathews J, Spencer RP. Splenectomy for splenic metastasis from carcinoma of the colon. Clin Nucl Med 1986;11: 491-492. [PubMed: 3731648]

234. Hirst AE Jr, Bullock WK. Metastatic carcinoma of the spleen. Am J Med Sci 223:414-417, 1952. [PubMed: 14914750]

235. Warren S, Davis H. Studies on tumor metastasis: V. The metastases of carcinoma to the spleen. Am J Cancer 21:517-533, 1934.

236. Marymont JH, Gross H. Patterns of metastatic cancer in the spleen. Am J Clin Pathol 1963;10:58-63.

237. Harmon JW, Dacorso P. Spread of carcinoma to the spleen. Arch Pathol 1975;45:179-186.

238. Berge T. Metastasis of carcinoma with special reference to the spleen. Acta Pathol Microbiol Scand Suppl 188:1128, 1967.

239. Breitbart AS, Harris MN. Isolated metastatic breast carcinoma to the spleen. Contemp Surg 1991;38:42.

240. Schoket E, Dembrow VD. Splenic metastases from melanoma of the nasal mucosa. Am J Surg 16:949-953, 1963.

241. Jorgensen LN, Chrintz H. Solitary metastatic endometrial carcinoma of the spleen. Acta Obstet Gynecol Scand 679:91-92, 1988.

242. Klein B, Stein M, Kuten A. Splenomegaly and solitary spleen metastasis in solid tumors. Cancer 60:100-102, 1987. [PubMed: 3581023]

243. Waller RM, Fajman WA. An unusual case of an isolated, focal splenic defect demonstrated by liver-spleen scintigraphy. Clin Nucl Med 7:5-7, 1982. [PubMed: 7060295]

244. Murthy SK, Prabhakaran PS, Rao SR, et al. Unusual splenic metastases from oesophageal cancer. Indian J Cancer 28:81-83, 1991. [PubMed: 1937551]

245. Capizzi PJ, Allen KB, Amerson JR, Skandalakis JE. Isolated splenic metastasis from rectal carcinoma. South Med J 85:1003-1005, 1992. [PubMed: 1411716]

246. Mainprize KS, Berry AR. Case report: solitary splenic metastasis from colorectal carcinoma. Br J Surg 84:70, 1997. [PubMed: 9043458]

247. Indudura R, Vogt D, Levin HS, Church J. Isolated splenic metastasis from colon cancer. South Med J 90:633-636, 1997.

248. Dunbar WH, Beahrs OH, Morlock CG. Solitary splenic metastasis incidental to rectal carcinoma: report of a case. Mayo Clin Proc 44:40-45, 1969. [PubMed: 5767148]

249. Thomas ST, Fitzgerald JB, Pollock RE, et al. Isolated splenic metastases from colon carcinoma. Eur J Surg Oncol 19:485-490, 1993. [PubMed: 8405487]

250. Falk S, Stutte HJ. Splenic metastasis in an ileal carcinoid tumor. Pathol Res Pract 1989;185:238-244. [PubMed: 2798224]

251. Sharpe RW, Rector JT, Rushin JM, Garvin DF, Cotelingam JD. Splenic metastasis in hairy cell leukemia. Cancer 1993;71:2222-2226. [PubMed: 8453541]

252. Das Gupta T, Brasfield R. Metastatic melanoma: a clinicopathologic study. Cancer 1964;17:1323.

253. Meyer JE, Stolbach L. Pretreatment radiographic evaluation of patients with malignant melanoma. Cancer 1978;42:125. [PubMed: 667789]

254. Amer MH, Al-Sarraf M, Vaitkevicius VK. Clinical presentation, natural history and prognostic factors in advanced melanoma. Surg Gynecol Obstet 1979;149:687. [PubMed: 505243]

255. Balch CM, Houghton AN, Peters LJ. Cutaneous melanoma. In: DeVita VT Jr, Hellman S, Rosenberg SA. Cancer: Principles & Practice of Oncology (4th ed). Philadelphia: JB Lippincott, 1993.

256. Brown BC. Pathology of the spleen. Probl Gen Surg 1990;7:48-68.

257. Hull CC, Galloway P, Gordon N, Gerson SL, Hawkins N, Stellato TA. Splenectomy and the indication of murine colon cancer. Arch Surg 1988;123:462. [PubMed: 3348737]

258. Skandalakis LJ, Gray SW, Skandalakis JE. Splenic realities and curiosities. Probl Gen Surg 1990;7:28-32.

259. Sappington SW. Carcinoma of the spleen. JAMA 1922;78:953-955.

260. Kettle EH. Carcinomatous metastases in the spleen. J Pathol Bacteriol 1913;17:40-46.

261. Herbut PA, Gabriel FR. Secondary cancer of the spleen. Arch Pathol 1942;33:917.

262. Pollard BR. Role of the spleen in resistance to experimental tumors. Texas Rep Biol Med 1953;11:48. [PubMed: 13038712]

263. Woglam WH. Immunity to transplantable tumors. Cancer Rev 1929; 4:129.

264. Small AG, Trainin N. Kinetics of the response of spleen cells from tumor-bearing animals in an in vivo tumor neutralization assay. Int J Cancer 1976;18:813-819. [PubMed: 992909]

265. Sato M, Michaelides MC, Wallack MK. Effect of splenectomy on the growth of murine colon tumors. J Surg Oncol 1983;22:73. [PubMed: 6823129]

266. Wanebo HJ, Kennedy BJ, Winchester DP, Stewart AK, Fremgen AM. Role of splenectomy in gastric cancer surgery: adverse effect of elective splenectomy on longterm survival. J Am Coll Surg 185: 172-176, 1997.

267. Davis CJ, Ilstrup DM, Pemberton JH. Influence of splenectomy on survival rate of patients with colorectal cancer. Am J Surg 1988; 155:173. [PubMed: 3341531]

268. Meyer JD, Argyzis BF, Meyer JA. Splenectomy suppression cell activity and survival in tumor bearing rats. J Surg Res 1980;29: 527. [PubMed: 6448937]

269. Ferrer ZF. Enhancement of the growth of sarcoma 180 in splenectomized and sham operated AKR mice. Transplantation 1968;6:160. [PubMed: 5654084]

270. Mercie P, Faure I, Viallard JF, Demeaux H, Dilhuydy MS, Leng B, Pellegrin JL. [Splenic vascular occlusion in the course of pancreatic cancer]. Rev Mal Intern 2000;21:628-631. [PubMed: 10942980]

271. Warshaw AL, Chesney TM, Evans GW, McCarthy HF. Intrasplenic dissection by pancreatic pseudocyst. N Engl J Med 1972; 287:72. [PubMed: 5040037]

272. Okuda K, Taguchi T, Ishihara K, Konno A. Intrasplenic pseudocyst of the pancreas. J Clin Gastroenterol 1981;3:37. [PubMed: 7276491]

273. Byrd BF, Couch OA Jr. Pancreatitis with rupture of spleen and hemorrhagic pleural effusion. JAMA 1955;157:1112. [PubMed: 14353649]

274. Catanzaro FP, Abiri M, Allegra S. Spontaneous rupture of spleen and pleural effusion complicating pancreatitis. RI Med J 1968; 51:328. [PubMed: 5240619]

275. Nath BJ, Warshaw AL. Pulmonary insufficiency. In: Bradley EL (ed). Complications of Pancreatitis. Philadelphia: WB Saunders, 1982.

276. Frey CF, Eckhauser F, Stanley JC. Hemorrhage. In: Bradley EL (ed). Complications of Pancreatitis. Philadelphia: WB Saunders, 1982.

277. Nishiyama T, Iwao N, Myose H, Okamoto T, Fujitomi Y, Chinen M, Komichi Y, Kobayashi T. Splenic vein thrombosis as a consequence of chronic pancreatitis: a study of three cases. Am J Gastroenterol 1986;81:1193-8. [PubMed: 3788930]

278. Bradley EL. The natural history of splenic vein thrombosis due to chronic pancreatitis: indications for surgery. Int J Pancreatol 1987;2:87-92. [PubMed: 3500243]

279. Ferguson CM. Human immunodeficiency virus-related immune thrombocytopenia. Probl Gen Surg 7(1):149-150, 1990.

280. Tsoukas CM, Bernard NF, Abrahamowicz M, Strawczynski H, Growe G, Card RT, Gold P. Effect of splenectomy on slowing human immunodeficiency virus disease progression. Arch Surg 133:25-31, 1998. [PubMed: 9438754]

Copyright ©2006 The McGraw-Hill Companies. All rights reserved.
Privacy Notice. Any use is subject to the Terms of Use and Notice. Additional Credits and Copyright Information.

Leave a Reply

Time limit is exhausted. Please reload the CAPTCHA.


apply_now Pepperstone Group Limited