INTRODUCTION
The spleen provides important phagocytic clearance of senescent red cells and platelets as well as entrap- ment and destruction of encapsulated bacteria, e.g., Streptococcus pneumoniae and Niseria meningococ- cus. This normal clearing mechanism becomes path- ological when target red cells or platelets are seen as abnormal by the spleen or when increasing splenic mass sequesters or destroys otherwise normal cells.
In childhood, most commonly, congenital spherocy- tosis, sickle cell disease and auto-immune haemolyt- ic anaemia can precipitate acute haemolytic crises, profound anaemia and jaundice as well as a chronic compensated anaemia from splenic hyperfunction.
Idiopathic thrombocytopenic purpura (ITP) sec- ondary to splenic platelet destruction manifests as petechiae, bruising and, rarely, non-active overt bleeding, e.g., mucous membrane bleeding. Giant splenomegaly can produce combinations of throm- bocytopenia, anaemia and possibly leucopenia.
Infiltrated processes such as lipid deposition disor- ders, e.g., Gaucher’s disease and malignancy such as Hodgkin disease or juvenile chronic myeloid leukae- mia and portal hypertension, can create enormous splenic enlargement, hyperfunction and risk of rup- ture from minor trauma
Splenectomy will reverse some of the above adverse consequences but at the cost of thrombocy- tosis and increased senescent red cells (Howell-Jowel bodies on blood smear). With loss of efficient clear-
ance of encapsulated bacteria comes an increased risk of overwhelming post-splenectomy infection (OPSI). In general OPSI is a small risk when com- pared with the pathological effects of the spleen. In the presence of a dysfunctional reticuloendothelial system, e.g., immunosupression, malignancy, radia- tion therapy or in the very young (<5 years), OPSI is seen with greater frequency. Caution is recommend- ed when considering splenectomy in the presence of these clinical states.
Pre-operative immunization is obligatory in elec- tive splenectomy. Commercial vaccinations are avail- able for pneumococcus, meningococcus and Haemophilus influenzae and ideally they should be administered at least three to four weeks pre-opera- tively if possible. Splenic preservation is therefore the surgical objective when laparotomy is needed for uncontrolled splenic bleeding secondary to abdomi- nal trauma.
Splenectomy traditionally is carried out as an open procedure. In recent years, increasingly lapar- oscopic splenectomy is becoming more widely applied, initially to small spleens and when concom- itant cholecystectomy is indicated. With experience moderate or giant spleens can be removed as a com- plete laparoscopic procedure, or as laparoscopic- assisted or hand-assisted laparoscopic splenectomy (HALS).
Peter Borzi
Figure 37.1
Splenectomy can be performed in the supine, semi- lateral or lateral positions. Except in the presence of enormous splenomegaly when there is a need to access the splenic hilum early in dissection, it is pref- erable to utilize gravity and positioning to enhance exposure by encouraging stomach, liver, colon and small bowel to fall away from the operative site. The semilateral and lateral positions with the patient supported and strapped to the operating table allow reasonable intraperitoneal positioning including reverse Trendelenberg during laparoscopic splenec- tomy. Intra-operative orogastric decompression is imperative to enhance exposure especially at the upper short gastric vessels
With elective splenectomy a transverse subcostal incision with possible extension across the midline allows good exposure and the ability to retrieve the spleen after mobilization and devascularization. Port sites for laparoscopy are somewhat variable but a more commonly used strategy is shown. The dorsal and epigastric ports may change depending on the size of the spleen. The need for other procedures such as cholecystectomy requires additional port placements. The epigastric or right-sided port may be extended to allow the insertion of a hand-assisted device for HALS.
Figure 37.2
Knowledge of the anatomical attachments and vas- cular anatomy is essential for completing an uncom- plicated splenectomy. In particular, the splencolic, splenorenal and phrenosplenic ligaments maintain splenic attachment to the posterior abdominal wall and diaphragm. The gastrosplenic ligament above and the gastrocolic ligament below cover the omen- tal bursa, the distal pancreas and splenic vessels.
Initial release of the phrenocolic and splenocolic ligaments allow the splenic flexure and adjacent transverse colon to fall away from the inferior splen- ic pole. Extending this dissection superomedially, one may encounter the left gastro-epiploic artery before entering the lesser sac. Division of the lower short gastrics creates a window onto the distal pan- creas and allows isolation of the splenic artery and vein in its more accessible and tortuous distal seg- ment before entering the splenic hilum. These vessels can be tied or clipped in continuity more proximally if hilar dissection seems difficult, particularly when dealing with an enormous spleen. Continued release of the upper short gastrics completes the anterior dissection.
Medial retraction of the spleen gives good expo- sure to the splenorenal ligament and the embedded tail of the pancreas. This posterior mobilization is continued with release of the phrenosplenic liga- ment. In this stage of mobilization, the spleen can be retrieved from the splenic bed onto the abdominal wall for closer inspection of the pancreatic tail and vascular pedicle.
With laparoscopic splenectomy, splenic mobiliza- tion usually progresses with a similar anatomical dissection. Following complete release of the short gastric vessels, the dissection returns to detachment of the splenorenal ligament inferiorly only. This allows access to the retropancreatic and hilar plane passing superiorly above the pedicle through the posterior peritoneum of the upper lesser sac. The splenic pedicle is then isolated on all sides leaving the upper splenorenal and phrenosplenic ligaments intact gives better stability and controlled exposure to the pedicle than a floppy and totally mobilized spleen. Early ligation of the splenic vessels above the pancreas is preferable if hilar exposure difficulties are expected, but it is generally not manditory.
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Dorsal retraction port Retrieval
Visualization Working port
Figure 37.1
Phrenocolic ligament Short gastric arteries and veins
Splenic artery and vein Splenorenal ligament Gastrosplenic ligament
Phrenocolic ligament
Figure 37.2
Figure 37.3
The prevalence of accessory spleens at the time of splenectomy has been variably reported to occur between 10 and 31%. Greater than 90% occur in the supra-colic compartment in and around the splenic hilum. In particular, they are found along the line of the distal splenic artery and adjacent hilum, and the gastrosplenic and splenorenal ligament, as well as adjacent to the greater omentum. After entering the abdominal cavity, these sites of accessory spleniculi
need to be sought out early. At splenic mobilization, again one needs to be observant and remove any accessory splenic tissue encountered. This will avoid possible recurrent haemolysis or thrombocytopenia at a later stage resulting from hypertrophy of the spleniculi.
In most patients (63.3%), there is only one acces- sory spleen present, with 17% having three or more to find.
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Figure 37.3
Figure 37.4
In the presence of a traumatic splenic injury with continuing uncontrolled haemorrhage, rapid mobil- ization and isolation of the pedicle is the priority to reduce continued blood loss and maximize the chance of splenic preservation. The incision may need to be modified depending the possibility of other visceral injuries. After rapid entry into the per- itoneal cavity, large clots and free blood are removed and air is introduced into the left subphrenic space from which often the spleen becomes more mobile descending closer to the wound. The splenic mass and fossa is packed with surgical sponges. With medial retraction of this splenic mass, lateral inci-
sion of the splenorenal and upper phrenosplenic lig- aments superiorly and medially allows greater mobility. Delivery of the inferior splenic pole into the wound can achieve progressive retrieval of the spleen onto the anterior abdominal wall taking care not to avulse the upper short gastric vessels or dam- age the splenic flexure. In this position the potential for splenic salvage can be assessed. Polar devascular- ization may be required or direct suture with haem- ostatic gauze and/or omental plug may be necessary to preserve the integrity of functioning splenic tis- sue.
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Figure 37.5
Early splenic devascularization by splenic vessel liga- tion through the lesser sac is generally considered safe practice in elective splenectomy and giant sple- nomegaly, or where there is expected dense dia- phragmatic and gastric adherence to the spleen.
Alternatively, initial anterior and posterior ligamen- tous splenic release and subsequent pedicle ligation can be applied also in the setting of elective splenec- tomy but is definitely indicated in the presence of splenic trauma. Laparoscopic splenectomy can be performed by either above methods with the polar vessels either divided individually with clips or suture ligation as well as with a linear stapling device
after initial mobilization of the tail of the pancreas.
Care must be taken to avoid splenosis during splenic retrieval, particularly in the presence of haemolytic disorders. Laparoscopically, the mobilized and devascularized spleen is placed in a sturdy, impermeable bag with the open end delivered through the retrieval port site. The wound edges are protected while the specimen is fragmented and removed. Devices such as Endocatch II (Tyco Healthcare, Mansfield, MA, USA) allow somewhat easier insertion of the spleen into the retrieval pouch.
Figure 37.4
Figure 37.5
CONCLUSION
Depending on the size of the spleen, the circum- stances at the time of removal and the need for con- comitant cholecystectomy, post-operative paralytic ileus from the intraperitoneal and retroperitoneal dissection may be expected. Nasogastric decompres- sion during the peroperative period may need to be extended for 24–48 h post-operatively. Persistent ileus and continuing vomiting raises the suspicion of a possible pancreatic injury. Slow mobilization and inadequate diaphragmatic movement predisposes to left lower lobe pulmonary collapse. Subphrenic col- lections can similarly attract a sympathetic pleural effusion and pulmonary infection. Finally, injury to the stomach, although very uncommon, can evolve where extensive adhesions between the greater curve of the stomach and an inflammatory spleen are encountered.
OPSI should be minimized by pre-operative immunization, intra-operative and continued post- operative antibiotic prophylaxis. In the long term,
any procedures such as dental, gastrointestinal or genitourinary surgery that increases the risk of potential sepsis needs antibiotic prophylaxis for the duration of the operation and immediate convales- cence. Rebound thrombocytosis is generally not of clinical concern in childhood in the presence of pre- operative ITP. In more than 90% of cases, it would be expected to achieve complete reversal of symptomat- ic thrombocytopenia and return of the platelet count to the normal range or above. Unfortunately, in the presence of more non-specific haemolytic disorders, 60–70% will recover with the majority of the rest having some transient recovery of platelet count and with bleeding tendency remaining subclinical.
Clinically significant recurrent thrombocytopenia needs further evaluation for missed accessory spleens. Contrast computed tomography or red cell labelled-isotope scans are suggested with considera- tion being given to a second-look laparotomy or laparoscopy being undertaken.
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SELECTED BIBLIOGRAPHY
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King H, Shumacker HB Jr (1952) Splenic studies. 1.
Susceptibility to infection after splenectomy performed in childhood. Ann Surg 136 : 239–242
Poulin EC, Thibauly C (1993) The anatomical basis of laparos- copic splenectomy. Can J Surg 36 : 484–488
Rescorla FJ (2002) Laparoscopic Splenectomy. Semin Pediatr Surg 11 : 226–232
