‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ Anatomy Splenic function Hypersplenism Splenectomy Lap vs open splenectomy Outcomes Complications Splenic trauma Splenic repairs Conservative treatment

‡ The spleen is situated principally in the left hypochondriac region, but its superior extremity extends into the epigastric region; it lies between the fundus of the stomach and the diaphragm. ‡ It is the largest of the ductless glands, and is of an oblong, flattened form, soft, of very friable consistency, highly vascular, and of a dark purplish color. ‡ The normal size and weight vary somewhat. The approx size is 12cm(length) x 7cm(width) x 3-4cm(thickness) with an average weight of 150g (range 80-300g).

Tail of Pancreas -Direct contact with spleen in 30% -Otherwise within 1 cm

external or phrenic surface) is convex. and to the left. tenth. which separates it from the ninth. It is in relation with the under surface of the diaphragm. and the intervening lower border of the left lung and pleura.RELATIONS ‡ The diaphragmatic surface (facies diaphragmatica. except at its upper end. smooth. backward. . and is directed upward. and eleventh ribs of the left side. where it is directed slightly medialward.


Drawing .Visceral surface of the spleen illustrating the splenorenal ligament and the vessels contained within .

upward. and is in contact with the posterior wall of the stomach. and below this with the tail of the pancreas. It presents near its medial border a long fissure. is broad and concave. It is somewhat flattened. This is pierced by several irregular apertures. which is directed forward.‡ The visceral surface is divided by a ridge into an anterior or gastric and a posterior or renal portion. ‡ ‡ . The renal surface (facies renalis) is directed medialward and downward. termed the hilum. and is in relation with the upper part of the anterior surface of the left kidney and occasionally with the left suprarenal gland. and medialward. for the entrance and exit of vessels and nerves. is considerably narrower than the gastric surface. The gastric surface (facies gastrica).


more rounded and blunter than the anterior. and rests upon the left flexure of the colon and the phrenicocolic ligament. and is often notched. ‡ The inferior border (internal border) separates the diaphragmatic from the colic surface. ‡ The posterior border (margo posterior). especially below. triangular in shape. it corresponds to the lower border of the eleventh rib and lies between the diaphragm and left kidney. and thin. where it lies on a level with the eleventh thoracic vertebra. ‡ The anterior border (margo anterior) is free.‡ The superior extremity (extremitas superior) is directed toward the vertebral column. . ‡ The lower extremity or colic surface (extremitas inferior) is flat. it separates the diaphragmatic from the gastric surface. The intermediate margin is the ridge which separates the renal and gastric surfaces. and is generally in contact with the tail of the pancreas. sharp. separates the renal from the diaphragmatic surface.


creating folds which form the suspensory ligaments of the spleen. ‡ The splenocolic and the splenophrenic ligaments are relatively avascular . It is held in position by two folds of this membrane. The peritoneum extends superiorly. which is firmly adherent to its capsule.LIGAMENTS ‡ The spleen is almost entirely surrounded by peritoneum. ‡ The parietal peritoneum adheres firmly to the splenic capsule. except at the splenic hilum. laterally and inferiorly.

. where they meet between the spleen and stomach. the short gastric and left gastroepiploic branches of the splenic artery run between its two layers. derived from the general cavity and the omental respectively. the gastrosplenic ligament. The lower end of the spleen is supported by the phrenicocolic ligament.LIGAMENTS ‡ The splenorenal ligament runs from the anterior left kidney to the hilum of the spleen as a two layered fold in which the splenic vessels and the tail of the pancreas are invested. ‡ The other fold. is also formed of two layers.

Suspensory Ligaments Gastrosplenic Ligament Short Gastric Vessels Gastroepiploic Vessels Splenorenal Ligament Splenic Vessels Tail of Pancreas Splenocolic Ligament Phrenicocolic Ligament Phrenicosplenic ligament .

and in 82% of specimens divides into three primary branches The left gastric artery The hepatic artery The splenic artery . ‡ Arises above the body of the pancreas.BLOOD SUPPLY ‡ The celiac axis ± largest but shortest branch of the abdominal aorta: 15-20mm long.

which means that the aorta must be crossed to reach the spleen and that selective angiography is likely to be difficult at times ‡ Acounts for approximately 5% of cardiac output . and even less often a second splenic artery arises from the celiac axis. the middle colic artery. ‡ Other variations include the splenic artery originating from the Superior mesenteric artery. or the accessory right hepatic artery ‡ As a rule the splenic artery arises from the celiac axis to the right or the midline. the left gastric artery. the hepatic artery.Splenic Artery ‡ In rare instances the splenic artery originates directly from the aorta.


Am J Anat 70: 21. the short gastric branches. the left gastroepiploic artery and the terminal splenic branches ‡ Splenic arterial geography can be divided into 2 types ± Distributed or Magistral (Michels NA The variational anatomy of the spleen and splenic artery . 1942) .‡ It courses along the superior border of the pancreas and the branches include numerous pancreatic branches.

30% .Magistral -Branches originate 3-13cm from hilum -Transverse Anastomoses ± why embolization / clipping may fail -Pancreatica Magna ± embolic debris from angio may cause pancreatitis .

Distributed -Branches originate within 3.70% .5 cm of hilum -L Gastroepiploic artery± Most varied of splenic branches (72% arise several cm from splenic artery proximal to terminal branching .

red pulp ( 75%) and white pulp ‡ A narrow marginal zone exists at the interface of the red and white pulps .HISTOLOGY ‡ The spleen is invested in a fibroelastic capsule from which trabeculae pass into the parenchyma. branching to form a trabecular network that subdivides the gland into small compartments. ‡ Parenchyma has 2 main elements : .

helper lymphocytes Intermediate follicular zone is the B. the Cords of Billroth macrophages. plasma cells.lymphocyte zone µRed pulp¶ consists of large thin walled sinuses that are filled with blood and separated by thin plates / cords of lymphoid tissue. lymphocytes.Pseudo-Segmental Blood Supply µWhite pulp¶ contains end arterioles surrounded by sheaths of densely packed small lymphocytes subdivided into central. granulocytes. intermediate and peripheral marginal zones Central zone -> CD4+T. red blood cells and platelets .

properdin -T-Cells Red Pulp (75% of parenchyma) -Phagocytosis -³Pitting´ damaged RBCs. WBCs -Opsonized Pathogen Clearance . IgG. tuftsin.White Pulp -Opsonins ± IgM.

Splenic Function .


and Destroying blood cells ‡ Results in reduction of blood cell counts Bone marrow function usually normal Sometimes by sequestration alone Cytopenia corrected following splenectomy . Sequestering.HYPERSPLENISM ‡ ³Hematologic effects of splenomegaly´ ‡ Hypersplenism is a disorder which causes the spleen to rapidly and prematurely destroy blood cells. ‡ Enhanced capacity of the enlarged spleen: Pooling.

weakness. . legs and feet. tuberculosis. and ulcerations of the mouth. rheumatoid arthritis. ‡ Secondary hypersplenism results from another disease such as chronic malaria. or polycythemia vera ‡ Symptoms of hypersplenism include easy bruising. fever. and from the gastrointestinal or urinary tracts.Causes and symptoms ‡ Primary hypersplenism ± caused by problem with the spleen itself. Individuals may also bleed unexpectedly and heavily from the nose or other mucous membranes. easy contracting of bacterial diseases. heart palpitations.

Hypersplenism±Many Etiologies .

Hypersplenism Platelet Sequestration Healthy Hypersplenism PALPABLE SPLEEN IS AT LEAST TWICE ITS NORMAL SIZE .

but an adjunctive therapy ‡ Failed medical management ‡ Reduce number of required transfusions ‡ Pain or abscess secondary to splenic infarction (sickle cell. Platelets Temporize underlying condition ‡ Rarely curative. thalassemia) Staging Procedure .Hypersplenism ‡ Why Splenectomy in Hypersplenism? Treat Splenomegaly ‡ Compressive symptoms ‡ Risk for splenic injury if active Improve blood counts ± RBC¶s.

O¶Brien Victim stabbed in LUQ while committing a rape 1826 .Quittenbaum. 1st elective splenectomy Portal HTN .SPLENECTOMY 1549 ± First reported by Zacarello in Italy 1816 ± First in North America.

7% in 49 patients with leukemia ‡ 1916 ± Kaznelson reports good results for thrombocytopenic purpura 1952 ± OPSS reported 1962 ± Christo in Brazil: Splenic salvage prevents OPSS 1991 ± Laparoscopic splenectomy reported by four different groups ‡ ‡ ‡ .‡ 1866 ± Bryant. 1st splenectomy for leukemia ‡ 1908 ± Johnson reports mortality of 87.


DVT prophylaxis Antibiotics .2 ± 4 units ? Platelet transfusion Parental corticosteroids periopratively if on steroids.1st generation cephalosporin NGT after intubation .PATIENT PREPARATION ‡ ‡ ‡ ‡ ‡ ‡ Counseled Vaccination .at least 7-14 days prior Transfusion if needed to achieve Hb >10g/dl Cross match .

multiple prior operations. . portal hypertension. ‡ Other situations where OS may be favored include massive splenomegaly. extensive splenic radiation. open splenectomy (OS) is still widely practiced. ‡ The most common indication for OS is traumatic rupture of the spleen. ascites. and possibly splenic abscess.SPLENECTOMY TECHNIQUES ‡ Although laparoscopic surgery (LS) is recognized as the standard approach for normosplenic patients requiring surgery.

and even pregnancy. .g.Laparoscopic Splenectomy ‡ LS has steadily surpassed OS as the approach of choice for most elective splenectomies . ‡ Several large series have shown the benefits of LS to patients with normal sized spleens ‡ Recent literature supports LS in expert hands in situations that were previously reserved for OS e. morbid obesity. multiple prior surgeries. splenomegaly.

or Sarcoid ‡ ‡ ‡ ‡ ‡ ‡ .Laparoscopic Splenectomy Indications ‡ ‡ ‡ ‡ ‡ ITP Most Common Hereditary Spherocytosis TTP Autoimmune Hemolytic Anemia Lymphoma Hodgkin¶s Dz (Staging) Non-Hodgkin¶s (hypersplenism) Leukemia (hypersplenism) Hemoglobinopathies Thalassemia. Sickle Cell ‡ ‡ ‡ ‡ Splenic Abcess Splenic Cyst Gaucher¶s Dz (storage) Felty¶s Syndrome RA neutropenia Splenomegaly Myelofibrosis Extramedullary hematopoiesis Splenic Infarct AIDS Thrombocytopenia Hypersplenism Portal HTN. SLE.


Lap vs Open Splenectomy .

Laparoscopic Splenectomy .


Laparoscopic Splenectomy ‡ Patient Positioning Usually right lateral decubitus position Anterior approach for large spleens(>25-30cm) ‡ Trocar placement lateral ± 3 or 4 ports anterior ± 5-6 ports .



the spleen is placed in a nylon or freezer bag. Short gastrics divided by individual application of clips. After retracting the lower pole of the spleen. Once excised. the splenic hilum is then accessible to clips or stapling device. resulting in medial mobilization of the spleen. The spleen is then morcellated and extracted piecemeal ‡ ‡ ‡ ‡ . the neck of which is pulled through one of the trocar sites. A thorough search is made for accessory spleens. endovascular stapler or haemostatic energy sources.Laparoscopic Splenectomy Procedure: ‡ The stomach is retracted medially to expose the spleen. Splenocolic ligament divided as are the lateral peritoneal attachments. Any accessory spleens found should be removed immediately as they are considerably harder to locate once the spleen is removed and the field is stained with blood.


RTA¶s. bicycle crashes.SPLENIC TRAUMA ‡ Most common indication for laparotomy following blunt trauma ‡ MVA¶s most common source ‡ Other mechanisms include: motorcycle crashes. and sports. compression. falls. ‡ Splenic injuries are produced by rapid deceleration. energy transmission through the posterior lateral chest wall over the spleen. or puncture from adjacent rib fractures ‡ Rapid deceleration results in the spleen continuing to move forward while tethered at the point of attachment .

. ‡ Injuries cause by assaults or falls are usually the result of direct blows over the lower chest wall. ‡ Because of this extensive supply. even small lacerations or capsular avulsions yield substantial hemorrhage.Splenic Trauma cont¶d ‡ Injuries produced by decelerating forces result in capsular avulsion along the various ligamentous attachments and linear or stellate fractures of varying depths. energy transfer is relatively efficient. ‡ Because of the solid structural characteristics and density. The splenic artery divide into several segmental vessel supplying the poles and midportion. ‡ The spleen receives about 5% of the cardiac output. and these vessels divide into 2nd and 3rd order vessels that course transversely within the spleen. with transmission of energy resulting in splenic lacerations.

Splenic Trauma ‡ Most frequently injured intraabdominal organ in blunt trauma ‡ Fractured left ribs and pulmonary contusion most common associated Injuries ‡ Hematuria most common nonspecific finding Renal injury .

000 RBC¶s/HPF Food Particles Very Sensitive Many False +¶s ‡ Intermediate: CT Scan ‡ New: FAST Looking for Blood only NOT looking for organ detail! Wait for foley: may get more detail if bladder full .Diagnosis ‡ Old: Peritoneal Lavage >100.Splenic Trauma .

intraparenchymal <5 cm in diameter Capsular tears. intraparenchymal hematoma >5cm or expanding >3cm parenchymal depth or involving trabecular vessels Laceration involving segmental or hilar vessels 4 producing major devascularisation (>25% of spleen) Completely shattered spleen Hilar vascular injury that devascularises spleen 5 5 3 3 2 2 2 Laceration IV V Laceration Laceration Vascular . 1-3cm parenchymal depth. >50% surface area or expanding: ruptured subcapsular or parenchymal hematoma. does not involve a trabecular vessel Subcapsular.American Association for the Surgery of Trauma (AAST) splenic injury scale (1994) Grade Injury description Score I II Hematoma Laceration Hematoma Laceration III Hematoma Subcapsular <10% surface area Capsular tear <1cm parenchymal depth Subcapsular 10-50% surface area.

Splenic Trauma
‡ Treatment has come full circle 1890¶s ± Nonoperative Management 1900¶s ± Operative Management 1970¶s-1990¶s ± Nonoperative Management ‡ OPSS ± Not as likely following Trauma Partial Splenectomy Accessory Spleens Splenosis


Spleen Removal (Splenectomy). This exhibit illustrates the splenectomy procedure in which the spleen is removed. The first image shows the midline incision in the abdomen through which the damaged spleen is exposed. The second image depicts the mobilization of the lacerated spleen and ligation (binding) of the splenic vessels which will be clipped. An enlargement of the removed spleen is pictured off to the side to highlight the specific injuries.

Splenic repairs ‡ Splenic conservation historically performed in Children: ‡ .More likely to develop OPSS.Capsule more amenable to repair (adults tear) ‡ -Lower arterial pressure in splenic arterial system ± easier hemostasis . saving splenic function protective ‡ .




SPLENECTOMY OUTCOMES Results in characteristic changes to blood composition. These include : appearance of Howell Jolly bodies and siderocytes Leukocytosis ± WBC raises within one (1) day and may remain elevated for several months Increased platelets occur wihin 2 days (but may not peak for several weeks) .

a rise in hemoglobin levels to above 10g/dl without the need for transfusion signifies a successful response to splenectomy successful in 60-80%of cases For patients with hereditary spherocytsis the success rate is 90-100% ‡ .HEMATOLOGIC OUTCOMES ‡ ‡ Divided into initial and long term responses: For thrombocyopenia : Initial response : rise in platelets within several days Long term response is defined as a platelet count > 150 000/ml more that 2 months after surgery with out medication LS long term response obtained in 85% OS has success rate of 60-90% For chronic hemolytic anemias.

COMPLICATIONS ‡ Classified as : Pulmonary Hemorrhagic Infectious Pancreatic Thromboembolic Functional .

Most common (16% of patients) Pleural effusions and pneumonia (10%) Hemorrhagic Usually occurs intra op and corrected then. but may present as a subphrenic hematoma Transfusions have become less frequent with LS and depend on the indication for splenectomy Across all elective cases ± need for transfusion occur in 3-5% of cases .Pulmonary : Left lower lobe atelectasis .

Infectious : Subphrenic abscess (usually associated with drain placement) OPSS (see below) Pancreatic Pancreatitis Pseudo cyst formation Pancreatic fistula These may all be due to trauma to the pancreas especially to the tail during the dissection of the splenic hilum .

myeloproliferative disorders and splenomegaly. portal vein thrombosis.‡ Thromboembolic: eg. deep vein thrombosis Occurs in 5-10% of patients and DVT prophylaxis is recommended The risk is even higher in patients with hemolytic anemia. Functional: Persistence of hyperspleenism (unresected accessory spleen) .

a.k. Certain factors however do influence the degree of risk: Age : Younger patients have greater risk Underlying disease : Risk with underlying immunodeficiency > thalassemia > sickle cell anemia > traumatic splenectomy Time since splenectomy : Recent splenectomy has greater risk than many years post-operatively with 80% of cases occurring within 2 years of splenectomy .OVERWHELMING POST. OPSS. OPSI RISK: ‡ All post splenectomy patients have an increased risk of overwhelming bacterial infection.SPLENECTOMY SEPSIS a.

Martha¶s Vineyard. influenza (2030%). Nantucket.Pathogens: ‡ The most common cause of overwhelming post-splenectomy sepsis is S. however all of the pathogens listed below can be a source of serious infection in these patients: · · Encapsulated bacteria: S. H. pneumoniae. (the latter usually acquired from a dog bite) · Malaria · Babesia (acquired from ticks in the Eastern seaboard particularly Cape Cod. meningitidis (10-20%) S. pneumoniae. pneumoniae (50-60%). and Capnotcytophagia sp. aureus · Numerous gram negatives including E. K. N. Block Island) . Salmonella sp. coli.

neck stiffness. petechiae ‡ Meningitis ± Headache.Clinical manifestations ‡ Fever ± Any fever must be viewed as possible PSS ‡ Bacteremia ‡ Coagulopathy ± Purpura. respiratory failure ‡ GI symptoms ± Nausea. vomiting. seizure ‡ Respiratory symptoms ± Cough. dyspnea. diarrhea. GI bleeding ‡ Shock .

Labs ‡ ‡ ‡ ‡ ‡ ‡ CBC Blood smear DIC profile Lumbar puncture CXR Blood culture .

influenzae ± General suggestion ‡ Ceftriaxone + Vancomycin ‡ Levofloxacin + Vancomycin ‡ Life-support measures ± ± ± ± H/D or CVVH for ARF Ventilator Inotropic agents Fluid .Management ‡ Broad-spectrum antibiotics ± Based on expert opinion ± Must cover: ‡ penicillin-resistant pneumococcus ‡ beta-lactamase producing H.

Trauma) Operative splenorrhaphy Intentional splenosis when appropriate ‡ Immunization ± Timing ‡ 14 days before splenectomy ‡ 14 days after splenectomy (not immediately) ± Pneumococcal vaccine ‡ PPV-23 for adults ‡ PCPV-7 for children and some adults ± ± ± ± Haemophilus B vaccine Meningococcal vaccine Re-immunization Other vaccines: influenza vaccine .Prevention ‡ Avoid unnecessary splenectomy Splenic salvage highly desirable when safe Selective nonoperative management (i.e.

It has not been well studied in older patients and provides protection against only 7 serotypes. . 2) a 7-valent Protein-Conjugated Vaccine. This vaccine is immunogenic only in those > 2 years of age and provides protection against the greatest number of clinically relevant serotypes. PPV23 (Pneumovax®). PCV-7 (Prevnar®). which is immunogenic and safe beginning at 6 weeks of age.Vaccinations ‡ There are currently 2 licensed pneumococcal vaccine: ‡ 1) a 23-valent Pnemococcal Polysaccharide Vaccine.

followed > 2 months later by a dose of PPV-23. Quadrivalent conjugated meningococcal vaccine should be given to all asplenic individuals > 2 years of age. Hemophilus influenza vaccine should be given once to all individuals > 2 years of age and at the time of routine vaccination for younger children. A booster PPV23 should be given approximately 5 years after the initial vaccine/series. 6 and 12-15 months of age.Vaccination: Recommendations Current recommendations for this use of these vaccines post splenectomy are as follows: ‡ Children less than 2 years of age should receive PCV-7 at the usual ages recommended for children their age: 2. Children 2 to 5 years of age should receive two doses of PCV-7 given 2 months apart. ‡ ‡ ‡ ‡ ‡ . 4. Older children and adults should receive the PPV23. These children should be given PPV-23 at 2 years of age.

o. (less than 5 years. b.d. ‡ The patients who are most likely to benefit from prophylaxis are: Children < 5 years of age. p. so it¶s efficacy is currently presumed to be lower. Those with an underlying immunodeficiency in addition to splenectomy ‡ Regimens for children: Penicillin G : Pediatrics: 250 mg. In addition. No data are available in adults and antibiotic prophylaxis is generally not recommended this population . Resistance to penicillin (and other antibiotics) is a growing concern. allergy to the penicillins should be assessed carefully. Alternatives: Amoxicillin: Pediatrics: 20mg/kg/day divided b.i.d.Prophylactic Antibiotics The only regimen which has been studied is penicillin prophylaxis for patients with functional asplenia from sickle cell anemia. b. 125 mg p.o.) . As there are currently no ideal second line oral agents. compliance with an indefinite daily regimen is extremely difficult.i.d. Individuals who have had splenectomy within the past year.

Post-Splenectomy Sepsis * Pre-op for distal pancreatectomy in case splenectomy performed .

consider angiography .NONOPERATIVE MANAGEMENT ‡ With careful patient selection. success rate now approaches 95% (85-95%) Hemodynamic stability No contrast µpooling¶ on CT No other intraabdominal injuries requiring laparotomy ‡ Follow frequent serial vital signs and H/H Treat persistently falling RBC with pRBC¶s Rebleeding most likely within 1st 48 hours Likely failure if patient requires • 2 u pRBCs If still falling after 2u. consider angio for embolization If hypotension develops.

No need for repeat CT scan if H/H and vitals stable Grade III: CT¶s on case-by-case basis Consider U/S for monitoring if necessary Contact Sports: Complete resolution on CT required before can return to activity ‡ 2-5% of patients treated nonoperatively will develop parenchymal infarction or infection .Nonoperative Management ‡ Follow-up CT scans rarely necessary Indicated for falling BP or H/H during observation Grade I-II: rarely show progression of lesion or other complications on CT.

Nonoperative Management .

Nonoperative Management ‡ Delayed Rupture 75% occur within 2 weeks in several series ‡ Hematoma liquifying? Can occur anytime! (1 month ± years) Actual incidence of delayed rupture very low Need to inform patients of this prior to Dischage .

Failure of nonoperative management of Blunt Splenic Injury ‡ Increasing or persistent fluid requirements to maintain normal hemodynamic status ‡ Failed angioembolization of arteriovenous fistula / pseudoaneurysm ‡ Transfusion requirement to maintain hematocrit and hemodynamic stability ‡ Increasing hemoperitoneum associated with hemodynamic instability ‡ Peritoneal signs/rebound tenderness .

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