Spleen surgical aspects

Spleen surgical aspects
Masoud Amini M.D. G.S. Laparoscopist & Bariatric Surgeon

AMINI MD

???????????????????????????????????????????? largest reticuloendothelial organ(?) from…derm(?) ligaments of spleen(?) Vascular most of spleen’s blood derives from(?) three main branches of the celiac artery(?) accessory spleen Present in up to (?%) Spleen size & weight (?) Splenomegaly ,Hypersplenism erythrocyte's, neutrophil & Platelets, life span (?) splenectomy should be delayed if possible to at least ??? age AMINI MD

Embryology & anatomy Spleen is the largest reticuloendothelial organ in the body From the primitive mesoderm Evident in the fifth week of gestation in an 8 mm embryo The most common variation of splenic embryology is the accessory spleen . Present in up to 20% of the population AMINI MD

Ligaments of the spleen
(splenocolic ligament), to the colon (phrenosplenic ligament),to the diaphragm (splenorenal ligament) to the kidney, adrenal, and tail of the pancreas (gastrosplenic ligament),to the stomach The gastrosplenic ligament contains the short gastric vessels; the remaining ligaments are avascular AMINI MD

Anatomy cont. the tail of the pancreas has been demonstrated to lie within one cm of the splenic hilum 75% of the time and in 25% of patients actually to abut the spleen AMINI MD

ligaments AMINI MD

AMINI MD

The spleen derives most of its blood from the splenic artery , the longest and most tortuous of the three main branches of the celiac artery AMINI MD

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Accessory spleens Present in up to 20% of the population
Over 80% in the hilum and vascular pedicle Other locations in descending order gastrocolic ligament, greater omentum, stomach's greater curve, splenocolic ligament, small and large bowel mesentery, left broad ligament in women, and the left spermatic cord in men AMINI MD

Locations of accessory spleens
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splenic artery & vein The distributed type :is the most common (70%) and is distinguished by a short trunk with many long branches. The less common magistral type of splenic artery (30%) has a long main trunk dividing near the hilum into short terminal branches. The splenic vein joins the superior mesenteric vein to form the portal vein and accommodates the major venous drainage of the spleen. AMINI MD

Spleen size The average adult spleen is 7 to 11cm in length and weighs 150 g (range 70 to 250 g). palpable below the left costal margin are at least double normal size, with an estimated weight of 750 g Spleen size and weight both diminishing in the elderly AMINI MD

Definitions , function The spleen can cause significant hematologic disturbance if it becomes hyper functioning ( hypersplenism) or hypertrophied ( splenomegaly) AMINI MD

Definitions Splenomegaly:( ?>1 kg or a pole-to-pole length of ?>15 cm) Hypersplenism :the presence of one or more cytopenias with normally functioning bone marrow.(e.g., hemolytic anemia ) AMINI MD

Massive splenomegaly Splenomegaly NL Spleen Spleen >1 kg 500 g
70—250(150) gm Wt >22 cm and / or 15 cm. 7—11 cm Length AMINI MD

immunologic role spleen plays a key immunologic role in defense against a number of organisms, particularly encapsulated bacteria AMINI MD

physiology The red pulp dynamic filtration system, enabling macrophages to remove microorganisms, cellular debris, antigen- antibody complexes, and senescent erythrocytes from the circulation. white pulp nodules that are <1 mm in size can increase to several centimeters in certain lymphoproliferative disorders AMINI MD

Physiology cont. Storage spleen :in many mammals , autonomic stimulation contract the spleen to expel large volumes of stored blood into the general circulation. defense spleen: human splenic function is largely related to immunologic protection. Total splenic inflow of blood is approximately 250 to 300 ml/min. AMINI MD

Physiology cont. A minimum of 2 days of the erythrocyte's 120- day life cycle is spent sequestered in the spleen. Daily, approximately 20 mL of aged red blood cells are removed. The spleen plays a significant role in host immunity, both humoral and cell-mediated. lymphocytes and locally produced immuno-globulins ultimately enter the systemic circulation AMINI MD

Physiology cont. A neutrophil half-life is approximately 6 hours, hypersplenism may result in neutropenia. Platelets, survive for 10 days. Thrombocytopenia may result from excessive sequestration or accelerated platelet destruction in the spleen. AMINI MD

physiopathology Under normal circumstances one third of the total platelet pool is sequestered in the spleen. Splenomegaly may result in sequestration of up to 80% of the platelet pool. The spleen may also contribute to the immunologic alteration of platelets, leads to thrombocytopenia in the absence of splenomegaly (e.g., ITP). AMINI MD

Physiology After an antigen challenge, an acute Ig M response(predominantly) results in the release of opsonic antibodies from the white pulp of the spleen. The spleen also produces opsonins, tuftsin, and properdin (major source). Circulating monocytes are converted within the red pulp into fixed macrophages that account for the spleen's remarkable phagocytic activity. AMINI MD

Splenic imaging Ultrasound :least invasive ,rapid, easy to perform, no ionizing radiation. It is often the first imaging modality. CT :high degree of resolution and less operator dependent. CT has become an invaluable tool in the evaluation and management of the blunt trauma patient. In the nontrauma setting, CT is extremely useful for assessment of splenomegaly, identification of solid and cystic lesions, and guidance of percutaneous procedures. The use of iodinated contrast material adds diagnostic clarity. AMINI MD

Splenic imaging MRI offers excellent detail in abdominal imaging , but it is more expensive than CT scanning or ultrasound. Angiography (controversy); splenic arterial embolization(SAE). For treatment of hemorrhage in select trauma patients; delivery of therapies in cirrhosis or portal and sinistral hypertension, and in transplant patients; and as an alternative to splenectomy for hematologic disorders such as ITP. Radioscintigraphy with Tc 99m sulfur colloid ;may be helpful in locating accessory spleens after unsuccessful splenectomy and in diagnosing splenosis (no benefit before splenectomy) AMINI MD

Autoimmune hemolytic anemias(AIHA)
AIHAs are characterized by the destruction of red blood cells, by autoantibodies. positive Coombs' test confirms the AIHA diagnosis AIHA is classified as :primary or secondary, depending on cause. AIHA is also divided into:"warm" and "cold", based on the temperature at which the autoantibodies exert their effect. AMINI MD

Autoimmune hemolytic anemias
In cold-agglutinin disease severe symptoms are uncommon and splenectomy is almost never indicated The mainstay treatment for both primary and secondary forms of symptomatic, unstable AIHA is corticosteroids AMINI MD

INDICATIONS FOR SPLENECTOMY
Splenic rupture (trauma) Red blood cell disorders and hemoglobinopathies. White blood cell disorders, Platelet disorders, Bone marrow disorders (myeloproliferative disorders), Cysts and tumors, Infections and abscesses, Storage diseases and infiltrative disorders, miscellaneous disorders and lesions AMINI MD

Splenectomy in trauma Overall, the most common indication for splenectomy is trauma to the spleen, (external trauma (blunt or penetrating) or iatrogenic injury) AMINI MD

Curative or palliative splenectomy in nontraumatic diseases
can be categorized as Red blood cell disorders(hemoglobinopathies) White blood cell disorders, Platelet disorders, Bone marrow disorders, Infections and abscesses, Cysts and tumors, Storage diseases and infiltrative disorders, miscellaneous conditions. AMINI MD

Red Blood Cell Enzyme Deficiencies
1-enzymes involved in glycolytic pathways , such as pyruvate kinase (PK) 2-enzymes needed to maintain a high ratio of reduced to oxidized glutathione in the red blood cell, protecting it from oxidative damage, such as glucose-6-phosphate dehydrogenase (G6PD) deficiency. AMINI MD

Hemolytic Anemia Erythrocyte Enzyme Deficiency
Pyruvate kinase deficiency is an autosomal recessive disease that results in decreased red blood cell deformability and the formation of echinocytes. the cell will be trapped and destroyed by the spleen, which results in splenomegaly, hemolytic anemia, and associated transfusion requirements, which can be mitigated with splenectomy

G6PD deficiency X-linked condition splenectomy is rarely indicated
Hemolytic anemia occurs after infection or exposure to certain foods, medications, or chemicals. Primary treatment, therefore, is avoidance of exacerbation of the condition

Sickle cell anemia During conditions of low oxygen tension, these hemoglobin S molecules crystallize, distorting the cell into a crescent shape. These misshapen cells are unable to pass through the microvasculature, which results in capillary occlusion thrombosis, and ultimately microinfarction These episodes of infarction result in autosplenectomy , although splenomegaly may occasionally persist

sickle cell disease Splenomegaly, hypersplenism, and splenic infarction, common in sickle cell disease, are also seen commonly in the thalassemias.

Other red blood cell membrane abnormalities
Hereditary elliptocytosis, hereditary pyropoikilocytosis, hereditary xerocytosis, and hereditary hydrocytosis also result in anemia secondary to red blood cell membrane abnormalities. Splenectomy is indicated in cases of severe anemia with these conditions, except hereditary xerocytosis, which results in only mild anemia of limited clinical significance

Other conditions thrombotic thrombocytopenic purpura
chronic disseminated intravascular coagulation congenital thrombocytopenia myelodysplasia autoimmune disorders (e.g., systemic lupus erythematosus) lymphoproliferative disorders (e.g., chronic lymphocytic leukemia, non-Hodgkin’s lymphoma). Approximately 10% to 20% of otherwise asymptomatic patients with HIV will develop ITP. Splenectomy is a safe treatment option for this cohort of patients and may actually delay HIV disease progression

Hereditary Spherocytosis
an autosomal dominant disease affecting the production of spectrin, a red blood cell cytoskeletal protein. Loss of this protein causes erythrocytes to lack their characteristic biconcave shape also, results in rigid, small and sphere- shaped cells that have increased osmotic fragility The resulting clinical features are anemia, occasionally with jaundice, and splenomegaly Diagnosis is made by examination of a peripheral blood smear, increased reticulocyte count, increased osmotic fragility, and a negative Coombs’ test

Hereditary Spherocytosis
The resultant anemia can be successfully treated with splenectomy, but normalization of the erythrocyte morphology does not occur Just as with other hemolytic anemias, the presence of pigmented gallstones is common. if gallstones are present, cholecystectomy may be performed at the same time as splenectomy

Hemoglobinopathies Sickle cell disease and thalassemia are two disorders in which the hemoglobin molecules exhibit qualitative or quantitative defects. These lead to abnormally shaped erythrocytes, which may lead to splenic sequestration and subsequent destruction Sickle cell anemia results from a single amino acid substitution (valine for glutamic acid) in the sixth position of the β chain of hemoglobin A, which causes those hemoglobin chains, under reduced oxygen conditions, to become rigid and unable to deform within the microvasculature

Hypersplenism and acute splenic sequestration
are life-threatening disorders in children with thalassemia and sickle cell disease. which results in and may require multiple blood transfusions. Patients present with rapid splenomegaly ,severe pain ,severe anemia, and an acute bone marrow response, with erythrocytosis, and circulatory collapse Resuscitation with hydration and transfusion may be followed by splenectomy in these patients

splenectomy Symptomatic massive splenomegaly that interferes with daily activities may also be improved by splenectomy Hypersplenism related to sickle cell disease requiring transfusions; transfusions may be reduced by performing splenectomy in children with sickle cell disease who exhibit growth delay or even weight loss because of increased metabolic rate and whole-body total protein turnover, splenectomy may relieve these symptoms.

Splenic abscesses and a may be seen in patients with sickle cell anemia , present with fever, abdominal pain, tender enlarged spleen, leukocytosis, as well as thrombocytosis and Howell-Jolly bodies indicating a functional asplenia. Salmonella and Enterobacter spp. and other enteric organisms are commonly seen in those with a splenic abscess. These patients require resuscitation with hydration and transfusion and may require urgent splenectomy after stabilization

Pyruvate Kinase Deficiency
The most common RBC enzyme deficiency to cause congenital chronic hemolytic anemia is PK deficiency. Clinical manifestations vary widely, from transfusion-dependent severe anemia in early childhood to well-compensated mild anemia in adolescents or adults. AMINI MD

Pyruvate Kinase Deficiency
Splenomegaly is common, and in severe cases splenectomy can alleviate transfusion requirements. splenectomy should be delayed if possible to at least 4 years of age to reduce the risk of infection. AMINI MD

G6PD deficiency The most common red blood cell enzyme deficiency overall is G6PD deficiency The mainstay of therapy is avoidance of drugs known to precipitate hemolysis the overwhelming majority of patients with G6PD deficiency will neither require nor benefit from splenectomy AMINI MD

Hereditary spherocytosis (HS)
An inherited dysfunction or deficiency in one of the erythrocyte membrane proteins. The spherocytic erythrocytes are sequestered and destroyed in the spleen, so hemolytic anemia ensues. HS is the most common hemolytic anemia for which splenectomy is indicated. [autosomal dominant fashion(1 in 5000 in west)]. Dramatic clinical improvement often occurs after splenectomy in patients with severe disease. AMINI MD

Gallstones & HS Gallstones are more likely to develop in HS, prophylactic cholecystectomy is recommended at the time of splenectomy. AMINI MD

sickle cell disease sickle cell disease; is due to mutation of adenine to thymine in globin gene, Deoxygenated HbS is insoluble and becomes polymerized and sickled. Sequestration splenomegaly, early in the disease course. In most cases infarction autosplenectomy occur later AMINI MD

sickle cell disease The most frequent indications for splenectomy are
Recurrent sequestration crises Hypersplenism, and Splenic abscess Major acute sequestration crisis, Rapid painful enlargement of the spleen and circulatory collapse, generally is considered sufficient grounds for splenectomy. Adequate hydration and avoidance of hypothermia AMINI MD

Thalassemia Inherited disorders of hemoglobin synthesis affected , classified according to the hemoglobin chain (α, β, or,γ). In all forms of thalassemia the primary defect is absent or reduced production of hemoglobin chains. Because α chains are needed to form both fetal hemoglobin and adult hemoglobin,α-thalassemia becomes symptomatic in utero or at birth. AMINI MD

Thalassemia By contrast, β -thalassemia becomes symptomatic at 4 to 6 months, because chains are involved only in adult hemoglobin synthesis Heterozygous carriers are usually asymptomatic. Homozygous individuals, typically present before 2 years of age with pallor, growth retardation, jaundice, and abdominal swelling due to liver and spleen enlargement. AMINI MD

Thalassemia treatment
Thalassemia Treatment involves transfusions to maintain a Hb >9 mg/dL, with intensive parenteral chelation therapy with deferoxamine. AMINI MD

Thalassemia major Other characteristics are
intractable leg ulcers, head enlargement, frequent infections, the need for periodic blood transfusions. Untreated individuals usually die in late infancy or early childhood from severe anemia. Splenectomy is indicated for patients with excessive transfusion (>200 mL/kg per year) AMINI MD

Thalassemia patients are at high risk for pulmonary hypertension after splenectomy
AMINI MD

Lymphomas Hodgkin’s Disease:
Hodgkin’s disease is a malignant lymphoma that usually affects young adults in their 20s and 30s. Rarely, patients present with constitutional symptoms such as night sweats, weight loss, and pruritus but, more typically, asymptomatic lymphadenopathy usually involving the cervical nodes

staging Hodgkin’s disease
Staging methods have evolved to include imaging techniques— computed tomography (CT), 18F-fluorodeoxyglucose positron emission tomography (FDG-PET), and lymphangiography

staging laparotomy Hodgkin’s disease
Historically, included splenectomy liver biopsy splenic hilar lymphadenectomy retroperitoneal node biopsy biopsy of a hepatoduodenal node and oophoropexy in premenopausal women common in stages I and II disease to rule out splenic or subdiaphragmatic involvement.

Early-stage Hodgkin’s disease is often cured with radiation therapy alone.
Laparotomy is no longer indicated for patients likely to relapse, those with evidence of intra-abdominal involvement on imaging, and those with B symptoms. These patients should receive systemic chemotherapy

Non-Hodgkin’s Lymphoma (NHL)
Splenomegaly or hypersplenism is common Splenectomy is indicated for NHL patients with massive splenomegaly leading to abdominal pain, early satiety, and Fullness also indicated in hypersplenism (anemia, neutropenia, and thrombocytopenia)

NHL Splenectomy may also be instrumental in the diagnosis and staging of patients with isolated splenic disease. The most common primary splenic neoplasm is NHL 50% to 80% of patients with NHL have involvement of the spleen but less than 1% of patients present with splenomegaly without lymphadenopathy Most patients have low-grade NHL, with frequent involvement of the splenic hilar lymph nodes, extrahilar nodes, bone marrow, or liver .Approximately 75% of these patients have clinically apparent hypersplenism

NHL In patients with spleen-predominant features, survival is significantly improved after splenectomy compared with similar patients who did not undergo splenectomy

Hairy Cell Leukemia Hairy cell leukemia, a rare disease that approximately 2% of adult leukemias This disease affects older men who presents with palpable splenomegaly. Approximately 10% of patients require no treatment because of the indolent course Treatment for cytopenias or splenomegaly typically begins with purine analogue chemotherapy. For more refractory cancers, a second-line immunotherapy may be instituted

splenectomy in hairy cell leukemia
If chemotherapy or immunotherapy failed in symptomatic anemia, infections from neutropenia, or hemorrhage from thrombocytopenia can lead to splenectomy. Patients with diffusely involved bone marrow without massive splenomegaly are less responsive to splenectomy. Patients with hairy cell leukemia are also at a two- to threefold risk for developing other malignancies (solid tumors)

Chronic lymphocytic leukemia (CLL)
is disease of B lymphocytes characterized by the progressive accumulation of relatively mature but functionally incompetent lymphocytes. CLL is seen mainly after the age of 50 Medical treatment is indicated for symptomatic patients or those exhibiting evidence of rapid disease progression. Monoclonal antibodies are also used in the treatment of CLL. Bone marrow transplantation currently offers the only known cure for CLL. Splenectomy is indicated for patients with refractory splenomegaly and pancytopenia, which results in improvements in blood counts in 60% to 70% of patients

Chronic myelogenous leukemia (CML)
is a myeloproliferative disorder & may occur in patients from childhood to old age characterized by the progressive replacement of normal diploid elements of the bone marrow with mature-appearing neoplastic myeloid cells Although CML can be asymptomatic at presentation, patients commonly present with fever, fatigue, malaise, effects of pancytopenia (infections, anemia, easy bruising), and occasionally splenomegaly

CML Bone marrow transplantation is an option but prognosis has improved dramatically with the advent of recent therapies, making transplantation less common Symptomatic splenomegaly and hypersplenism in CML can be effectively treated with splenectomy, but there does not appear to be a survival benefit when performed during the early chronic phase. Surgery is therefore reserved for patients with significant symptoms.

CML the Philadelphia chromosome, is highly associated with CML

Non-Hematologic Tumors of the Spleen
The spleen can also be the site of metastatic disease, seen in up to 7% of autopsies of cancer patients. most frequently spread to the spleen are carcinomas of the breast, lung, and melanoma. Any primary malignancy, however, can metastasize to the spleen splenectomy may provide palliation for carefully chosen patients with symptomatic splenic metastases

white blood cell disorders
Splenectomy for white blood cell disorders can be effective therapy for symptomatic splenomegaly and hypersplenism, improving some clinical parameters but generally not altering the course of the underlying disease. Splenectomy is indicated to improve cytopenias and was shown to be 75% effective in a combined group of patients who had either CLL or nonmalignant Hodgkin's disease. AMINI MD

Splenectomy in Benign Hematologic Conditions
Aged red blood cells with decreased plasticity (>120 days) become trapped and destroyed in the spleen. SPLENECTOMY in Benign Hematologic Conditions Immune (idiopathic) Thrombocytopenic Purpura (ITP), is characterized by a low platelet count despite normal bone marrow and the absence of other causes of thrombocytopenia. Autoantibodies are responsible for the disordered platelet destruction mediated by the overactivated platelet phagocytosis within the reticuloendothelial system.

Platelet Disorders Is an autoimmune disorder
IDIOPATHIC (immune)THROMBOCYTOPENIC PURPURA (ITP) Is an autoimmune disorder Antiplatelet immunoglobulin G autoantibodies produced in the spleen premature removal of platelets opsonized by antiplatelet immunoglobulin G autoantibodies. Characterized by a low platelet count and mucocutaneous and petechial bleeding & ….. AMINI MD

Dif. Dx. Of ITP

ITP presentation purpura Epistaxis gingival bleeding.
Less commonly, gastrointestinal bleeding and hematuria are noted. Intracerebral hemorrhage is a rare but sometimes fatal presentation. The diagnosis of ITP involves the exclusion of other relatively common causes of thrombocytopenia—pregnancy, drug-induced thrombocytopenia (e.g., heparin, quinidine, quinine, sulfonamides), viral infections, and hypersplenism

Management of ITP Asymptomatic patients with platelet counts higher than 50,000/mm3 may be observed without further intervention. Platelet counts of 50,000/mm3 and higher are rarely associated with clinical sequelae, even with invasive procedures. Patients with platelet counts, between 30,000 and 50,000/mm3, may always be observed but with more routine follow-up because they are at increased risk for progressing to severe thrombocytopenia.

Initial medical treatment is glucocorticoid
prednisone, 1 mg/kg body weight/day) for patients with platelets counts <50,000 /mm3 and symptoms such as mucous membrane bleeding, high-risk conditions (e.g., active lifestyle, hypertension, peptic ulcer disease), OR platelet counts <20,000 to 30,000 /mm3, even without symptoms Clinical response with increases in platelet levels to >50,000 /mm3 is seen in up to two thirds of patients within 1 to 3 weeks of initiating treatment

ITP Of patients treated with steroids, 25% will experience a complete response. Patients with platelet counts >20,000 /mm3 who remain symptom-free, or who experience minor purpura as their only symptom, do not require hospitalization

ITP Hospitalization may be required for patients whose platelets counts remain below 20,000/mm3 with significant mucous membrane bleeding and is required for those who have life-threatening hemorrhage. Platelet transfusion is indicated only for those who experience severe hemorrhage. IV immunoglobulin is important for the treatment of acute bleeding, in pregnancy, or for patients being prepared for operation, including splenectomy. The usual dose is 1 g/kg body weight/day for 2 days.

ITP This dose usually increases the platelet count within 3 days; it also increases the efficacy of platelet transfusions For patients with severe thrombocytopenia, with counts less than 10,000/mm3 for 6 weeks or longer, those with thrombocytopenia refractory to glucocorticoid treatment, or those who require toxic doses of steroid to achieve remission, the treatment of choice is to proceed to splenectomy

ITP Splenectomy is also the treatment of choice for patients with incomplete response to glucocorticoid treatment and for pregnant women in the second trimester of pregnancy who have also failed steroid treatment or IV Ig therapy with platelet counts less than 10,000/mm3 without symptoms or less than 30,000/mm3 with bleeding problems.

ITP It is not necessary to proceed to splenectomy for patients who have platelet counts higher than 50,000/mm3, have had ITP for longer than 6 months, are not experiencing bleeding symptoms, and who are not engaged in high-risk activities. A recent review of short-term and long-term failure of laparoscopic splenectomy has reported an overall approximate failure rate of 28% at 5 years after splenectomy

ITP A systematic review has showed that 72% of patients with ITP had a complete response to splenectomy. Relapse occurred in a median of 15% of patients (range, 1% to 51%), with a median follow-up of 33 months Younger patients had improved responses Preoperative indium-111 labeled platelet scintigraphy with platelets sequestered predominantly within the spleen had a significantly higher response rate than those noted to have hepatic sequestration

ITP Durable platelet responses are associated with patients who have platelet counts of 150,000/mm3 by postoperative day 3 or more than 500,000/mm3 by the postoperative day 10 the long-term failure rate of laparoscopic splenectomy at approximately 8% and approximately 44/1000 patient-years of follow-up. Another study has estimated the complete response of ITP patients postsplenectomy to be 66%

ITP evaluation for a missed accessory spleen must be undertaken in patients who experience a relapse. Other treatment options for these patients include observation of stable nonbleeding patients with platelet counts higher than 30,000/mm3, long-term glucocorticoid therapy, and treatment with azathioprine or cyclophosphamide. Recent evidence regarding thrombopoietin receptor agonists may offer a novel medical therapy for patients with no response to steroids, IV immunoglobulin therapy, or splenectomy.

ITP Gingival bleeding, epistaxis, menorrhagia, hematuria, or even melena. Platelet >50,000/cc present with incidental findings; 30,000 <Platelet<50,000/cc often have easy bruising; 10,000 < platelet < 30,000/cc may develop spontaneous petechiae or ecchymosed; <10,000/mm3 are at risk for internal bleeding AMINI MD

ITP Children often present at a young age (peak age of approximately 5 years) with sudden onset of petechiae or purpura several days to weeks after an infectious illness. In contrast, adults experience a more chronic form of disease with an insidious onset. Splenomegaly is uncommon with ITP(Up to 10%) AMINI MD

TTP Thrombotic thrombocytopenic purpura
Petechiae, fever, neurologic symptoms, renal failure, infrequently, cardiac symptoms such as heart failure or arrhythmias. Neurologic changes range from generalized headaches to altered mental status, seizures, and even coma. Generally, however, the mere presence of petechiae and thrombocytopenia are sufficient to lead to the diagnosis of TTP and consideration of treatment AMINI MD

Primary tumors of the spleen
are commonly vascular neoplasms. Hemangiomas are frequent findings in spleens removed for other reasons. Angiosarcomas (or hemangiosarcomas) of the spleen usually occur spontaneously, but have been linked to environmental exposures, such as thorium dioxide or monomeric vinyl chloride

Lymphangioma Lymphangiomas, come to attention because of splenomegaly secondary to cyst enlargement. Splenectomy is appropriate for the diagnosis, treatment, and/or palliation of these conditions. lymphangiosarcoma has been found within lymphangiomas

Angiosarcoma(lymphangiosarcoma)
These tumors are aggressive and have a poor prognosis Patients with angiosarcomas may present with splenomegaly, hemolytic anemia, ascites, pleural effusions, or even spontaneous splenic rupture

Splenic Cysts They are classified as true cysts, which can be parasitic or nonparasitic, or as pseudocysts. Tumors of the spleen may also appear to be cystic; these include lymphangiomas and cavernous hemangiomas True cysts are lined with a squamous epithelium and many are considered congenital. These epithelial cells are often positive for carbohydrate antigen 19-9 (CA19-9) and carcinoembryonic antigen (CEA) by immunohistochemistry

True splenic cysts often asymptomatic discovered incidentally.
Patients may complain of abdominal fullness, early satiety, pleuritic chest pain, shortness of breath, and/or left shoulder or back pain. They may also experience renal symptoms from compression of the left kidney. On physical examination, an abdominal mass may be palpable. Rarely, splenic cysts present with acute symptoms related to rupture, hemorrhage, or infection. Diagnosis is best made by CT and operative intervention is indicated for those with symptomatic or large cysts. Total or partial splenectomy may provide appropriate treatment; 25% of the spleen appears to be sufficient to protect against pneumococcal pneumonia.

true splenic cyst Most true splenic cysts are parasitic cysts and occur in areas of endemic hydatid disease (Echinococcus spp.). Radiographic imaging reveals cyst wall calcifications or daughter cysts Rupture of the cyst and expulsion of contents into the abdomen may precipitate anaphylactic shock and can also lead to intraperitoneal dissemination of the infection

Pseudocysts 70% to 80% of nonparasitic splenic cysts. not lined with epithelium A history of prior trauma Sono or CT: smooth, unilocular, thick-walled lesion, sometimes with focal calcifications. Asymptomatic, small (<4-cm) pseudocysts do not require treatment and may involute with time. Symptomatic pseudocysts are treated surgically with total or partial splenectomy Percutaneous drainage has also been reported although, recurrence was common and subsequent complications were deemed too high.

Splenic Abscess is an unusual but potentially life threatening illness (0.7% in autopsy series). The mortality rate (15% to 20% in previously healthy patients, with single unilocular lesions to 80% for multiple abscesses in immunocompro-mised patients) as malignancies, polycythemia Vera, endocarditis, prior trauma, osteomyelitis, hemoglobinopathies, urinary tract infections, IV drug use, and AIDS Gram-positive cocci (commonly Staphylococcus, Streptococcus, or Enterococcus spp.) and gram- negative enteric organisms are typically involved. Mycobacterium tuberculosis, Mycobacterium avium, and Actinomyces spp.

Splenic Abscess Fungal abscesses (e.g., Candida spp.) also occur, typically in immunosuppressed patients present with nonspecific symptoms—vague abdominal pain, fever, peritonitis, and pleuritic chest pain. Splenomegaly is not typical. CT is the preferred method for diagnosis; however, the diagnosis can also be made with ultrasound. Unilocular abscesses are often amenable to percutaneous drainage, along with antibiotics, (success rates 75% to 90%). Multilocular lesions are usually treated with splenectomy, drainage of the left upper quadrant, and antibiotics Laparoscopic splenectomy for abscess has been reported

Wandering Spleen rare finding,
failure to form normal splenic peritoneal attachments (seen in children and in women between the ages of 20 and 40 years). the splenic pedicle is unusually long and prone to torsion Splenomegaly(resulting from venous congestion) ,Intermittent abdominal pain, or severe persistent pain (suggestive of tension or intermittent torsion of the splenic pedicle )

Wandering Spleen CT, with IV contrast of the abdomen, provides confirmation of the diagnosis, with the spleen located outside its usual position Rx. : Splenopexy or splenectomy

SPLENIC ARTERY ANEURYSM PORTAL HYPERTENSION FELTY'S SYNDROME
The triad of rheumatoid arthritis, splenomegaly, and neutropenia AMINI MD

Elective Laparoscopic Splenectomy
Laparoscopic splenectomy is now the preferred method for resecting the spleen barring trauma or cases of massive splenomegaly. Disadvantages are longer operating times and difficulty removing large organs; however, reduced hospital stay and more rapid postoperative recovery alleviate these limitations

Laparoscopic Splenectomy
Spleens measuring more than 22 cm in craniocaudal dimension, more than 19 cm in width, or more than g estimated weight will require hand-assisted laparoscopy, if not open splenectomy (Melman and Matthews) The reported conversion to open splenectomy is between 0% and 20% most are caused by intraoperative bleeding, lack of surgical experience, prohibitive adhesions, massive splenomegaly, and obesity contraindications (e.g., portal hypertension, major medical comorbidities)

Vaccination Vaccinations for N. meningitidis, S. pneumoniae, and H. influenzae should be given 15 days prior to elective splenectomy or within 30 days of an emergent splenectomy to reduce the risk of OPSI Several case series have compared the laparoscopic with the open approach and consistently favored the laparoscopic approach, particularly in regard to earlier resumption of diet, decreased postoperative pain, and shorter hospital stay but longer operative times. In published results to date, laparoscopic outcomes are equivalent to those of open splenectomy.

The laparoscopic technique
supine or lateral position, or a combination. General anesthesia and endotracheal intubation, nasogastric tube and urinary catheter Standard antithrombotic precautions the patient is placed so that the kidney rest can be raised to maximize the space between the iliac crest and costal margin. the patient is tilted in a reverse Trendelenburg position to facilitate retraction of the viscera caudally away from left upper quadrant

Camera port at the umbilicus or offset between the umbilicus and costal margin
Three to five 2- to 12-mm-diameter ports are used search of the abdomen for the accessory spleen. A 1-cm cuff of peritoneum is left along the lateral aspect of the spleen, which can then be grasped to facilitate medial retraction.

The devascularized spleen is suspended only from a small cuff of avascular splenophrenic tissue at the superior pole. This tissue facilitates transfer of the spleen into a retrieval bag

Post Splenectomy Mild thrombocytopenia may be seen in approximately 6% to 8% of otherwise normal pregnancies and in up to 25% of women with preeclampsia. Drug-induced thrombocytopenia in up to 40 cases/million users of common medications, such as trimethoprim-sulfonamide and quinine. Other medications, such as gold salts, have a higher incidence, almost 1% of users. Viral infection (e.g., hepatitis C virus [HCV], HIV, rarely, Epstein-Barr virus [EBV]) can be responsible for thrombocytopenia independent of splenic sequestration

Post Splenectomy Helicobacter pylori, has also been linked to infection- related thrombocytopenia that improves with eradication. ITP is predominantly a disease of young women; 72% of patients older than 10 years of age are women and 70% of affected women are younger than 40 years. ITP manifests somewhat differently in children — both genders are affected equally, onset is sudden, thrombocytopenia is severe, and complete spontaneous remissions are seen in approximately 80% of affected children. Girls older than 10 years with more chronic purpura are those in whom the disease seems to persist

LATE MORBIDITY AFTER SPLENECTOMY
Postsplenectomy thrombocytosis occurs particularly in patients with myeloproliferative disorders (e.g., CML, polycythemia vera, essential thrombocytosis), which can result in thrombosis of the mesenteric, portal, and renal veins and can be life-threatening because it can lead to hemorrhage and thromboembolism Also, there have been case reports of acute myocardial infarction in postsplenectomy patients with thrombocytosis

OPSI OPSI is the most common fatal late complication of splenectomy. Infection may occur at any time after splenectomy; most infections occurred more than 2 years after splenectomy and 42% occurred more than 5 years after splenectomy OPSI typically begins with a prodromal phase characterized by fever, rigors, and chills and other nonspecific symptoms, including sore throat, malaise, myalgias, diarrhea, and vomiting. Pneumonia and meningitis may be present. Many patients have no identifiable focal site of infection and present only with high-grade primary bacteremia. Progression of the illness is rapid, with the development of hypotension, disseminated intravascular coagulation, respiratory distress, coma, and death within hours of presentation

OPSI Despite antibiotics and intensive care, the mortality rate is between 50% and 70%. Also, survivors often have a long and complicated hospital course with multiple sequelae, such as peripheral gangrene requiring amputation, deafness from meningitis, mastoid osteomyelitis, bacterial endocarditis, and cardiac valvular destruction.

OPSI The most frequently involved organism in OPSI is S. pneumoniae and is estimated to be responsible for between 50% and 90% of cases. Other organisms are H. influenzae, N. meningitidis, Streptococcus and Salmonella spp., other pneumococcal organisms, and Capnocytophaga canimorsus, implicated in OPSI as a result of dog bites the risk for OPSI is greater among patients who have received splenectomy for malignancy or hematologic conditions than for those who underwent splenectomy for trauma

fatal OPSI The risk for fatal OPSI is estimated to be 1/300 to 350 patient-years follow-up for children and 1/800 to 1000 patient-years follow-up for adults In another large review in all age group ,septic fatalities were 2.1%

PROPHYLACTIC TREATMENT OF SPLENECTOMIZED PATIENTS
The standard of care for postsplenectomy patients includes immunization with polyvalent pneumococcal vaccine (PPV23) ,H. influenzae type b conjugate, and meningococcal polysaccharide vaccine within 2 weeks of splenectomy if the patient did not receive these prior to surgery education of patients, families, and caregivers must stress the need for prompt medical attention if these patients show signs of infection

PPV23 (polyvalent pneumococcal vaccine)
PPV23 (is composed of purified preparations of pneumococcal capsular polysaccharide antigens of 23 types of S. pneumoniae (25 mg each) that cause 88% of the bacteremic pneumococcal disease in the United States.) The relationship between antibody titer and protection from invasive disease has not been established. it has been clearly documented that after vaccination with PPV23, antibody levels decline after 5 to 10 years, and may fall to prevaccination levels

Candidates for revaccination with PPV23
include : asplenic patients who received the 14-valent vaccine Adults who received the 23-valent vaccine 6 years prior Adults who have shown a rapid decline in pneumococcal antibody levels (e.g., patients with nephrotic syndrome, those with renal failure, transplant recipients) Children at highest risk (e.g., asplenia, nephritic syndrome, sickle cell anemia) who would be 10 years old at revaccination Only one PPV23 revaccination dose is recommended for these high-risk individuals and it is administered 5 years after the initial dose.

CDC (U.S. Centers for Disease Control and Prevention) recommend that all splenectomy patients, including those with hereditary spherocytosis, be revaccinated and reeducated between 2 and 6 years after splenectomy determination of pneumococcal antibody titers after immunization of every splenectomized patient Subsequent follow-up of antibody titers at 3 to 5 years partial splenic salvage or splenic autotransplantation may improve the humoral immune response to PPV23

OPSI The most serious sequela is overwhelming postsplenectomy infection (OPSI), Older studies have demonstrated that the risk of OPSI is greatest within the first 2 years after splenectomy but recent studies have confirmed that a lifelong risk remains. One third of cases occur more than 5 years after surgery, with the overall incidence reported to be 3.2% to 3.5%. & mortality is between 40% and 50%. The risk is greatest in patients with thalassemia major and sickle cell disease. OPSI is typically caused by polysaccharide-encapsulated organisms, such as Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae

&OPSI Post Splenectomy
Encapsulated and other organisms are bound by antibodies and complement components in preparation for phagocytosis by macrophages in the spleen. After splenectomy, the antibodies continue to bind but digestion by splenic macrophages is no longer possible. Asplenic patients have been noted to express similar postvaccination immunoglobulin G (IgG) antibody levels but functional antibody levels, however, were lower

Post Splenectomy Also, asplenic patients have been found to express subnormal IgM levels and Their peripheral blood mononuclear cells exhibit a suppressed immunoglobulin response Other factors such as properdin and tuftsin, opsonins, exhibit reduced serum levels after splenectomy. Properdin (factor P), a globulin protein, initiates the alternate pathway of complement activation; this increases the destruction of bacteria, foreign, or otherwise abnormal cells.

Post Splenectomy Tuftsin, a tetrapeptide, enhances the phagocytic activity of mononuclear phagocytes and polymorphonuclear leukocytes. The spleen also plays a key role in cleaving tuftsin from the heavy chain of IgG Methods of blood flow within the spleen, the closed and open systems . In open system cellular cleansing processes take place. These include removal of senescent cells, cellular inclusion (e.g., red cell nucleoli), parasites, and sequestration of red cells (for maturation) and platelets (reservoir).

Overwhelming Postsplenectomy Infection(OPSI)
Splenectomy imparts a small (<1 to 5%) but definite lifetime risk of fulminant, potentially life-threatening infection. After splenectomy, annual influenza immunization is advisable AMINI MD

OPSI Overwhelming postsplenectomy infection (OPSI) is an uncommon but potentially grave disease. Children and those undergoing splenectomy for hematologic malignancy are at elevated risk of OPSI. Encapsulated bacteria risk posed by Streptococcus pneumoniae, H.influenzae type B, and meningococcus to an asplenic patient. AMINI MD

OPSI Vaccination of the splenectomized patient remains the most effective prevention strategy against OPSI and should be given at least 2 weeks before surgery If the spleen is removed emergently ,vaccinations should be given as soon as possible after surgery AMINI MD

splenic autotransplantation
The most effective site of splenic autotransplantation was found to be the omental pouch, and approximately 50% of the spleen would be necessary for the prevention of pneumococcal sepsis. However it seems to have limited applicability in humans OPSI is preventable if appropriate precautions are taken.

CDC immunization guidelines for asplenic patients
tetanus (Td/Tdap), human papillomavirus (HPV), measles, mumps, rubella (MMR), varicella, zoster, influenza, pneumococcal polysaccharide, hepatitis A, hepatitis B, and meningococcal vaccines Several sources have reported that the conjugate pneumococcal vaccine is more effective in asplenic patients than the polysaccharide vaccine and should be given immediately postoperatively, as well as every 5 years to maintain efficacy

pneumococcal infection, is reported to be the cause of OPSI in 50% to 90% of patients
Significant controversy still exists regarding antibiotic prophylaxis in postsplenectomy patients OPSI secondary to penicillin-sensitive pneumococcal infection has been reported in children and adults receiving penicillin prophylaxis prophylaxis with penicillin is routinely practiced in children, at least during the first 2 postsplenectomy years

there is evidence that there is no difference in the incidence of sepsis in postsplenectomy sickle cell patients when the antibiotic prophylaxis is ceased after 5 years or given lifelong Other studies have reported significant differences in the incidence of sepsis, with and without antibiotic prophylaxis patients should be made aware that even with daily antibiotics, all infections may not be preventable

Education & aggressive empiric antibiotic Rx
the risk of OPSI is lowest in patients who exhibit the greatest understanding of the infectious risks of asplenia. This highlights the importance of patient education, particularly at follow-up visits, to ensure compliance with antibiotic and vaccine prophylaxis any asplenic patient who presents with rigors or fever must be started immediately on aggressive empiric antibiotic coverage, even without culture data.

Preoperative splenic artery embolization for elective splenectomy.
Partial splenectomy Preoperative splenic artery embolization for elective splenectomy. Laparoscopic splenectomy provides equal hematologic outcomes with decreased morbidity compared with the open operation. The laparoscopic approach has emerged as the standard for elective, nontraumatic splenectomy AMINI MD

AMINI MD

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