Throughout the past millennia, knowledge of splenic function has been elusive. The ancients considered the spleen to be essential for such diverse functions as laughter, humor, purification of the blood, and the maintenance of life. In contrast, many senior surgeons were taught that the spleen is a vestigial organ without function. Scientific reconciliation of these conflicting opinions awaited twentieth-century investigations.

These philosophical controversies had no clinical relevance until Riegner, in 1892, introduced the modern era of splenic surgery when he performed a successful splenectomy following a blunt injury. This 14-year-old construction worker fell from a scaffold and sustained a grade V splenic injury (Table 1), with portions of the spleen lying free in the peritoneal cavity. This operation helped to establish two principles. First, laparotomy with definitive control of bleeding, rather than extraabdominal compression for refractory intraabdominal bleeding, leads to a better outcome. Second, splenectomy is safe and well tolerated, thus laying to rest the ancient concept that the spleen was necessary for life.

During most of the nineteenth century, the spleen was considered an unimportant organ. Early twentieth-century authors supported that view despite data suggesting the contrary. For example, Pearce, in 1918, noted that 25% of animals undergoing splenectomy died from either peritonitis or pneumonitis; unfortunately, these deaths were thought to be unrelated to the asplenic state as reflected in the conclusion that animals survived splenectomy with “relative impunity.” Pearce also noted that splenectomy leads to eosinophilia and leukocytosis, which were of unknown significance. Shortly thereafter, Morris and Bullock documented the importance of the spleen as an immune organ. Asplenic rats, subjected to a Pasteurella bacterial challenge, did poorly when compared to their normal controls; they suggested that the spleen was important for immunity. The surgical leadership in the Western world, however, rejected these findings by concluding that fears of infection after splenectomy were poppycock; thus, routine splenectomy for even the smallest of injuries became the norm for the ensuing generation.

The seed that gave rise to our current appreciation of splenic function was planted when King and Shumacker reported two deaths in five children, who died of an overwhelming postsplenectomy infection (OPSI) after splenectomy for spherocytosis. Smith, in 1957, reported the first death from OPSI following splenectomy in an injured patient without preexisting comorbidities. Subsequent studies demonstrated that OPSI occurs in about 2% of children and 1% of adults; the mortality in the non-vaccinated patient was <50%. These findings led to a reassessment of splenic function.

The spleen at birth is small and remains immature throughout the neonatal period. During this phase, there are few lymphoid follicles and a relative absence of germ centers. Throughout childhood, the spleen slowly increases in size and reaches its maximal weight during puberty when it represents about 25% of the total body lymphoid mass. Perfusion through the mature spleen facilitates leukocyte sequestration and the production of both immunoglobulins
and antibodies to circulating antigens. This immunologic protection is thought to be mediated through the perifollicular lymphoid cells. The result is enhanced opsonization and phagocytosis of bacteria. The resultant enhancement of bacterial clearance is directed primarily toward the encapsulated Gram-positive bacteria, but also affects Gram-negative bacteria. These protective responses may also affect bacteria accessing the body by way of the respiratory route.

Once the spleen became recognized as a vital link in the immune response to infection, operative attempts at splenic salvage became fashionable. A few far-sighted surgeons, however, practiced splenic salvage before their less prescient colleagues. Zikoff, in 1897, may have performed the first splenorrhaphy; Dretzka, in 1930, published the first splenorrhaphy performed on a child. This early report by Dretzka and the subsequent report by Morganstern and Shapiro highlight the technical factors involved with achieving successful splenorrhaphy. These authors emphasized the importance of a generous incision, proper exposure, and gentle manipulation when using the open approach to splenic salvage.

Typically, in the injured patient, this involves a midline incision, although a left subcostal incision provides excellent exposure in patients who are known to have injury limited to the left upper quadrant. The actively bleeding spleen should be packed in order to obtain temporary hemostasis while full splenic exposure is accomplished. The lesser sac is entered through the greater omentum outside the arcades of the gastroepiploic vessels (Fig. 1). As this dissection is carried superiorly along the greater curvature of the stomach, the proximal branches of the left gastroepiploic vessels may need to be divided; this facilitates the dissection near the apical fat pad and the cardiophrenic ligament. Dissection of the apical fat pad helps expose and control the highest short gastric branch. Mobilization of the proximal stomach anteriorly and medially allows one to visualize the short gastric vessels coming from the superior branches of the splenic artery as these branches enter into the superior segment of the spleen. Careful dissection of these vessels permits safe division. The splenic flexure of the colon is then mobilized. Typically, there will be two (sometimes one) short vessels extending from the colonic mesentery to the inferior pole of the spleen. These are the same “aberrant” vessels that are notoriously avulsed from the splenic capsule when too much anterior and medial tension is placed on the omentum during gastric mobilization for truncal vagotomy. These vessels are always present; they should be identified and made hemostatic by coagulation or ligation prior to division.

The spleen can then be detached from its “avascular” diaphragmatic and retroperitoneal attachments, remembering that small vessels are often present in these attachments; they can be controlled by electrocoagulation. Patients with portal hypertension may have extensive collaterals in this “avascular” plane, necessitating suture ligation of the peritoneal edges. This can be achieved by dividing the retroperitoneal <2 cm from the spleen between clamps and suture ligating each side. The spleen shares in this hyperdynamic, hypertensive state, thereby, making successful splenorrhaphy unlikely in cirrhotic patients. Such patients are served best by splenectomy. When bleeding occurs, placement of packs posterior to the area of digital dissection controls bleeding and allows the operation to proceed as the spleen is mobilized. The plane posterior to both the spleen and the body and tail of the pancreas is then bluntly dissected, taking care to remain within this plane and not extend posteriorly, where one might injure the adrenal vessels or renal vessels. The pancreas with
spleen is then gently pushed anteriorly and medially; one must never pull on the spleen in an effort to lift the pancreas (Fig. 2). When the injured spleen is actively bleeding, control of hemorrhage can be achieved by compressing the splenic hilum with the fingers and thumb of the left hand while the right hand is used to continue the anterior and medial mobilization of both the pancreatic body with tail and spleen. Again, packs can be placed posteriorly in the plane that was previously occupied by these organs. When digital pressure does not control splenic bleeding, the operation will likely be hurried; this almost certainly will result in the patient requiring a total splenectomy. Therefore, this tedious and compulsive mobilization with digital hemostasis should be continued until the spleen has been fully delivered to the wound (Fig. 2).