SPLEEN Flashcards
postsplenectomy sepsis is inversely related to
age.
In a younger child, the risk of developing this condition is greater and the impact of the infection will be more severe.
splenectomies are not performed for patients with hereditary erythrocyte syndromes until after ages 6 to 10 years.
These postsplenectomy septic episodes occur within what time periods for kids
the first 2 years after splenectomy in 80% of cases.
In adults, the reason for splenectomy related to the incidence of sepsis.
In trauma, the incidence of sepsis in a large series was 1.4%,
thalassemia, the incidence was 24.8%!
Patients with any associated immunodeficiency such as malignancy or patients undergoing chemotherapy for treatment of Hodgkin disease are also at increased risk for sepsis.
The mortality rate of postsplenectomy sepsis is between 50% and 60% in most series.
The types of organisms that account for infection are
typically encapsulated organisms, with the most common being Streptococcus pneumoniae, which accounts for 50% of septic episodes in most series. In decreasing order of frequency, other bacteria associated with postsplenectomy sepsis are Haemophilus influenzae, Neisseria meningitidis, β-hemolytic Streptococcus, and Staphylococcus aureus. The current recommendation for patients who are having elective splenectomy is to vaccinate susceptible individuals with Pneumococcus strains, which is ideally performed 2 weeks before operation.
The operative approach for open splenectomy involves
either a midline abdominal or left subcostal incision.
A long midline incision should be employed in patients who have massive splenomegaly.
One approach, particularly for small spleens that are mobile, is to initially divide the lateral attachments and place packs in the left upper quadrant to elevate the spleen and then proceed with the vascular dissection. This technique should be discouraged particularly in patients who are thrombocytopenic or in patients with massive splenomegaly. In this situation, the splenectomy should start by obtaining vascular control before manipulating the spleen, which could lead to capsule rupture and significant blood loss.
For patients with immune thrombocytopenia purpura timing of platelets with surgery for splenectomy
not be given until the spleen is removed
or
at least until ARTERIAL flow is controlled because of the clearance of transfused platelets by the spleen in this disease.
The specific criteria for hypersplenism are
(a) documented anemia, thrombocytopenia, or leukopenia;
(b) normal compensatory response by the bone marrow to correct cytopenia;
(c) correction of the cytopenia by splenectomy.
Some definitions of hypersplenism may also include the criterion of splenomegaly.
The most important symptom of hypersplenism
is early satiety with accompanying weight loss
as the stomach is compressed between the liver and the enlarged spleen.
treatment of hypersplenism
Hypersplenism is the most important indication for elective isolated splenectomy to reverse the cytopenia and often to relieve compressive symptoms from splenomegaly.
Hereditary spherocytosis,
mild to moderate anemia,
splenomegaly
jaundice.
30% and 60% of patients have been reported to have pigmented gallstones due to breakdown of hemoglobin.
The treatment for hereditary spherocytosis is splenectomy and is indicated in virtually all patients.
This treatment does not remove the spherocytes, but it does relieve all symptoms.
The major question involving management of these patients is the time of the splenectomy because of the increased incidence of overwhelming postsplenectomy sepsis in very young children. It is usually recommended that patients wait until after age 4 to 6 years before undergoing to splenectomy.
The primary hematologic function of the spleen is
removal of senescent erythrocytes or REMODELING of abnormal red blood cells with various abnormalities.
This physiologic filtration function is increased in disease states to produce hypersplenism.
The spleen may play a minor role in hematopoiesis and storage of blood cells that can be mobilized for circulation, with the stored cells being predominately platelets.
Pathologic destruction of red cells occurs in diseases such as hereditary spherocytosis or elliptocytosis in which a genetic defect creates abnormal red cell pliability, limiting its passage through the red pulp of the spleen.
A second physiologic process involving circulating erythrocytes is remodeling or pitting, which is partial removal of the cell membrane typically associated with cytoplasmic inclusions.
The destruction of other circulating cellular elements of the blood (platelets and leukocytes) is more in the realm of pathophysiology of the spleen than normal physiologic function. The disease process in which these cells are removed are either related to autoantibodies to cell surface elements or related to hypersplenism. The spleen serves as a potential source of hematopoiesis of all cell types during gestation. In healthy humans, there is thought to be very little if any production of red blood cells, granulocytes, or platelets. The immunologic function of the spleen is to generate an immune response to antigens that are identified and cleared from the bloodstream. Either opsonized antigens or specific encapsulated microorganisms are important examples of target antigens trapped by the spleen. The spleen is an ideal environment for generation of either a cellular or humoral immune response. Many cell types are necessary for stimulation of the immune response, including phagocytic cells, dendritic cells, T cells, and B cells, which may form general follicles to generate a specific antibody response. The spleen is also involved in nonspecific immune responses. It is the site of synthesis of both properdin and tuftsin, which are opsonins.
The splenic artery
is one of the three major trunks along with the left gastric artery and common hepatic artery branching off from the celiac axis. The splenic artery generally travels outside the parenchyma of the pancreas just at the superior border, although curves that travel inferiorly may be completely covered by the posterior surface of the pancreas, whereas superior curves may be well away from the pancreatic surface. It is these curves, which become more cranial, that are the optimal place to provide a ligature to control the splenic artery during procedures in which there is significant thrombocytopenia or for enlarged spleens. The first major splenic branch occurs approximately 2 to 3 cm from the hilum and is called the superior polar artery. The main artery then divides into anywhere between three and five segmental branches that enter along the trabecula of the spleen. Additional blood supply to the spleen comes from the left gastroepiploic artery via the short gastric vessels. The splenic vein is formed by segmental venous branches that leave the trabecula and coalesce into the main splenic vein in the hilum of the spleen. The splenic vein is intimately associated with the posterior surface of the tail and body of the pancreas to its junction with the superior mesenteric forming the portal vein. The blood flow to the spleen in the typical adult is estimated to be 200 to 300 mL/min or approximately 5% of the cardiac output.
hematologic changes following splenectomy
The changes in circulating blood cells after splenectomy or in cases of hyposplenism may affect the erythrocytes, leukocytes, and platelets.
Over time, the intracytoplasmic inclusions in the red cells that are normally cleared by the spleen accumulate, resulting in the presence Howell-Jolly bodies, Heinz bodies, and Pappenheimer bodies as well as target cells with excess red blood cell membrane and occasionally increases in circulating nucleated red blood cells or reticulocytes.
As the spleen is the organ of storage for large proportions of platelets, a splenectomy often results in thrombocytosis, with platelet counts postsplenectomy ranging from 500,000/mm3 up to 1 million/mm3 in some cases.
This increased platelet count is usually transient and may be a reflection of the fact that the spleen, while being a storage organ for platelets, may not be a primary area of platelet destruction after the typical half-life of 10 days.
Immediate response after splenectomy in white blood cells is leukocytosis, again reflecting the storage of a large proportion of white blood cells in the spleen. As in thrombocytosis, the effect is transient; however, there may be long-term increases in the proportion of circulating lymphocytes and monocytes after splenectomy. Preserving even a small amount of spleen can preserve splenic function in the clearance of senescent blood cells.
Acute ITP
generally occurs in children younger than age 8 years following a viral upper respiratory illness. Of all children with acute ITP, spontaneous remission occurs in 80% to 90% of cases.
adults who develop ITP have remission;
Only 8% to 10% of patients of adults who develop ITP have remission; most develop chronic ITP.
Chronic ITP accounts for most cases considered for splenectomy. The average age at diagnosis is the fourth decade of life, and the disease affects women more commonly than men. The pathophysiology of ITP is development of immunoglobulin G antibody to a platelet antigen. The spleen plays a predominate role in this disease because it may be the site of initial antibody production, it is almost certainly the site of continued antibody production, and in most patients it is the primary site of platelet destruction.
