Download The Spleen

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5
The Spleen
Hugo W. Tilanus
Aims
To describe the development and anatomy
of the spleen. To describe the effects of a
splenectomy.
Embryology
The spleen starts to develop in the fourth week
of gestation as a mesenchymal condensation
in the dorsal mesogastrium of the lesser sac. In
the following weeks these early mesenchymal
cells differentiate to a vascular lymphatic
pedicle that eventually forms the spleen. Smaller
condensations that develop near the hilum of
the spleen form accessory spleens. When the
embryo is about 10 cm in length the dorsal
mesogastrium can be divided into a posterior
part and an anterior part. The posterior part,
from the posterior abdominal wall to the spleen,
is eventually invaded by the pancreatic bud,
which grows as far as the hilum and later
fuses with the peritoneum of the posterior
abdominal wall ventral to the left kidney to
form the splenorenal ligament. In this dorsal
structure the splenic artery and vein develop.
The anterior part of the dorsal mesogastrium
develops into the gastrosplenic ligament and
contains the short gastric vessels. It is now clear
that the spleen is of mesenchymal origin and
does not originate from the embryonic entodermal gut.
The splenic condensation forms a trabecular
structure resulting in a mesh and ending up
in the connective supportive structure of the
spleen. The isolated free cells in this network
differentiate into hematopoietic cells in the next
months of gestation. Other cells derived from
the sinusoids of the splenic artery specialize to
participate in the reticuloendothelial system [1].
Anatomy
The normal spleen cannot be palpated as it lies
at the dorsal side of the left upper quadrant
of the abdomen and its surface covers an oval
area of the diaphragm, the hilum being projected ventrally depending on the distension of
the stomach. As the tail of the pancreas is the
Achilles heel of splenectomy, detailed knowledge of the peritoneal reflections of the spleen
is essential. Starting from the gastrosplenic ligament it divides at the hilum. The anterior sheet
covers the surface of the spleen and reflects to
the anterior surface of the left kidney. The posterior sheet encloses the splenic vessels and
reflects to the dorsal peritoneum. The inferior
part rests upon the phrenicocolic ligament
and is, if connected with this ligament, a preferential place for rupture of the capsule and
bleeding.
The abundant arterial vasculature of the
spleen arises from the splenic artery and comes
from the celiac trunk, running, sometimes
tortuously, all along the upper border of the
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pancreas and ending in a number of smaller
branches that vascularize the spleen. Two
branches, the superior polar artery and the
left gastroepiploic artery, serve a special function. The superior polar artery is one of the
early branches of the splenic artery and divides
into the short gastric vessels before entering
the spleen. The intrasplenic arterial supply in
divided into three segments, creating a superior,
middle and inferior segment.
The left gastroepiploic artery, one of the most
inferior branches of the splenic artery, vascularizes the greater curvature distal to the short
gastric vessels and mostly anastomoses with the
right gastroepiploic artery.
Some large veins join at the splenic hilum to
form the splenic vein, which runs a straight
course to the portal vein, and receiving the inferior mesenteric vein.
The spleen is created in units called the red
pulp and the white pulp. The red pulp contains
the vascular structures: the pulp sinuses and
pulp cords that are lined by reticuloendothelial
cells and filled with blood. The white pulp consists of arterioles surrounded by periarteriolar
T lymphocytes. A zone of B lymphocytes that
also contain the germinal centers made up of B
cells and macrophages surrounds this central
area of the white pulp. The most peripheral
layer of the white pulp is another B-cell layer,
the marginal zone.
Once inside the spleen, the blood flow from
the branches of the splenic artery enters firstly
the trabeculae and from there goes into the
small central arteries dividing into the arterial
capillaries. The periarteriolar lymphoid sheet of
T cells surrounded by B cells continues along
the arterial vessels until they become small arterioles. Red blood cells pass from the central
arteries to pulp cords and further through critical small openings in the sinus endothelium
to the spleen sinuses and the spleen venous
system. During this passage through the white
pulp, aged red blood cells, nuclear material,
denaturated hemoglobin and other debris are
retained in the pulp cords and phagocytosed by
macrophages [2].
Physiology and Function
The role of the spleen as an important functional organ, not only in childhood but also in
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adults, should not be underestimated. For the
surgeon this should lead to careful handling of
the spleen in elective abdominal surgery in
order to avoid injury, preventing splenectomy
and to a conservative approach in case of
trauma of the spleen without jeopardizing the
patient’s health. It is therefore important to
remember the four major physiologic functions
of the spleen.
1. The spleen is an important organ in
the clearance of microorganisms and
unwanted antigens from the circulation. Moreover it generates immune
responses to foreign antigens, especially
by the production of IgM antibodies.
Opsonic proteins produced in the spleen
promote phagocytosis and initiate complement activation, resulting in destruction of bacteria and foreign or abnormal
cells. Especially against bacteria in the
bloodstream that are not recognized by
the host’s immune system, the spleen is
a major second line of defense. When a
specific antibody in the liver is missing
for bacterial removal, the spleen
becomes the site for this action.
2. In addition to sequestration and removal
of older normal red blood cells, the
spleen is able to remove abnormal red
blood cells, e.g. morphologically abnormal erythrocytes such as spherocytes
and sickled cells. As the spleen removes
immunoglobin-coated blood cells it is
the place of destruction in a variety of
autoimmune diseases. Intraerythrocytic parasites as in malaria are also
removed in the white pulp. In addition,
the blood flow rate plays an important
role in the filtering function of the
spleen. In splenic vein thrombosis resulting in stasis this leads to increased red
cell removal.
3. The spleen has a “buffer-like” function
in regulation of the portal flow and in
pathological conditions like portal
hypertension.
4. The spleen has an important auxiliary
function in the production of red blood
cells when normal hematopoiesis in
bone marrow fails as in hematological
diseases [3].
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THE SPLEEN
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Splenomegaly
Enlargement of the spleen is a symptom of
a large variety of diseases. The enlargement is
due to an increase in cellularity and vascularity
and the most important groups of diseases
are:
1. Infections like bacterial septicemias,
viral and parasitic infections and splenic
abscess.
2. Diseases related to abnormal red blood
cells like spherocytosis and sickle cell
anemia.
3. Infiltrative enlargement as seen in
benign amyloidosis and Gaucher’s
disease or in malignant leukemias and
lymphomas.
4. Altered splenic blood flow. This group of
diseases can be divided into an isolated
outflow obstruction of the splenic vein
only as in splenic vein thrombosis or
enlargement of the spleen as in generalized portal hypertension.
5. Immune disorders like rheumatoid
arthritis or systemic lupus erythem
atosus.
6. Hypersplenism. The spleen removes
excessive quantities of blood cells from
the circulation leading to anemia and
platelet
reduction.
Hypersplenism
occurs in the course of an underlying
disease or is idiopathic.
The degree of the splenomegaly and the
symptoms vary with the underlying disease.
A fast increase in diameter provokes upper
abdominal discomfort and local tenderness
becoming extreme pain when splenic infarction
occurs in acute disease. Massive enlargement
can be completely asymptomatic as in portal
hypertension or hemolytic anemias or other
more chronic diseases. At physical examination
splenomegaly can easily be missed if the examination is not started in the left lower quadrant of the abdomen with the patient in a leftsided position. Other techniques to assess the
size of the spleen are ultrasound scanning, computed tomography and 99Tc-colloid liver-spleen
scan [4].
Indications for
Splenectomy
The indications for splenectomy can be arbitrarily divided into two large groups – hematologic disorders or trauma. The hematologic
disorders comprise platelet disorders like idiopathic thrombocytopenic purpura, thrombotic
thrombocytopenic purpura and hypersplenism
in which low platelet count is accompanied by
depression of one or more of the formed elements of blood, red cells white cells and
platelets. Splenectomy for staging of Hodgkin’s
and non-Hodgkin’s lymphoma has decreased
over the last 10 years and is no longer the most
important diagnostic test for these diseases.
Splenectomy for trauma can be divided into surgical trauma of the spleen, especially during
upper abdominal surgery leading to accidental
splenectomy, and accidents involving blunt
trauma of the spleen.
Splenectomy for
Hematologic Disorders
Immune Thrombocytopenic
Purpura (ITP)
ITP is caused by a circulating antiplatelet factor
identified as an IgG antibody directed towards
a platelet-associated antigen. There is no evidence for a clear autoimmune entity. Most
patients are women in their late thirties but the
percentage of men is increasing, as is the total
incidence. Spontaneous and easy bruising and
bleeding are the most common first symptoms.
Petechiae, epistaxis, mucosal bleeding and menorrhagia are often seen and reflect the number
of platelets being mostly under 20 000/mm3
in serious blood loss. ITP is diagnosed after
exclusion of other underlying illnesses or medications like sulfonamides and quinine, which
can induce thrombocytopenia. An otherwise
normal blood count, a normal bone marrow
aspirate and a not enlarged spleen support the
diagnosis. There is an increased megakaryocyte
mass in combination with a greatly shortened
platelet survival. The amount of circulating
antiplatelet-associated antibodies mirrors the
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severity of the disease. These antibodies are
preferentially produced in the spleen: liver and
bone marrow are less involved. One-third of the
total circulating platelets are harbored within
the spleen so most platelets are destroyed there.
Prednisone therapy does not prevent destruction but the increased platelet count is the
result of increased platelet production. Most
patients improve with corticosteroid therapy
but complete and sustained remission of ITP
is only achieved in up to 25% of patients.
Splenectomy is performed in patients who are
completely or partially refractory to corticosteroids. Sustained remission is more probable in
patients who showed an initial response to corticosteroid therapy. Most patients are referred
after failure of the initial corticosteroid therapy,
which should be continued during surgery.
Immunization with polyvalent pneumococcal
vaccine should be administered preferably 10 to
14 days before splenectomy. High dose intravenous gammaglobulin is effective in increasing
the platelet count in patients refractory to
corticosteroids especially in urgent cases such
as intracranial hemorrhage. Nearly 80 to 90% of
patients develop a normal sustained platelet
count after splenectomy [5–7].
Thrombotic Thrombocytopenic
Purpura (TTP)
In thrombotic thrombocytopenic purpura
platelet microthrombi depositions occlude arterioles and capillaries resulting in intravascular
depositions of hyaline material consisting of
platelets and fibrin. The etiology is unknown
but the disease may be initiated by connective
tissue disorders like lupus erythematosus, bacterial and viral stimuli, malignancies and AIDS.
The clinical picture is dominated by hemolysis. Anemia occurs in association with fragmented red blood cells in the peripheral blood,
an elevated reticulocytes and thrombocytopenia. As the disease progresses over weeks or
months, patients, primarily young adults and
more often women, die of progressive renal
failure and brain involvement with a 1-year survival of less than 10% in untreated patients.
Treatment consists of plasmapheresis with
infusion of fresh frozen plasma, antiplatelet
agents and high dose corticosteroids in combination with removal of a normal to moderately
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enlarged spleen. The explanation of the
response to splenectomy is not clarified but
the majority of long-term survivors have undergone this procedure [8].
Hodgkin’s Disease
Hodgkin’s disease, described by Thomas
Hodgkin in 1832, usually presents with localized
lymphomas that spread to lymphoid structures
elsewhere in the body. Half of the patients
present with lymph nodes in the neck or the
supraclavicular region and half of them present
with mediastinal lymphadenopathy. The disease
is characterized by the unique multinuclear
giant cell, the Sternberg–Reed cell.
Most patients are asymptomatic at first presentation but weight loss, fever, night sweats
and pruritus, the so-called B symptoms, sometimes accompanied by the characteristic intermittent high, Pel–Ebstein fever, are signs of
widespread disease and carry a bad prognosis.
Anemia, leucocytosis, and eosinophilia are
common. In 1966 the Rye classification was
introduced and has been unaltered since then.
There are four histologic subgroups identified
in decreasing order of prognosis: the lymphocyte predominant group, the nodular sclerotic
group, the mixed cellular group and the lymphocyte depleted group. Staging is based on the
lymph node region involved. In stage 1 disease,
the lymph nodes of one region, above or below
the diaphragm, are involved. Stage 2 includes
two affected lymph node regions on one side of
the diaphragm. Stage 3 refers to lymph node
involvement above and below the diaphragm
and stage 4 describes disseminated disease
to extranodal organs on both sides of the
diaphragm. It is important to remember that
treatment and prognosis in Hodgkin’s disease
are dependent on stage of the disease whereas
in non-Hodgkin’s lymphoma, treatment and
prognosis are largely based on histologic
subtype.
Controversy exists regarding the role of
staging laparotomy and splenectomy in the
diagnosis and treatment of Hodgkin’s disease
as the introduction of non-invasive diagnostic
tests and less toxic chemotherapy make this
procedure less and less indicated. Today,
staging laparotomy is indicated in selected
patients only and includes splenectomy, liver
biopsy, intra-abdominal and retroperitoneal
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lymph node sampling according to clinical findings and the outcome of preoperative diagnostics. A review of the different therapeutical
strategies for the different stages of Hodgkin’s
disease is beyond the scope of this chapter [9].
Non-Hodgkin’s Lymphomas
Non-Hodgkin’s lymphomas (NHL) are mostly
detected as an abdominal mass or as hepatic
and/or splenic enlargement in addition to mediastinal and peripheral lymphadenopathy and
in combination with general symptoms such
as night sweats, weight loss and fever. NHL
spreads fast to distant nodal and extranodal
sites through the bloodstream.
Chemotherapy and radiation are the first-line
therapeutic options based on histologic features
and the stage of the disease. Splenectomy is only
indicated in patients with primary NHL in the
spleen presenting with symptomatic splenic
enlargement due to parenchymal tumor infiltration or in order to correct hypersplenism,
which is the result of hematological depression
with anemia and thrombocytopenia. In this situation splenectomy relieves the discomfort of
splenomegaly and the systemic effects of hypersplenism [10].
The Spleen in Chronic Leukaemia
The spleen is often involved in different forms
of leukemia like chronic lymphocytic, chronic
myeloid and hairy cell leukemia.
In chronic lymphocytic leukemia (CLL)
lymph node enlargement is the most common
finding and progressive splenomegaly is present
in most patients. There is as yet no curative
therapy but due to effective medical treatment
with chemotherapeutic agents and corticosteroids combined with irradiation most patients
can be palliated for up to 10 years or more. In
later stages CLL is often complicated by autoimmune hemolytic anemia, which is an indication
for the removal of an often very large spleen, up
to more than 6 kg in severe cases. This leads to
hematologic improvement in the large majority
of patients but does not improve survival.
In chronic myeloid leukemia splenomegaly
is a common finding together with lymphadenopathy, hepatomegaly and sternal tenderness. A myeloblastic crises results in death
from infection or bleeding within weeks or
months. Splenectomy is only indicated in a
small group of patients with severe thrombocytopenia and anemia or for relief of pain due to
splenomegaly or infarction.
Hairy cell leukemia (HCL) is an uncommon
form of leukemia presenting with moderate splenomegaly, hepatomegaly and lymphadenopathy. It is characterized by malignant
cells with “hairy” cytoplasmic filamentous projections in the peripheral blood. The majority
of patients are elderly men presenting with
moderate to severe pancytopenia resulting in
anemia, thrombocytopenic bleeding, neutropenia and recurrent infections. For patients with
diffuse manifestations of HCL especially in bone
marrow and severe cytopenia, interferon in
combination with pentostatin is remarkably
effective. Splenectomy especially in an early
stage of the disease leads to improvement of
symptoms in half of the patients [11,12].
Hereditary Hemolytic Anemias
Hemolysis resulting in hemolytic anemia must
be quite severe as the normal bone marrow
can produce erythrocytes up to eight times the
normal production. Congenital disorders have
an intrinsic defect involving different metabolic
functions and structures of the red cell. The
clinical picture consists of pallor and/or jaundice and biliary complications due to the excessive amount of bilirubin to be disposed of by
the biliary system. Mild to moderate symptoms
often already manifest at a young age. Hereditary spherocytosis, sickle cell anemia and thalassaemia are the most common hereditary
disorders that benefit from splenectomy [13,14].
Autoimmune Hemolytic Anemias
Autoimmune hemolytic anemia (AIHA) is an
acquired disease caused by antibody production
against the own red cells. A positive direct
Coombs test is discriminating for AIHA. There
are two forms, which are classified as warm
or cold reactive depending on the affinity of
the antibody to the red cell at 37°C and at
temperatures approaching 0°C. Warm antibodies are usually IgG whereas cold antibodies
mostly concern IgM immunoglobulins. The
latter bind to red cells in the peripheral, cold
circulation leading to immediate or delayed
hemolysis.
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AIHA may be associated with drugs especially
penicillins, with viral infections such as infectious mononucleosis and with leukemias and
lymphoproliferative disorders. Treatment directed at the hemolytic anemia consists of transfusion of blood, corticosteroids and splenectomy when conservative medical therapy fails.
The response rate to splenectomy is high, up to
80% of patients, especially when there is a high
degree of sequestration in the spleen [15].
Principles of Elective
Splenectomy
Before elective splenectomy is planned, patients
should receive polyvalent pneumococcal
vaccine, polyvalent meningococcal vaccine and
Haemophilus influenzae vaccine. Blood products should be ordered at an early stage, as
cross-matching is sometimes difficult, especially in acquired haemolytic anemias and
isoantibodies. Some patients may have developed cold hemagglutinins so blood and blood
products should be warmed before transfusion.
Open Splenectomy
The midline upper abdominal incision is preferred in virtually all splenectomies. Neither in
very large spleens, nor in trauma, are thoracoabdominal incisions necessary. The lateral surface
is palpated carefully in order to rule out adhesions. If present they can be divided sharply. In
rare cases the spleen can be firmly adhered to
the lateral abdominal wall and laceration of the
capsule should be prevented by sharp division of
its posterior attachments. During splenectomy
it is important to remember the local anatomy.
The gastrosplenic ligament covers the vascular
structures at the ventral side, divides at the
hilum and covers the surface of the spleen. The
dorsal part envelops the vessels and reflects to
the dorsal peritoneum. After division of this
dorsal part of the splenic ligament the spleen can
be mobilized in most cases, leaving the tail of the
pancreas in place. Thereafter the splenic artery
and vein and the short gastric vessels can be
divided. The tail of the pancreas is the Achilles
heel of the procedure.
Mobilization of the tail can lead to pancreatitis and injury to the pancreatic duct of the tail
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can lead to pseudocyst formation. Special care
should be taken of the stomach fundic vessels.
A ligature can very easily catch a small part
of the stomach wall leading to perforation.
Especially in very large spleens some authors
prefer an early and more central ligation of
the splenic vessels in order to prevent massive
hemorrhage during the splenectomy phase.
Draining of the left upper abdominal space is
not routinely advised and should be restricted
to cases with large blood loss or pancreatic
damage [16].
Laparoscopic Splenectomy
Laparoscopic splenectomy has gained wide
acceptance since the first reports in 1999. There
is no longer an absolute contraindication and
some large series highlighted the many advantages of the laparoscopic procedure especially in
adults and children with hematological disorders. There are relative contraindications, e.g. a
higher complication rate is seen in patients with
or after portal hypertension or splenic abscess
predisposing for perisplenitis. Massive spleens
remain a challenge with a high failure rate in
early series. Successful laparoscopic removal of
spleens with a diameter over 30 cm has been
reported; but rather than the absolute diameter,
the relationship between the patient’s body size
and the size of the spleen, the splenic index,
is the limiting factor. A splenic index of 0.2
being normal, a patient with an index exceeding
0.76 is unlikely to benefit from a laparoscopic
approach. In a series of over 200 splenectomies
for mostly hematologic disorders the laparoscopic procedure was successful in 97% of
patients.
In the right decubitus position, open insertion of the first trocar is advised and pneumoperitoneum is obtained. three to four ports
are placed along an arch concentric to the
spleen and 3 cm distal to the costal margin. The
lateral splenic attachments are divided leaving
the uppermost fibrous bands intact to facilitate
exposure. The two layers of the gastrosplenic
ligament are opened and the short gastric
vessels are elevated and divided. Not before
the spleen is completely mobilized is the hilum
divided with an endoscopic linear stapler,
avoiding damage to the tail of the pancreas. This
last step is more difficult in large spleens as
they tend to turn dorsally, which complicates
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placement of the stapler. A nylon bag is manipulated around the spleen after which the last
superior fibers are severed. The spleen is morcellated or completely retrieved through the
largest trocar opening [17].
The Spleen in Trauma
In cases of blunt and especially high velocity
trauma information regarding direction of the
force, vertical or horizontal, and the nature
of the force, compression or deceleration, is of
the utmost importance. Information should be
obtained about prior operations or diseases of
the spleen, as the enlarged spleen is especially
prone to injury.
Splenic injury produces vague abdominal
symptoms with occasionally left shoulder pain
caused by free intra-abdominal blood which
causes only a mild irritation of the peritoneum.
Skin lesions may be helpful in the diagnosis, as
are lower left rib fractures and pelvic fracture.
Shock and hypotension are late symptoms that
are seen after major loss of circulating volume
of 30% or more. Physical findings are more
often than not disappointing, especially in the
polytraumatic patient with multiple fractures
that provide another explanation for sometimes
major blood loss and instability.
Effective resuscitation in the shock room
is mandatory before evaluation is performed.
Direct laparotomy is performed in persisting
unstable patients but mostly there is time for
further evaluation with diagnostic peritoneal
lavage to confirm intra-abdominal blood loss,
ultrasound and or CT scan. Delayed symptoms
in case of rupture of a subcapsular hematoma
can develop days or weeks after the primary
trauma. Splenic injury is classified according to
a number of grading systems in order to standardize the impact and to formulate therapeutic guidelines. The most current of these is
the Organ Injury Scaling of the American
Association for the Surgery of Trauma, which
grades the injury from grade 1: subcapsular
haematoma, to grade 5: a completely shattered
spleen.
Non-operative management by observation
alone is historically associated with a mortality
approaching 90%. With current diagnostic
modalities, however, there is a place for conservative treatment which should be weighed
against the grading of the injury, the age of the
patient, the risk of mortality of the asplenic condition and the risk of blood transfusion [18–20].
Planned observation in children with splenic
injury has gained acceptance. The juvenile
spleen contains more connective tissue than the
spleen in adults, which is a possible explanation
for the relative resistance of the parenchyma
to hematoma formation. Several series report
success rates for conservative treatment in
children of 90% or more. Furthermore, due
to their expected long lifespan they are more
patient-years prone to overwhelming postsplenectomy infection as compared to adults,
which is a further argument for conservative
treatment or spleen-saving surgery [21].
Splenectomy after Trauma
Splenectomy in trauma follows essentially the
same guidelines as in elective splenectomy.
A midline upper abdominal incision should
suffice in virtually all patients. Close collaboration with the anesthesiologist is mandatory
before entering the abdominal cavity as the
sudden drop in intra-abdominal pressure due
to the evacuation of a large quantity of blood
may lead to sudden hypotension. The large
amount of free intra-abdominal blood should
be removed carefully: injury to other organs
should be prevented at this sometimes rather
hectic stage. After removal of the free and
clotted blood the left upper abdomen is packed
before careful assessment of the splenic injury
is performed and other causes of major bleeding are excluded. Splenic injury is graded from
grade 1, injury of the splenic capsule to grade 4,
complex splenic fractures. Total splenectomy
should be performed in all patients who remain
in shock or who have other life-threatening
injuries intra- or extra-abdominally. In the
absence of extrasplenic sources of bleeding
the choice of treatment is mainly dictated by the
grading of the bleeding. Grade 1 bleedings are
better left alone in most cases, but if hemostasis is needed direct pressure with the addition
of topical hemostatic material like thrombin
fleece will suffice. Grade 2 injuries include
larger hematomas and deeper lacerations and
are initially also treated with compression
and hemostatic agents. The procedure can be
repeated once or twice, evaluating the blood
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loss in between. Grade 3 bleeding is not
stopped with the above-mentioned measures
and needs careful suture transfixion over protecting Gelfoam or Surgicel pledgets. The firmer
capsule and parenchyma in children permits
direct suturing in most cases. In grade 3, multiple deep lacerations and extensive capsule loss,
the bleeding may be treated by wrapping the
spleen in an absorbable woven polyglycolic acid
mesh. The mesh is wrapped around the spleen
under controlled tension and the vascular
inflow and outflow in the hilum is left uncompromised by a keyhole in the wrap to prevent,
especially venous, obstruction that could add to
the bleeding. In grade 4, complex splenic fractures, partial resection is possible with suturing
of the cutting edge over Teflon pledgets, but
total splenectomy is performed in most cases.
All efforts to prevent total splenectomy in
trauma of the spleen should be weighed against
the possibility of persistent bleeding or rebleeding and the possibility of post-splenectomy
infection [22,23].
Post-splenectomy
Complications
Rebleeding after splenic repair or splenectomy
results from inadequate hemostasis of the short
gastric vessels or the splenic hilar vasculature
and occurs in 1.5–2.5% of cases, repair being
more prone to persistent bleeding than excision.
Early re-operation is advised in most cases.
Thrombocytosis of more than 400 000/cm3
occurs in half of the patients after splenectomy,
suggesting an increased risk of deep venous
thrombosis and pulmonary embolism, but
antiplatelet therapy is not recommended unless
the platelet count exceeds 1 million/cm3.
Pneumonia, pleural effusion and subphrenic
abscess are the most frequent complications
after splenectomy. The rate of abscess formation is possibly higher in patients with bowel
perforation after trauma and after drainage of
the left upper quadrant.
Postoperative infections are possibly less
frequent after a splenic salvage procedure than
after total splenectomy but splenectomy alone
may not be an independent risk factor for
the development of postoperative infectious
complications.
66
The risk of overwhelming post-splenectomy
infection, first suggested by Morris and Bullock
in 1919, is considered the greatest in children
under 5 years of age and during the first years
after splenectomy but it is in fact a lifelong one.
It is estimated to be between 0.8% and 0.026%
in children and adults but the mortality rate is
extremely high. A recent survey by Waghorn
[24] suggests that the increased risk of lifethreatening post-splenectomy sepsis persists in
adults and that the mortality rate varies between
50 and 70%. The majority of patients are under
50 years of age and in good health without
further underlying disease. In contrast to earlier
findings, which suggest that there is a decreasing risk with increasing interval, this analysis
showed that the increased risk is indeed lifelong.
The clinical picture is typified by the onset of
nausea, vomiting and confusion leading to
coma and death within hours after the onset
of symptoms. Disseminated intravascular coagulation, hypoglycemia and electrolyte disturbances are symptoms of progressive and often
fatal septicemia. Streptococcus pneumoniae,
Meningococcus, Escherichia coli, Staphylococcus
and Haemophilus inflenzae are the most
common microorganisms in decreasing order
of frequency [24]. The recommendations for
prevention include splenic autotransplantation,
immunization with, at least, pneumococcal
vaccine, antibiotic prophylaxis before surgery
and prevention of animal and tick bites.
Splenic autotransplantation was thought to
prevent overwhelming post-splenectomy infection but remains controversial as, experimentally, the critical amount of splenic tissue needed
to keep its function is at least 30%. Although
splenic tissue can be autotransplanted successfully, the number of transplanted splenocytes
seems insufficient to function against microbial
challenge.
The current pneumococcal vaccines,
although not completely protecting, cover the
serotypes responsible for 90% of bacteremias.
Protection is not lifelong and revaccination is
recommended possibly best based on antibody
measurements. Moreover the protection by vaccination is not complete and prophylaxis with
penicillin has been recommended, especially
in children under the age of 5 years, gradually
changing to antibiotic therapy at the first signs
of infection in patients over 18 years of age
[25,26].
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THE SPLEEN
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Conclusion
The normal spleen is, in infancy and in adulthood, an important and immunocompetent
organ that should be preserved in elective and
in trauma surgery. Removal of a diseased spleen
especially in hematologic disorders carries a
high morbidity, although this has dramatically
decreased with the introduction of laparoscopic
splenectomy, which is now the treatment of
choice. Overwhelming post-splenectomy sepsis
is a lifelong risk that requires adequate prevention and treatment.
Questions
1. What is the tissue of origin of the spleen?
2. Describe the vascular supply of the
spleen.
3. What is the risk of a splenectomy?
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