AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Splenic anatomy and function

The spleen is a functionally diverse organ with active roles in immunosurveillance and hematopoiesis. A normal spleen weighs 150 g, is approximately 11 cm in craniocaudal length, and is not easily palpable. Spleens that are prominent below the costal margin typically weigh 750-1000 g. Spleens weighing 400-500 g indicate splenomegaly, and some authors consider spleens weighing more than 1000 g to indicate massive splenomegaly. Poulin et al define splenomegaly as moderate if the largest dimension is 11-20 cm and severe if the largest dimension is greater than 20 cm.

In many instances, the spleen enlarges as it performs its normal functions. The 4 most important normal functions of the spleen are (1) clearance of microorganisms and particulate antigens from the blood stream; (2) synthesis of immunoglobulin G (IgG), properdin (ie, an essential component of the alternate pathway of complement activation), and tuftsin; (3) removal of abnormal red blood cells (RBCs); and (4) embryonic hematopoiesis in certain diseases.

Pathophysiology

Many of the mechanisms of splenic enlargement are exaggerated forms of normal spleen function. While a wide variety of diseases are associated with enlargement of the spleen, 6 etiologies of splenomegaly are considered primary, including (1) immune response work hypertrophy such as in subacute bacterial endocarditis or infectious mononucleosis; (2) RBC destruction work hypertrophy such as in hereditary spherocytosis or thalassemia major; (3) congestive such as in splenic vein thrombosis or portal hypertension; (4) myeloproliferative such as in chronic myeloid metaplasia; (5) infiltrative such as in sarcoidosis and some neoplasms; and (6) neoplastic such as in chronic lymphocytic leukemia and the lymphomas. Miscellaneous causes of splenomegaly include trauma, cysts, hemangiomas, metastasis, giant abscess, and certain drugs (eg, RhoGAM).

Frequency

United States

Two large series report the presence of a palpable spleen in 2% and 5.6% of patients. An enlarged or palpable spleen is not necessarily of clinical significance. Certain individuals with broadly splayed costal margins have readily palpable, but small, spleens.

International

Tropical splenomegaly syndrome has the highest predilection for indigenous persons and visitors of the malarial belt in tropical Africa (see Sex).

Mortality/Morbidity

• Morbidity and mortality principally stem from associated disease states or surgical procedures, rather than from the splenomegaly itself. The rates for morbidity and mortality are highly variable and relate to the presence or absence of comorbidities, hemorrhage, and organ failure.
• Patients with enlarged spleens are more likely to have splenic rupture from blunt abdominal or low thoracic trauma. These patients are unlikely to undergo nonoperative management of their splenic injury or splenic salvage maneuvers because their spleen is abnormal with regard to architecture, capsule tensile strength, and, commonly, hemostatic function.

Race

• No race predilection is recognized for splenomegaly. However, note that African American persons may have hemoglobin SC disease, a disorder related to sickle cell disease. Unlike sickle cell disease that results in a small, autoinfarcted spleen, patients with hemoglobin SC disease may have splenomegaly that accompanies their pigment gallstones.

Sex

• Tropical splenomegaly syndrome (or hyperactive malarial syndrome) has a female-to-male ratio of 2:1. Otherwise, no sex predilection is documented for splenomegaly.

Age

• No age predilection is recognized for splenomegaly. Nonetheless, the capsules of older spleens are much thinner than younger counterparts. The combination of capsular thinning with increased spleen weight and size makes splenic injury more common in elderly persons. These factors account for the increased likelihood of splenectomy for trauma in this subgroup.

CLINICAL

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History

The most common history is mild abdominal pain that is vague in nature. Increased abdominal girth is less common. Early satiety from gastric displacement occurs with massive splenomegaly. Associated symptoms or signs may include the following:

• Febrile illness (infectious)
• Pallor, dyspnea, bruising, and/or petechiae (hemolytic process)
• History of liver disease (congestive)
• Weight loss, constitutional symptoms (neoplastic)
• Pancreatitis (splenic vein thrombosis)
• Alcoholism, hepatitis (cirrhosis)

Physical

Spleen size is not a reliable guide to splenic function, and palpable spleens are not always abnormal. Patients with chronic obstructive pulmonary disease and low diaphragms commonly have palpable spleens. In one study, 3% of college freshmen had palpable spleens; an additional study showed that 5% of hospitalized patients with normal spleens based on scan results were thought to have palpable spleens by their physicians.

• Examination should include palpation with the patient in the supine and right lateral decubitus position, with knees up and hips flexed. Apply light fingertip pressure as the patient slowly inspires. The use of the reverse Trendelenburg position may aid in bringing the spleen into contact with the examiner's fingers. This is especially helpful in patients with morbid obesity.
• Additional signs that identify possible etiologies of splenomegaly include the following:
• • Signs of cirrhosis (eg, asterixis, jaundice, telangiectasias, gynecomastia, caput medusa, ascites)
  • Heart murmur (endocarditis, congestive failure)
  • Jaundice
  • Scleral icterus (spherocytosis, cirrhosis)
  • Petechiae (any cause of thrombocytopenia)

Causes

The causes of splenomegaly are diverse, but they may be conveniently grouped into the following categories:

• Inflammatory splenomegaly: This is acute enlargement of the spleen that develops in association with various infections or inflammatory processes and results from an increase in the defense activities of the organ. The demand for increased antigen clearance from the blood may lead to increased numbers of reticuloendothelial cells in the spleen and stimulate accelerated antibody production with resultant lymphoid hyperplasia.
• Hyperplastic splenomegaly: In this setting, splenomegaly is thought to reflect work hypertrophy resulting from the removal of abnormal blood cells from the circulation (either cells with intrinsic defects or cells coated with antibody) or, in some cases, as the result of extramedullary hematopoiesis (ie, myeloproliferative disease).
• Congestive splenomegaly: This condition develops as a result of cirrhosis with portal hypertension, splenic vein occlusion (thrombosis), or congestive heart failure (CHF) with increased venous pressure.
• Infiltrative splenomegaly: In this setting, splenomegaly is the result of engorgement of macrophages with indigestible materials (eg, Gaucher disease, amyloidosis, metastatic malignancy).
• Infectious: Splenic filtering of blood-borne pathogens, especially encapsulated organisms, may lead to abscess formation. Because many splenic abscesses may be indolent in presentation, spleen size may be increased as the abscess enlarges. This is a relatively uncommon but important process to recognize and treat.

DIFFERENTIALS

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Other Problems to be Considered

Symptomatic HIV infection
Leukocyte disorders
Trypanosomiasis
Immune hemolytic anemias
Angioimmunoblastic lymphadenopathy
Drug reactions with serum sickness syndromes
Splenic vein obstruction
Congestive heart failure
Banti disease
Gaucher disease
Niemann-Pick disease
Mucopolysaccharidosis
Hyperlipidemias
Lymphomas
Histiocytosis X
Idiopathic splenomegaly
Ovalocytosis

WORKUP

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Lab Studies

• Perform a CBC count with platelet count.
• The term hypersplenism describes some of the sequelae often observed with splenomegaly. Criteria for a diagnosis of hypersplenism include the following:
• • Anemia, leukopenia, thrombocytopenia, or combinations thereof, plus cellular bone marrow, splenomegaly, and improvement after splenectomy
  • Thrombocytopenia: Approximately 30% of the total platelet mass exists as an exchangeable pool in the spleen. Increased splenic platelet pooling is the primary cause of the thrombocytopenia of hypersplenism. In patients with hypersplenism, as much as 90% of the total platelet mass can be found in the spleen. In hypersplenism, the platelet count is usually 50,000-150,000/µL.
  • Anemia: The etiology of the anemia observed in splenomegaly is the result of sequestration and hemodilution.
  • Leukopenia: Increased destruction or sequestration of leukocytes causes the leukopenia observed in splenomegaly. Leukopenia is closely related to neutropenia. Neutropenia (absolute neutrophil count <2000) is the result of an increase in the marginated granulocyte pool, a portion of which is located in the spleen. Sequestration also may play a role in the genesis of neutropenia.

Imaging Studies

• Craniocaudal measurement: A craniocaudal measurement of 11-13 cm is frequently used as the upper limit of normal for splenic size. However, because of wide variations in shape, no consistent correlation has been recognized between the spleen's length and its overall volume, as has been determined for other organs (eg, kidney).
• Computed tomography
• • The underlying histologic anatomy of the spleen largely determines its characteristic appearance on abdominal CT scan images. On unenhanced CT scan images, the spleen has an attenuation similar to that of the liver, approximately 40 henry (H). Normally, the liver and spleen densities are within 25 H on dynamic contrast-enhanced scan images.
  • A CT scan remains the most useful preoperative investigation to measure splenic volume; to exclude lymph nodes at the splenic hilum; and to detect accessory spleens, splenic abscess, and perisplenitis.
  • Findings that indicate radiologic distinction between benign and malignant lesions are inconsistent and cannot be relied upon to establish or refute a diagnosis of malignancy.
  • CT scan is the study of choice for identification of inflammatory changes.
  • CT scan is sensitive for detecting mass lesions, infarcts, and cysts.
• Splenoportography
• • This is used to evaluate portal vein patency and the distribution of collaterals before shunt operations for cirrhosis.
  • Findings can help identify the cause of idiopathic splenomegaly, especially in children.
• Angiography: Findings are used to differentiate splenic cysts from other splenic tumors.
• Spleen scans
• • Label erythrocytes with chromium Cr 51, mercury Hg 197, rubidium Rb 81, or technetium Tc 99m, and alter the cells by treatment with heat, antibody, chemicals, or metal ions so that the spleen sequesters them after infusion.
  • A spleen scan is a good noninvasive technique for evaluating spleen size; a close correlation exists between spleen length on scan images and spleen weight after splenectomy.
  • A spleen scan is useful for detecting space-occupying lesions in the splenic substance, evaluating loss of spleen functions, assessing for the absence of a spleen, or determining the presence of an accessory spleen.
• Ultrasound: This is a noninvasive, highly sensitive, and specific technique for the evaluation of spleen size.

Histologic Findings

When referring to an enlarged spleen as hypertrophied, the underlying cause may be hypertrophy or hyperplasia of individual cells. In specific diseases, splenic architecture is remodeled. For example, in Niemann-Pick disease, sphingomyelin and cholesterol accumulate within large foamy cells, which is characteristic of this disease. With amyloidosis involving the spleen and resulting in splenomegaly, large hyaline masses are seen as lesions occupying the white pulp space. Two forms exist, including the "sago spleen," in which amyloid deposits are limited to follicles, and the "lardaceous spleen," in which amyloid is deposited in the walls of the splenic sinusoids. In a rare complication of typhoid fever, reactive splenic vasculitis may develop.

TREATMENT

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Medical Care

Successful medical treatment of the primary disorder can lead to regression of the hypersplenism without the need for surgery.

• Chemotherapy is used for hematologic malignancy.
• Antibiotics are used for infection, with the exception of that associated with splenic abscess. This requires surgical intervention.
• Immunosuppression is used for autoimmune or inflammatory disorders, treatment of cirrhosis, and CHF.
• All patients scheduled for elective splenectomy (either diagnostic or therapeutic) should receive a pneumococcal vaccine. Also consider administering prophylaxis against Haemophilus influenzae and Neisseria meningitidis.

Surgical Care

• Splenectomy is indicated to help control or stage basic disease. These diseases can include hereditary spherocytosis, autoimmune thrombocytopenia or hemolysis, or Hodgkin disease (as part of a staging celiotomy.
• Splenectomy is also indicated for the treatment of chronic, severe hypersplenism. This can occur in conditions such as hairy cell leukemia, Felty syndrome, agnogenic myeloid metaplasia, thalassemia major, Gaucher disease, hemodialysis splenomegaly, or splenic vein thrombosis.
• Splenectomy allows treatment of hematologic disease.
• • Thrombotic thrombocytopenic purpura (TTP) is a rare hematologic disease that may manifest with fatigue, cephalgia, hematuria, petechiae, and hematomas.
  • Although the pathophysiology of TTP is still poorly understood, current opinions include endothelial damage, the presence of abnormally large factor VIII multimeric structures, and a platelet-aggregating factor.
  • TTP is a rapidly fatal disease if left untreated, although current treatment with combination corticosteroids, antiplatelet agents (eg, aspirin, dipyridamole), and vincristine have reduced the mortality rate to 20%.
  • Splenectomy was originally used in patients in whom plasma exchange failed to improve hematologic values, but this was associated with a high mortality rate. Much better results have been achieved when splenectomy is performed at the time of TTP relapse, and some authors now believe that a laparoscopic approach is safe and is associated with low morbidity and fast recovery.
  • Overall, splenectomy is effective in increasing the disease-free intervals in most patients and should be considered early in the course of chronic, relapsing TTP. However, further studies are warranted and are in progress.
• The use of open versus laparoscopic splenectomy (LS) is now a controversy that has yet to be decided.
• • The greatest danger in either approach is hemorrhage. The value of preoperative splenic artery control or embolization remains unclear, but this issue is applicable to either approach.
  • The technical feasibility of LS has been established.
  • A teaching institution offers the optimal environment for LS.
  • LS has replaced the open approach for many elective splenectomies.
  • LS is associated with reduced pain, a more rapid resumption of regular diet, shortened hospitalization, and an earlier return to normal activities.
  • The complication rate for LS remains low, with extremely rare wound or bleeding complications.
  • Problems inherent to laparoscopic treatment of splenomegaly include structural friability of the spleen, increased difficulties in the manipulation of an enlarged spleen, and exposure and access to the splenic hilum.
• Occasionally, severe thrombocytosis occurs following splenectomy, and this requires therapy to reduce the platelet count and prevent thrombotic complications.
• • This is most common in patients with massive splenomegaly from myeloproliferative disorders.
  • Monitoring the platelet count following splenectomy in patients at risk of this complication permits early detection and prompt initiation of therapy.
• An onset of fever several days following splenectomy can be due to a recrudescence of malaria.
• • This should be considered as a cause of fever in patients who have lived in areas commonly associated with malaria and in persons who abuse intravenous drugs who share needles.
  • With Plasmodium malariae infection, this may occur decades after the initial infection. Malaria from Plasmodium vivax (3-7 y) and Plasmodium falciparum (~1 y) remain active for shorter intervals after the initial infection.

Consultations

• Consultation with a hematologist is ideal prior to surgery in order to secure necessary blood products. Postoperative management does not usually require intervention from a hematologist.

Activity

• The usual postoperative activity restrictions imposed on a patient who has undergone a laparotomy or laparoscopy also apply to this patient population after splenectomy.
• Patients with uncorrected splenomegaly should be counseled to refrain from contact sports or activities that would predispose them to blunt abdominal trauma. Examples include skydiving, horseback riding, soccer, football, and ice hockey, among other activities. These restrictions reduce the likelihood that blunt injury will lead to splenic rupture and uncontrolled hemorrhage.

MEDICATION

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The goals of pharmacotherapy are to reduce morality and to prevent complications. Recall that in the absence of a functional spleen, patients have a defect in bacterial clearance due to impaired opsonization. In particular, these patients are at risk for overwhelming postsplenectomy sepsis due to infection with encapsulated organisms such as H influenzae, N meningitidis, and Streptococcus pneumoniae.

Drug Category: Vaccines

Aid in the generation of an anamnestic response to invasion with the target organism.

FOLLOW-UP

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Further Inpatient Care

• Inpatient care depends on the treatment modality used to treat the underlying cause and on the complications of that care. These therapies are not unique to splenomegaly treatment and, therefore, are not discussed.

Further Outpatient Care

• Outpatient care consists of 2 main focus areas: (1) monitoring for thrombocytosis and (2) monitoring for overwhelming postsplenectomy sepsis (OPSS).
• • Thrombocytosis may require treatment when the platelet count exceeds 1 million/µL. Multiple modalities have been used, including hydroxyurea and aspirin. No randomized, placebo-controlled studies demonstrate a better survival benefit with one therapy over the other. Whether any discrete benefit is gained by also controlling the platelet count remains unclear.
  • OPSS is a relatively rare condition that may follow a splenectomy. Infection is with encapsulated organisms (S pneumonia, H influenza, N meningitidis). Because these organisms are encapsulated and the spleen is integral in the removal of opsonized bacteria, these patients are at increased risk for unimpeded sepsis. Rapid therapy is essential because of the increased risk of death from a rapidly progressive infection. A prototype infection is meningococcemia (ie, Waterhouse-Friderichsen syndrome), which is complicated by adrenal hemorrhage and infarction.

Transfer

• Transfer is not generally required except for complications of surgery or OPSS. Patients undergoing elective splenectomy for splenomegaly may develop significant hemorrhaging during their operation if difficulty occurs controlling the splenic hilum. Such patients may require abdominal packing and transfer to a tertiary center with personnel who have expertise in angioembolization and splenic resection for splenomegaly. Such centers usually have the additional resources (eg, well-stocked blood bank, tertiary level intensive care unit) to support the organ systems in these patients. Multisystem organ failure is not uncommon following severe hemorrhage, and these patients are no exception.

Deterrence/Prevention

• The only applicable prevention is attempts at preventing droplet transfer/infection in patients with known mononucleosis and splenomegaly as an accompanying feature. This maneuver may decrease the risk of mononucleosis and splenomegaly in others, but it does nothing to aid the index patient.

Complications

• Postsplenectomy infection
• • Fulminant, life-threatening infection represents a major long-term sequela after splenectomy. Splenic macrophages play a major role in filtering and phagocytizing bacteria and parasitized blood cells from the circulation. In addition, the spleen is a significant source of antibody production.
  • Overwhelming postsplenectomy infection (OPSI), also known as postsplenectomy sepsis syndrome, begins as a nonspecific flulike prodrome that is followed by a rapid evolution to full-blown bacteremic septic shock accompanied by hypotension, anuria, and clinical evidence of disseminated intravascular coagulation, thus making this syndrome a true medical emergency. The subsequent clinical course often mirrors that of the Waterhouse-Friderichsen syndrome, with bilateral adrenal hemorrhages noted at autopsy.
  • Despite appropriate antibiotics and intensive therapeutic intervention, the overall mortality rate in older published studies of established cases of OPSI varied from 50-70%. More recent information suggests that if patients seek medical attention promptly, the mortality rate may be reduced to approximately 10%. Of those patients who die, more than 50% die within the first 48 hours of hospital admission.
  • Most instances of serious infection are due to encapsulated bacteria, such as pneumococci (eg, S pneumoniae). Pneumococcal infections account for 50-90% of cases reported in the literature and may be associated with a mortality rate of up to 60%. H influenza type B, meningococci, and group A streptococci account for an additional 25% of infections.
  • Possible OPSI involving an asplenic individual constitutes a medical emergency. The critical point in management remains early recognition of the patient at risk, followed by subsequent aggressive intervention. The diagnostic workup should never delay the use of empiric therapy. Possible choices of empiric antimicrobial agents include cefotaxime (adult dose of 2 g IV q8h, pediatric dose of 25-50 mg/kg IV q6h) or ceftriaxone (adult dose of 2 g q12-24h, pediatric dose of 50 mg/kg IV q12h). Unfortunately, some penicillin-resistant pneumococcal isolates are also resistant to cephalosporins. If such resistance is suggested, consider using vancomycin.
  • The precise incidence of OPSI remains controversial. Overall, the most reliable data related to incidence estimate approximately 1 case occurring per 500 person years of observation. Asplenic children younger than 5 years, especially infants splenectomized for trauma, may have an infection rate of greater than 10%.
  • Splenectomy performed for a hematologic disorder, such as thalassemia, hereditary spherocytosis, or lymphoma, appears to carry a higher risk than splenectomy performed as a result of trauma. A major contributing factor is the frequent existence of splenic implants or accessory spleens in traumatized patients.
  • Preventative strategies for OPSI fall into 3 major categories: education, immunoprophylaxis, and chemoprophylaxis.
    • Education represents a mandatory strategy in attempting to prevent OPSI. Asplenic patients should be encouraged to wear a Medi-Alert bracelet and carry a wallet card explaining their lack of a spleen. Patients should also be aware of the need to notify their physician in the event of an acute febrile illness, especially if associated with rigors or systemic symptoms.
    • An appropriate factor in preventing OPSI entails vaccination. This has best been defined for S pneumoniae. Unfortunately, the most virulent pneumococcal serotypes tend to be the least immunogenic, and evidence indicates that the efficacy of the vaccine is poorest in younger patients, who would be at higher risk. However, under ideal conditions in a healthy immunocompetent host, the vaccine offers a 70% protection rate. Pneumococcal vaccine should be performed at least 2 weeks before an elective splenectomy. If the timeframe is not practical, the patient should be immunized as soon as possible after recovery and before discharge from the hospital.
    • Most authorities recommend antibiotic prophylaxis for asplenic children, especially for the first 2 years after splenectomy. Some investigators advocate continuing chemoprophylaxis in children for at least 5 years or until aged 21 years. However, the value of this approach in older children or adults has never been adequately evaluated in a clinical trial.

Prognosis

• Prognosis is usually excellent and not substantially different from age-matched controls, but it is impacted by the underlying disease state rather than the presence of splenomegaly or the postsplenectomy state.

Patient Education

• Patients with splenomegaly need education regarding decreasing their risk of splenic hemorrhage. These patients must be cautioned about contact sports and other activities that may acutely increase their intra-abdominal pressure or place excessive forces on the left upper quadrant, left flank, or lateral back. This decreases the likelihood of splenic rupture in a patient with an abnormal splenic mass and capsule. The routine use of seat belts is essential while driving or riding in a motor vehicle.
• Additional education regarding the signs and symptoms of postsplenectomy sepsis cannot be overstressed. Prompt antibiotic therapy may be lifesaving.
• Preoperative and preprocedure antibiotic prophylaxis is equally important in procedures associated with a high likelihood of bacteremia.
• For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center. Also, see eMedicine's patient education article Mononucleosis.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to recognize the need for immunization after splenectomy for protection against encapsulated organisms such as H influenzae, N meningitidis, and S pneumoniae

Special Concerns

• The major special concern is antibiotic use in splenectomized patients. Those who have undergone splenectomy should receive antibiotic prophylaxis prior to undergoing procedures associated with a risk of transient or sustained bacteremia. Antibiotics should cover encapsulated organisms and organisms likely found at the operative site. This is an important maneuver to decrease the risk of overwhelming postsplenectomy sepsis.

MULTIMEDIA

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Media file 1:  Splenomegaly. This patient has a splenic abscess due to pneumococcal bacteremia. Note that the massively enlarged spleen is readily visible with minimal retraction in the left upper quadrant.
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Media file 2:  Splenomegaly. Resected specimen from the patient in Image 1. Note the discrete abscesses adjacent to normal parenchyma.
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Media file 3:  Splenomegaly. The margins of this massive spleen were palpated easily preoperatively. Medially, this 7-lb spleen crosses the midline. Inferiorly, it extends into the pelvis.
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Media file 4:  Massive splenomegaly does not preclude splenectomy through a minimally invasive approach. A fragmented 3.2-kg spleen after removal via a hand-assisted laparoscopic technique.
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Media file 5:  Splenomegaly. A portion of a massive spleen extracted via hand-assisted laparoscopy.
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Media file 6:  Splenomegaly. Intraoperative photograph of a laparoscopic splenectomy being taken down using the hanging-pedicle technique. The tip of the spleen is visualized in the background, while the stapler is detailed in the foreground across a segment of the pedicle.
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Media file 7:  Splenomegaly. A massive spleen, which was removed from an elderly woman with lymphoma.
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REFERENCES

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• Al-Salem AH. Is splenectomy for massive splenomegaly safe in children?. Am J Surg. Jul 1999;178(1):42-5. [Medline].
• Eichner ER, Whitfield CL. Splenomegaly. An algorithmic approach to diagnosis. JAMA. Dec 18 1981;246(24):2858-61. [Medline].
• Eichner ER. Splenic function: normal, too much and too little. Am J Med. Feb 1979;66(2):311-20. [Medline].
• Flowers JL, Lefor AT, Steers J, et al. Laparoscopic splenectomy in patients with hematologic diseases. Ann Surg. Jul 1996;224(1):19-28. [Medline].
• Goldstone J. Splenectomy for massive splenomegaly. Am J Surg. Mar 1978;135(3):385-8. [Medline].
• Laws HL, Burlingame MW, Carpenter JT, et al. Splenectomy for hematologic disease. Surg Gynecol Obstet. Oct 1979;149(4):509-12. [Medline].
• Musser G, Lazar G, Hocking W, Busuttil RW. Splenectomy for hematologic disease. The UCLA experience with 306 patients. Ann Surg. Jul 1984;200(1):40-5. [Medline].
• Shaw JH, Print CG. Postsplenectomy sepsis. Br J Surg. Oct 1989;76(10):1074-81. [Medline].
• Wilhelm MC, Jones RE, McGehee R, et al. Splenectomy in hematologic disorders. The ever-changing indications. Ann Surg. May 1988;207(5):581-9. [Medline].

Article Last Updated: Oct 5, 2004