Chapter 34 Spleen Surgery II

Reference: Scwartz Principles in Surgery

EMBRYOLOGY

5th AOG, the spleen is evident

Accessory spleen

Most common anomaly of splenic embryology

20% of the population

30% with hematologic disease

80% found in the splenic hilum and vascular pedicle region

ANATOMY

Largest reticuloendothelial organ in the body

Capsule 1-2 mm thick, contains:

Collagen and elastin fibers

Average size 7-11 cm in lenght

Average weight 150g (70-250g)

If >500g and > 15 cm= Splenomegaly

In cadaveric anatomic series: Tail of pancreas

75% lies within 1 cm of the splenic hilum

30% abuts the spleen

Suspended in position by several ligaments and peritoneal folds
Colon

Splenocolic ligament

Avascular

Stomach

Gastrosplenic
ligament

Short gastric vessels

Diaphragm

Phrenosplenic
ligament

Avascular

Kidney, adrenal
gland, and tail of the
pancreas

Splenorenal ligament

Avascular

Blood Supply

Splenic artery (Main)

Short Gastric artery

Branches of the left gastroepiploic artery

Types of Splenic arteries
I Distributed type

70% Most common

Short trunk

Long branches

Entering over 75% of the medial surface

II Magistral type

30% Less common

Long main trunk

Short terminal branches

Entering over 2530% of the medial surface

Venous Supply

Splenic vein major venous drainage

Two elements of splenic parenchyma

I Red pulp

~ 75 % of total splenic volume

Comprised of large numbers of venous sinuses

Lined by long, narrow endothelial cells

Drain into tributaries of the splenic vein

Reticulum

Fibrocellular network

Consisting of collagen fibers and fibroblasts.

Within this network or mesh lie splenic macrophages.

Surrounded and separated the venous sinuses

Splenic cord

Intersinusoidal regions

Function

Dynamic filtration system

Enabling macrophages to remove microorganisms, cellular debris, antigen/antibody complexes, and senescent
erythrocytes from circulation.
II White pulp

Periarticular lymphatic sheath

Replaces the adventitia of the vessel splenic arterioles

Comprised of T lymphocytes and intermittent aggregations of B lymphocytes or lymphoid follicles.

Lymphoid follicles

Centers of lymphocyte proliferation,

Develop germinal centers

Regress as the stimulus or infection subsides

Normally consisting of nodules 1 mm in size

Can increase to several centimeters in size when nodules coalesce.

Marginal zone

Interface between the white and red pulp

Lymphocytes are more loosely aggregated

Blood is delivered to the red pulp

Lymphocytes and locally produced immunoglobulins ultimately enter the systemic circulation.
PHYSIOLOGY

Major organ clearing damaged or aged red blood cells; abnormal white blood cells and platelets.
Splenic function has historically been summarized as:

Filtration

Host Defense

Storage

Cytopoiesis.
Total splenic inflow of blood

~ 250300 mL/min.
Filtration function of the spleen occurs primarily via the slower circulation
Further evidence of selective slowing of blood cell flow versus plasma flow is indicated by a concentration of erythrocytes
(hematocrit) twice that of the general circulation within the spleen.

Erythrocytes 120-day life cycle

2-day minimum is spent sequestered in the spleen

20 mL of aged red blood cells are removed daily.

Act as a host defense

Significant, not indispensable role

Contributing to both humoral and cell-mediated immunity

The splenic RE system is better able to clear bacteria poorly or inadequately opsonized from the circulation than is the
hepatic RE system
Produces proteins such as:

Tuftsin

Stimulant to general phagocytic function in the host, facilitate clearance of bacteria.

Circulating monocytes converted into fixed macrophages with the red pulp account for the spleens remarkable
phagocytic activity.

Properdin

Important in the initiation of the alternate pathway of complement activation.

Physiologic capacity within the complement cascade to withstand the loss of tuftsin and properdin production
without increasing patient vulnerability postsplenectomy

Opsonins
PATHOPHYSIOLOGY

Splenectomy

Splenomegaly alone is an uncommon indication for splenectomy.

Most common indications

Hypersplenism

Presence of cytopenia (of one or more blood cell lines)

Disorders causing hypersplenism in an intrinsically normal spleen can be categorized as:

Increased destruction of abnormal blood cells

Increased sequestration and destruction of normal blood cells

Hypersplenism

May result in neutropenia or thrombocytopenia, and Alteration of splenic immune function

I Neutropenia

May result from sequestration of normal white blood cells or the removal of abnormal ones.
IIThrombocytopenia

May result from excessive sequestration of platelets and accelerated platelet destruction in the spleen.

Immunologic alteration of platelets

(-) splenomegaly
Platelet

Generally survive in the circulation for 10 days.

Under normal circumstances
33% or one third of the total platelet pool is sequestered in the spleen.
Up to 80% splenomegaly

III Alteration of splenic immune function

Alteration immune function often gives rise to antibody production,resulting in blood cell destruction.

EVALUATION OF SIZE AND FUNCTION

Before elective splenectomy, imaging of the spleen is frequently indicated to assess size and to determine
degree, if any, of splenomegaly
I Ultrasound

~98% sensitivity for detecting textural lesions of the spleen

II Computed tomography (CT) scanning

Affords a high degree of resolution and detail of the spleen

Useful for:

Assessment of splenomegaly

Identification of splenic lesions

Guidance for percutaneous procedures.

III Iodinated contrast material

Adds diagnostic clarity to CT imaging.

IV Plain radiography

Rarely used alone for splenic imaging

Can provide an outline of the spleen in the left upper quadrant, suggest splenomegaly

Demonstrate calcifications.
V Magnetic resonance imaging (MRI)

Offers no advantages in depicting anatomic spleen abnormalities.

VI Radioscintigraphy with 99mTc sulfur colloid

Demonstrates splenic location and size

Little benefit to its use as a preoperative scan.

The splenic index (SI)

Expresses spleen size as a volume in milliliters (mL)

Obtained by multiplying the spleens length, width, and height as determined by a reliable imaging modality.

Normal values for SI range = 120480 mL.

The normal ex vivo weight = 150 g.

INDICATIONS FOR SPLENECTOMY
The conditions for which splenectomy is therapeutic include:

Disorders of red blood cells

Myeloproliferative disorders (Early cell lines)

Disorders of white blood cells

Disorders of platelets

Miscellaneous disorders and lesions

Trauma to the spleen

The most common indication for splenectomy

Red Blood Cell Disorders

Acquired

Autoimmune hemolytic anemia

Warm-antibody AIHA

Congenital

Hereditary spherocytosis

Hemoglobinopathies

Sickle cell disease

Thalassemia
Autoimmune hemolytic anemia.

Set of disorders characterized by autoantibodies against antigens on red blood cells

Decrease the erythrocyte life span

Classified based on the temperature

Warm

Autoantibodies (IgG)

Bind erythrocytes at 37 C (98.6 F)

Best treated by splenectomy.

Cold

Ttypically IgM)

Cause erythrocytes to clump at cold temperatures.

Warm-antibody AIHA

Incidence

Approximately 1:100,000

More common among women

Principally seen in mid-life

50% cases are idiopathic

Clinical findings include:

Mild jaundice

Symptoms and signs of anemia

Splenomegaly 33-50%

occurs in one third to one half of patients, sometimes enough

Presentation

Acutely, with severe symptoms and signs

Gradually, with a relatively asymptomatic

In acute disease:

Signs of congestive heart failure may be observed.

Confirmation Diagnosis Direct Coombs test

Demonstrating hemolysis

Intravascular hemolysis

Extravascular hemolysis
Intravascular hemolysis

Red blood cells are opsonized by autoantibodies and are destroyed, directly within the circulation

Extravascular hemolysis

Removed from the circulation by tissue macrophages located primarily in the spleen and to a lesser extent in
the liver
Teatment of AIHA

Red blood cell transfusion.

For severe anemia (<4 g/dL), causing:

Pulmonary edema, tachycardia, postural hypotension, dyspnea, and angina

Corticosteroids

Act as the mainstay of treatment for both primary and secondary forms of symptomatic, unstable AIHA.

Splenectomy

Indicated for failure to respond to steroids, intolerance of steroid side effects, requirement for excessive steroid
doses to maintain remission, or inability to receive steroids for other reasons.

Favorable response up to 80 percent of patients with warm-antibody AIHA.

Hereditary spherocytosis

Prevalence: Western populations of 1 in 5000

Most common hemolytic anemia for which splenectomy is indicated.

Disorder of the red blood cell membrane resulting in hemolytic anemic

Underlying abnormality

Inherited dysfunction or deficiency in one of the erythrocyte membrane proteins:

Spectrin, ankyrin, band 3 protein, or protein 4.2

Rare fatal crises occur, usually in the setting of infection (e.g., parvovirus).

Clinical findings:

Relatively asymptomatic

Mild jaundice

Splenomegaly

Diagnosis:

Spherocytes are readily apparent on peripheral blood film.

Treatment: Splenectomy

Curative for typical forms of HS and serves as the sole mode of therapy.

Timing is important to reduce the very small possibility of overwhelming postsplenectomy sepsis.

At least age 4 but before age 7 unless the anemia and hemolysis accelerate

Early splenectomy

Indication for intractable leg ulcers

Heal only after removal

Sickle cell disease

Prevalence of sickle cell carriers

African Americans in the United States

Western Africa,

Inherited chronic hemolytic anemia

Due to mutant sickle cell hemoglobin (HbS) within the red blood cell.

Underlying abnormality

Substitution of valine for glutamic acid as the sixth amino acid of the beta-globin chain.

Results in microvascular congestion, which may lead to thrombosis, ischemia, and tissue necrosis.

Clinical Findings

Intermittent painful episodes

Treatment:

Palliative

Splenectomy

Blood transfusion

Splenectomy

Most frequent indications for splenectomy:

Hypersplenism

Acute sequestration crises

Splenic abscess

Does not affect the sickling process

Preoperative preparation includes:

Special attention to adequate hydration

Avoidance of hypothermia.
Transfusions

Indicated for anemia especially before splenectomy

For moderately severe episodes of the acute chest syndrome associated with new symptoms, such as fever,
cough, sputum production, or hypoxia.
Thalassemia

Group of inherited disorders of hemoglobin synthesis

Prevalent among people of Mediterranean extraction

As a group they are the most common genetic diseases defect.

The primary defect in all forms of thalassemia is reduced or absent production of hemoglobin chains

Two significant abnormalities:

Underproduction of hemoglobin

Excess production of unpaired hemoglobin subunits

Both factors contribute to the morbidity and mortality
The clinical spectrum of the thalassemias

Heterozygous carriers

Asymptomatic

Homozygous carriers

Present before 2 years of age

Pallor, growth retardation, jaundice, and abdominal swelling (Hepatosplenomegaly)

Other characteristic of thalassemia major include:

Intractable leg ulcers

Head enlargement

Frequent infections

Requirement for chronic blood transfusions.

Treatment for thalassemia consists:

Red blood cell transfusions

To keep the hemoglobin count > 9 mg/dL

Intensive parenteral chelation therapy

Deferoxamine.

Splenectomy

For patients with excessive transfusion requirements (> 200 mL/kg per year)

Discomfort because of splenomegaly

Painful splenic infarction.

Careful assessment:

Infectious morbidity following splenectomy is greater than in other patients undergoing splenectomy for
hematologic indications

BONE MARROW DISORDERS (MYELOPROLIFERATIVE DISORDERS)

Characterized by an abnormal growth of cell lines in the bone marrow.

The common underlying problem leading to splenectomy

Symptomatic splenomegaly.

Symptoms consist

Early satiety

Poor gastric emptying

Heaviness or pain in the left upper quadrant

Diarrhea.

Hypersplenism usually associated with splenomegaly

Chronic Myeloid Leukemia (CML)

Disorder of the primitive pluripotent stem cell in the bone marrow

Genetic hallmark

Transposition between the bcr gene on chromosome 9 and the abl gene on chromosome 22.

Clinical Findings

Frequently asymptomatic

Present with the gradual onset of fatigue, anorexia, sweating, and left upper quadrant pain and early satiety
secondary to splenomegaly.

Diagnosis

Significant increase in erythroid, megakaryotic, and pluripotent progenitors in the peripheral blood smear.

Treatment

Splenectomy

To ease pain and early satiety.

Acute Myeloid Leukemia (AML)

Characterized by a more rapid and dramatic clinical presentation than CML.

Increased risk for leukemic transformation to AML.

Polycythemia vera

Primary thrombocytosis

Myeloid metaplasia

Clinical Findings:

Viral-like illness with fever, malaise

Bone pain because of the expansion of the medullary space.

Splenomegaly is modest but palpable ~ 50%

Treatment

Splenectomy

If left upper quadrant pain and early satiety become unbearable.

Adds further risk of infection to immunocompromised by neutropenia and chemotherapy.

If untreated Death usually results within weeks to months

Chronic Myelomonocytic Leukemia

Associated with monocytosis in the peripheral smear (> 1 103/mm3) and in the bone marrow.

Splenomegaly occurs in one-half of these patients

Treatment:

Splenectomy can result in symptomatic relief.

Essential Thrombocythemia

Represents abnormal growth of the megakaryocyte cell line, resulting in increased levels of platelets in the
bloodstream.

Clinical manifestations of ET include:

Vasomotor symptoms

Thrombohemorrhagic events

Recurrent fetal loss

Transformation to myelofibrosis with myeloid metaplasia or acute myeloid leukemia

Splenomegaly 33%-50%
Treatment: Splenectomy
Not felt to be helpful in the early stages
Best reserved for the later stages of disease
Complication to surgery
Significant bleeding

Polycythemia Vera

Rare, chronic, progressive myeloproliferative disorder

Increase in red blood cell mass, frequently accompanied by leukocytosis, thrombocytosis, and splenomegaly.

Number of nonspecific complaints, including:

Headache, dizziness, weakness, pruritus, visual disturbances, excessive sweating, joint symptoms, and weight
loss.

Physical findings include

Ruddy cyanosis, conjunctival plethora, hepatomegaly, splenomegaly, and hypertension.

Treatment:

Phlebotomy

Aspirin

Chemotherapeutic agents.

Spelenctomy

Not helpful in the early stages

Best reserved for late-stage patients

Prognosis

Typically enjoy prolonged survival compared to others affected by hematologic malignancies.

Myelofibrosis (Agnogenic Myeloid Metaplasia)

Generic condition of fibrosis of the bone marrow

Specific, chronic, malignant hematologic disease

Associated with splenomegaly, red blood cell and white blood cell progenitors in the bloodstream, marrow
fibrosis, and extramedullary hematopoiesis

Underlying abnormality

Response to a clonal proliferation of hematopoietic stem cells.

Marrow failure often ensues, either:

Secondary to the fibrosis itself

Unknown malignant proliferation of cells

Clinical manifestations:

Asymptomatic ~ 20%

Most frequently related to ANEMIA

Including fatigue, weakness, dyspnea on exertion, and palpitations.

Others: Bleeding, fever, weight loss, gout/renal stones, night sweats, and symptoms because of an enlarged
spleen.

Nearly all patients with AMM

Nearly all have splenomegaly

35 % massive splenomegaly

67% hepatomegaly.

Diagnosis:

~ 96 cases = Nucleated red blood cells and immature myeloid elements in the blood are

Care must be taken, however, to exclude a history of a primary neoplasm or tuberculosis,

These conditions may develop secondary myelofibrosis.

Treatment

Asymptomatic patients

Closely followed and monitor

Symptomatic patients

Undergo therapeutic intervention targeted toward their symptoms.

Sprenectomy
Best treated with splenomegaly related symptoms
Effective palliation for nearly all patients with AMM
Preoperative workup:
Candidate must possess acceptable cardiac, pulmonary, hepatic, and renal reserve for the operation.
The coagulation system should be examined, including tests of coagulation factors V and VIII, fibrin split
products, platelet count, and bleeding time.
Low platelet counts may require adrenal steroids and/or platelet transfusion at the time of surgery.
Prognosis
Postoperative complications are more common in patients with AMM than in those with other hematologic
indications.

White Blood Cell Disorders

Leukemias

Chronic lymphocytic leukemia

Hairy cell leukemia

Both are amenable to treatment by splenectomy

Lymphoma

Non Hodgkin Disease

Hodgkin Disease
Chronic lymphocytic leukemia (CLL)

Symptoms of are nonspecific and include:

Weakness, fatigue, fever without illness, night sweats, and frequent bacterial and viral infections.

Splenomegaly

May be massive or barely palpable below the costal margin

Treatment:
Splenectomy
To improve cytopenias
May thus facilitate chemotherapy in patients whose cell counts were prohibitively low prior to spleen removal.
Palliative splenectomy also is indicated for symptomatic splenomegaly.

Hairy cell leukemia

Characterized by splenomegaly, pancytopenia, and large numbers of abnormal lymphocytes in the bone
marrow.

Number of complaints, including:

Anemia

Neutropenia

Thrombocytopenia,

Splenomegaly most common physical finding ~80%

Diagnosis

Lymphocytes contain irregular hair-like cytoplasmic projections identifiable on the peripheral smear

Treatment is indicated for:

Those with moderate to severe symptoms related to cytopenias, such as:

Repeated infections

Bleeding episodes

Splenomegaly.

Newer chemotherapeutic agents

Able to induce durable complete remission in most patients.

2-deoxycoformycin

2-chlorodeoxyadenosine

NonHodgkin lymphoma (NHL)

Encompasses all malignancies derived from the lymphoid system except classic Hodgkin disease.

Surgical staging is no longer indicated for NHL

History and physical examination, chest radiograph and abdominal/pelvic CT scan, biopsy of involved lymph
nodes and bone marrow biopsy is sufficient.

Splenomegaly

Exists in various, but not all, forms of NHL

Splenectomy

Indicated for symptoms related to an enlarged spleen

To improve cytopenias
Hodgkin disease (HD)

Disorder of the lymphoid systemcharacterized by the presence of Reed-Sternberg cells form the minority of the
Hodgkins tumor.

The spleen is often an occult site of spread

Massive splenomegaly is not common.

The staging procedure for HD begins:

Wedge biopsy of the liver

Splenectomy

Removal of representative nodes in the retroperitoneum,mesentery, and hepatoduodenal ligament.

Laparoscopic core biopsy of the liver

Performed under direct visualization, either using:

Tru-cut needle percutaneously or by

Wedge resection with shears and cautery.

Current indications for surgical staging include:

Clinical stage I

Stage II with nodular sclerosing histology

No symptoms referable to HD

Staging information affects treatment:

Radiotherapy

Early stage patients who have no splenic involvement

Chemotherapy or multimodality therapy

Splenic involvement
PLATELET DISORDERS
Idiopathic Thrombocytopenic Purpura (ITP)

Also called immune thrombocytopenic purpura

Autoimmune disorder characterized by a low platelet count and mucocutaneous and petechial bleeding.

Underlying abnormality:

Low platelet count stems from premature removal of platelets opsonized by antiplatelet IgG autoantibodies
produced in the spleen.

Patients with ITP typically present:

Petechiae

Ecchymosis

Some will experience major bleeding

Bleeding may occur from mucosal surfaces in the form:

Gingival bleeding

Epistaxis

Menorrhagia

Hematuria

Melena.

Risk for internal bleeding

Platelet counts < 10,000/mm3

The estimated incidence of ITP

~50% are children.

~ 1% major intracranial hemorrhage.
Children often present at a young age
Peak age approximately 5 years
Sudden onset several days to weeks after an infectious illness
Adults experience a more chronic form of disease with an insidious onset.
Splenomegaly with ITP is uncommon in both adults and children
Diagnosing ITP
Based on exclusion of other possibilities in the presence of a low platelet count and mucocutaneous bleeding:
Systemic lupus erythematosus,
Certain antimicrobials or other drugs
Laboratory findings:
Large, immature platelets (megathrombocytes) on peripheral blood smear.
Treatment
Oral Prednison
The usual first line of therapy
Dose of 1.01.5 mg/kg per day
Responses occur within the first 3 weeks, rates range from 5075%
Relapses are common.
Intravenous immunoglobulin
Dose of 1.0 g/kg per day for 23 days
Indicated for internal bleeding if below 5000/mm3 or when extensive purpura exists.
Immediate response is common, but a sustained remission is not
Splenectomy
Indicated for failure of medical therapy, or for most cases of first relapse
Provides a permanent response without subsequent need for steroids in 7585%
Management
Platelet replacement/transfusion
For lowplatelet counts (< 10,000/mm3)
Should not receive them preoperatively.
Given to those who continue to bleed after the splenic pedicle is ligated
Prognosis
In children with ITP, the course is self-limited, with durable and complete remission ~70%
Managed principally by observation, with shortterm therapy in select cases.

Splenectomy

Reserved for failure of medical therapy in children who have

Immune thrombocytopenic purpura for at least 1 year with symptomatic

Severe thrombocytopenia.

Urgent splenectomy may play a role in the rare circumstance of severe, life-threatening bleeding, in conjunction
with aggressive medical therapy.
Thrombotic thrombocytopenic purpura (TTP)

Serious, rare disorder characterized by thrombocytopenia, microangiopathic hemolytic anemia, and neurologic
complications.

Underlying abnormality:

Abnormal platelet clumping occurs in arterioles and capillaries

predisposing the patient to microvascular thrombotic episodes.

Clinical features of the disorder include:

Petechiae in lower extremities

Most common sign

Fever
Neurologic symptoms
Headaches to altered mental status, seizures, and even coma
Renal failure
Infrequently cardiac symptoms
Heart failure or arrhythmias
Differential Diagnosis by a negative Coombs test.
Evans syndrome (ITP and autoimmune hemolytic anemia)
Systemic lupus erythematosus
Treatment
Plasma exchange
The first line of therapy
Splenectomy
Plays a key role for patients who relapse or require multiple plasma exchanges to control symptoms
Generally well-tolerated without significant morbidity
Typically do not relapse.
Platelet transfusions are not recommended

MISCELLANEOUS DISORDERS AND LESIONS

Infections and abscess

Storage Diseases

Gauchers disease

Niemanns Pick Disease

Amyloidosis

Infiltrative Disorders

Felty Syndrome

Sarcoidosis

Cysts and Tumor

Portal Hypertension

Splenic Artery Aneurysm

Infections and Abscesses

Abscesses are uncommon, with incidence of 0.140.7 %,

Five distinct mechanisms of splenic abscess formation:

Hematogenous infection

Contiguous infection

Hemoglobinopathy

Immunosuppression, including hiv and chemotherapy

Trauma.

The most common origins for hematogenous spread are:

Infective endocarditis

Typhoid fever

Malaria

Urinary tract infection

Osteomyelitis

Clinical manifestations Presentation is frequently delayed

Fever

Left upper quadrant pain

Leukocytosis

Splenomegaly about 33%

Diagnosis

Confirmed by ultrasound or CT scan

95% sensitivity and specificity

Treatment

Broad-spectrum antibiotics for 14 days.

Splenectomy is the operation of choice
Percutaneous drainage
Optional
successful for patients with unilocular disease.
Open drainage
Options for patients who cannot tolerate splenectomy.

Gauchers disease.

Inherited lipid storage disease

Deposition of glucocerebroside in cells of the macrophage-monocyte system.

Clinical features

Early satiety

Abdominal discomfort

Hypersplenism

Includethrombocytopenia, normocytic anemia, and mild leukopenia.

Treatment

Splenectomy

Alleviates hematologic abnormalities in patients with hypersplenism

Does not correct the underlying disease process.

Niemann-Pick disease.

Inherited disease of abnormal lysosomal storage of sphingomyelin and cholesterol in cells of the macrophagemonocyte system.

Types A and B forms

Most likely to demonstrate splenomegaly with its concomitant symptoms.

Treatment

Splenectomy

Successfully treat symptoms of splenomegaly

Amyloidosis

Disorder of abnormal extracellular protein deposition.

Treatment

Splenectomy

Relieved symptoms of splenomegaly

To cure patients of factor X deficiency associated with primary amyloidosis

Felty Syndrome

The triad of:

Rheumatoid arthritis (RA)

Splenomegaly

Neutropenia

Spleen is 4x heavier than normal

Neutropenia

Causing frequent infections

Driving force behind the decision for splenectomy

Treatment of neutropenia

Hematopoeitic growth factors

Methothrexate

Splenectomy
Sarcoidosis

Inflammatory disease of young adults

Characterized by noncaseating granulomas in affected tissues.

Any organ system may be involved:

Lung most common
Spleen 2nd common
25% have Splenomegaly
Massive splenomegaly (>1 kg) is rare.

Treatment: Splenectomy
Indicated for symptomatic splenomegaly and hypersplenism
Relieves symptoms and corrects hematologic abnormalities such as anemia and thrombocytopenia.

Cysts

Splenic cysts are rare lesions

Most common etiology for splenic cysts
Parasitic infestation, particularly echinococcal.
Treatment for Symptomatic parasitic cysts are:
Splenectomy choice treatment
Also amenable to percutaneous aspiration, instillation of protoscolicidal agent, and reaspiration.
Nonparasitic cysts
Also called Pseudocyst
Most commonly result from trauma

Treatment and Management of Nonparasitic cysts

Asyptomatic patients

Observed with close ultrasound follow up to exclude significant expansion

Advised of the risk of cyst rupture with even minor abdominal trauma

Small symptomatic nonparasitic cysts

May be excised with splenic preservation

May be performed laparoscopically.

Large symptomatic nonparasitic cysts

May be unroofed. Both of these operations

May be performed laparoscopically.

Tumors

Sarcomatous
Most common primary tumor of the spleen
NonHodgkin lymphoma of the spleen
Rare, but splenectomy imparts an excellent prognosis.
Lung cancer
Most common tumor to spread to the spleen.

Portal Hypertension

Result from numerous causes

Usually is because of cirrhosis.

Often accompanied by splenomegaly and splenic congestion

Splenectomy

Not indicated for hypersplenism

No correlation exists between the degree of pancytopenia and long-term survival

Curable if Portal hypertension secondary to splenic vein thrombosis

Splenic vein thrombosis

Should be examined if with bleeding from isolated gastric varices in the presence of normal liver function tests

Especially with a history of pancreaticdisease,

Splenic Artery Aneurysm

Rare but most common visceral artery aneurysm

Usually arises in the middle to distal portion of the splenic artery.
The risk of rupture
Between 3 and 9 %
If rupture occurs, mortality is substantial 3550%.
If rupture during pregnancy, mortality:
Mother (70 %)
Fetus (95 %).
Indications for treatment include:
Presence of symptoms
Pregnancy
Intention to become pregnant, and
Pseudoaneurysms associated with inflammatory processes.
Indication for surgery:
For asymptomatic patients, size > 2 cm
Treatment:
Aneurysm resection or ligation alone
Acceptable for amenable lesions in the mid-splenic artery,
Splenectomy
For distal lesions in close proximity to the splenic hilum

PREOPERATIVE CONSIDERATIONS
Splenic Artery Embolization

Became available with advances in angiographic technology.

Theoretical advantages of SAE include:

Reduced operative blood loss from a devascularized spleen

Reduced spleen size for easier dissection and removal.

Potential disadvantages of the procedure include

Acute left-sided pain (although usually of limited duration)

Pancreatitis

Other embolization-related complications.

There is currently no consensus on the role of preoperative SAE for elective splenectomy.
Vaccination

Splenectomy imparts a small (<15%) but definite life-time risk of fulminant, potentially life-threatening infection.
Therefore, when elective splenectomy is planned,

Vaccinations against encapsulated bacteria

Should be given at least 2 weeks before surgery:

Streptococcus pneumonia

Haemophilus influenzae type B

Meningococcus

If the spleen is removed emergently (e.g., for trauma),

Should be given as soon as possible following surgery, allowing at least 12 days for recovery.

Booster injections of pneumococcal vaccine

Should be considered every 56 years

Annual influenza immunization is advisable.

Deep Venous Thrombosis Prophylaxis

For patients undergoing splenectomy

Deep venous thrombosis (DVT) is common following splenectomy, especially in cases involving:

Splenomegaly

Myeloproliferative disorders (MPD).

The risk of portal vein thrombosis (PVT) may ~ 40%

For patients with both splenomegaly and MPD.

Postsplenectomy PVT typically presents with:

Anorexia
Abdominal pain
Leukocytosis
Thrombocytosis
Keys to successful treatment for PVT: High index of suspicion
Early diagnosis with contrast-enhanced CT
Immediate anticoagulation
DVT prophylaxis
Compression devices with subcutaneous heparin (5000 U).
Patients risk factors for DVT
Obesity
History of prior VTE
Known hypercoagulable state
Age > 60
More Aggressive antithrombotic regimen, including low-molecular-weight heparin (LMWH)

SPLENECTOMY TECHNIQUES
Patient Preparation

Vaccination for elective splenectomy at least 1 week preoperatively with:

Polyvalent pneumococcal

Meningococcal

Haemophilus.

Blood product transfusion

Anemic patients

Transfused to a hemoglobin of 10 g/dL.

For more complex patients, including those with splenomegaly

Type and cross is recommended for at least 24 units of blood.

Platelet transfusions

May transiently correct thrombocytopenia

Preferably not preoperatively

Ideally not before intraoperative ligation of the splenic artery.

Perioperatively parenteral corticosteroid therapy

Patients who have been maintained on corticosteroid therapy preoperatively:

Deep vein thrombosis (DVT) prophylaxis

Intravenous administration of a first-gen. cephalosporin.

Nasogastric (NG) tube

To decompress the stomach.

Open Splenectomy (OS)

Widely practiced due to the standard approach of laparoscopic surgery (LS) for normosplenic patients

Indication for:

Traumatic rupture of the spleen Most indication

Massive splenomegaly

Ascites

Portal hypertension

Multiple prior operations

Extensive splenic radiation

Possible splenic abscess.

Open Splenectomy Technique

Incision
Left subcostal incision
Preferred for most elective splenectomies
Midline incision
If exposure of a ruptured
If massively enlarged spleen
If abdominal access is needed for a staging laparotomy.

Dividing ligamentous attachment to mobilizes the spleen

Splenocolic ligament
First to divide
Splenophrenic ligament
Spleens lateral peritoneal attachments
Further medial mobilization

Role of early ligation of the splenic artery

Safer manipulation of the spleen and dissection of the splenic hilum,
Spleen shrinkage
Autotransfusion of erythrocytes and platelets.
Pointers:
Early ligation of splenic artery for patients with significant splenomegaly
Avoid injuring the tail of the pancreas.
Splenic bed is not routinely drained.

Laparoscopic Splenectomy

Supplanted OS as the elective splenectomy approach of

Laparoscopic Splenectomy Tachnique/Procedure

Vital anatomy
Allowing for an intuitive dissection sequence.
Short gastric vessels and splenic hilum are divided by:
Individual clip applications
Endovascular staples
Hemostatic energy sources
Pointers
Lower spleen pole can be elevated
For accessible dissection of splenic hilum
Retract to spleen
For easily visualizes the tail of the pancreas and can avoid its injury. .
Surgeons hand
Introduced completely into the peritoneal cavity for palpation of appropriate tissues
Allows for identification, retraction, and dissection.

Partial Splenectomy

Amenable for certain lipid storage disorders and some forms of traumatic splenic injury

Indicated in children to minimize postsplenectomy sepsis risk

SPLENECTOMY OUTCOMES

Changes to blood composition

Appearance of Howell-Jolly bodies

Siderocytes.

Leukocytosis

Increased platelet counts commonly

Classification of Complications:

Pulmonary

Left lower lobe atelectasis,

~ 16%, most complication

Pleural effusion

Pneumonia

Hemorrhagic ~ 3%

Intraoperative hemorrhage

Postoperative hemorrhage

Infectious

Subphrenic abscess

Wound infection

Pancreatic

Pancreatitis

Pseudocyst

Pancreatic fistula

Thromboemboli ~ 5-10%
Hematologic Outcomes

Thrombocytopenia

Long-term response

Platelet count > 150,000/mL, > 2 months after surgery without medications.

Laparoscopic splenectomy provide a long-term platelet response in 85% with ITP.

Chronic hemolytic anemias

Rise in hemoglobin levels to >10 g/dL

Without the need for transfusion signifies a successful response to splenectomy.

Success rate 60-80% of splenectomy

Patients with spherocytosis

Success rate 90100% of splenectomy.

Laparoscopic approach typically results:

Longer operative times

Shorter hospital stays

Lower morbidity rates

Similar blood loss

Similar mortality rates.

Overwhelming Postsplenectomy Infection (OPSI)

OPSI usually develops within the first 2 years after splenectomy due the loss of spleens ability

More likely to occur:

Children > Adults

With hematologic disorders > splenic trauma.

Loss of the spleens ability:

To filter and phagocytose bacteria

Parasitized blood cells

Loss of a significant source of antibody production.

The most common source of infection:

Streptococcus pneumonia ~5090%

H. influenzae type

B, meningococcus

Group A streptococci

Clinical findings:

Mild-appearing prodrome:

Fever, malaise, myalgias, headache, vomiting, diarrhea, and abdominal pain.

May progress rapidly to fulminant bacteremic septic shock, with accompanying hypotension, anuria, and DIC
Risk factors for the development of OPSI:
Patients undergoing splenectomy for hematologic indications
Hodgkin disease
Those taking chemotherapy or radiation therapy
Prophylaxis and vaccination
Immunoprophylaxis consists of pneumococcal, meningococcal, and H. influenzae type B vaccination
Pneumococcal vaccine booster injections
Annual influenza immunization
Antibiotic prophylaxis
Penicillin or amoxicillin
Single Daily Dose for asplenic children for the first 2 years after splenectomy.