Gastrointestinal and Abdominal: Spleen Flashcards
(22 cards)
Spleen
The spleen is a lymphatic organ located in the left
upper abdominal quadrant. It contains the largest
accumulation of lymphoid cells in the body. In addi-
tion to filtering the blood, it plays an important role
in host defense. Splenic lymphocytes are involved
in antigen recognition and plasma cell production,
whereas splenic endothelial macrophages extract bac-
teria
and damaged red blood cells from circulation
by phagocytosis. White pulp of the spleen contains
high concentrations of antigen-presenting cells and
receives arterial blood supply first. Blood then trav-
els through an open-type circulation known as the
red pulp, where foreign particles are filtered and
antibody-coated cells are removed. Removal of red
blood cell imperfections is another function of the
spleen. These include Howell-Jolly bodies (Fig 8-1),
which are nuclear remnants, Pappenheimer bodies,
which are iron inclusions, and Heinz bodies, which
are denatured hemoglobin. Splenectomy or hypos-
plenism is associated with the presence of these
abnormalities in the peripheral blood.
Surgical issues regarding the spleen are multiple
and varied. Life-threatening hemorrhage from a lac-
erated spleen resulting from trauma is a common
problem, requiring swift surgical intervention. Certain
disease states, such as immune thrombocytopenic
purpura (ITP) and the hemolytic anemias, are often
treated with splenectomy when medical manage-
ment fails. Splenectomy may be necessary as part of
another operation, such as distal pancreatectomy. In
addition, the traditional staging workup for Hodgkin
disease has involved removal of the spleen to deter-
mine extent of disease, although this is now rarely
performed.
Spleen: Anatomy
The spleen is embryologically derived from condensa-
tions of mesoderm in the dorsal mesogastrium of
the developing gastrointestinal tract. In the mature
abdomen, the spleen is found attached to the stomach
by the gastrosplenic ligament and to the left kidney by
the splenorenal ligament. Other supporting attach-
ments include the splenocolic and splenophrenic liga-
ments (Fig. 8-2).
Accessory spleens are present in approximately
25% of patients. They are most often found in the
splenic hilum and in the supporting splenic ligaments
and greater omentum.
Arterial blood is mostly supplied via the splenic
artery, which is one of three branches of the celiac
axis (splenic, left gastric, common hepatic). At the
hilum, the splenic artery divides into smaller
branches that supply the several splenic segments.
Additional arterial blood is supplied via the short gas-
tric and left gastroepiploic vessels (Fig. 8-3).
Venous drainage is from segmental veins that join
at the splenic hilum to form the splenic vein.
Running behind the upper edge of the pancreas, the
splenic vein joins with the superior mesenteric vein
to form the portal vein.
Splenic Hemorrhage
The most common cause of splenic hemorrhage is
blunt abdominal trauma. Nonpenetrating injury may
cause disruption of the splenic capsule or frank lacera-
tion of the splenic parenchyma. Displaced rib fractures
of the left lower chest often cause splenic laceration.
Splenic injuries are graded from I to V based on the
extent of laceration and hematoma (Table 8-1).
Splenic hemorrhage may also be iatrogenic.
Intraoperative damage to the spleen may occur dur-
ing unrelated abdominal surgery that results in bleed-
ing controlled only by splenectomy. Estimates are
that 20% of splenectomies result from iatrogenic
causes. Infectious diseases (e.g., mononucleosis,
malaria) may damage the spleen to the point that
unnoticed blunt trauma can cause “spontaneous” splenic
rupture and hemorrhage.
Splenic Hemorrhage: History
Patients typically present with a recent history of
trauma, usually to the left upper abdomen or left flank.
Splenic Hemorrhage: Physical Examination
Depending on the degree of splenic injury and hemo-
peritoneum, a physical examination may reveal left
upper quadrant abdominal tenderness, left lower rib
fractures, abdominal distention, peritonitis, and
hypovolemic shock. Pain on the left shoulder is referred to as
Kerr’s sign and is referred pain from peritoneal irritation.
Splenic Hemorrhage: Diagnostic Evaluation
Computed tomography (CT) scan, abdominal ultra-
sound, and peritoneal lavage (see Chapter 27,
Trauma) can be used to detect intraperitoneal blood.
In hemodynamically stable patients, CT can demon-
strate the degree of both splenic injury and hemo-
peritoneum.
Splenic Hemorrhage: Treatment
For patients with splenic injury who are hemody-
namically stable and without evidence of ongoing
hemorrhage, nonoperative management with close
hemodynamic monitoring has become the accepted
treatment of choice. In children, nonoperative man-
agement is widely applied as a result of the incidence
of overwhelming postsplenectomy sepsis seen in the
pediatric population. Recent advances in interven-
tional radiology have made it possible to embolize
the spleen, or a portion, to obviate the need for
laparotomy. This can have the advantage of salvaging
enough of the spleen to prevent major complications,
such as postsplenectomy sepsis, but splenic abscess
may occur. For patients with known or suspected
splenic injury who are hemodynamically unstable,
operative intervention is indicated to control ongoing
hemorrhage.
Once in the operating room, the decision to per-
form splenic repair (splenorrhaphy) versus splenec-
tomy is based on the degree of injury to the par-
enchyma and blood supply of the organ. Relatively
minor injuries, such as a small capsular laceration
with minor oozing, may be repaired, whereas a frag-
mented spleen with involvement of the hilar vessels
necessitates surgical removal. If splenic repair is con-
templated, the spleen must be mobilized completely
to determine the extent of injury and the likelihood
of success. If there are other organs injured in addi-
tion to the spleen, splenectomy is generally recom-
mended.
Immune Thrombocytopenic Purpura
ITP is an autoimmune hematologic disease in which
antiplatelet IgG antibodies, produced largely in the
spleen, are directed against a platelet-associated antigen,
resulting in platelet destruction by the reticuloendothe-
lial system and subsequent thrombocytopenia. The dis-
ease is typically seen in young women, who may present
with complaints of menorrhagia, easy bruising, mucosal
bleeding, and petechiae. Men may present with com-
plaints of prolonged bleeding after shaving trauma.
Immune Thrombocytopenic Purpura: Treatment
Initial therapy is with corticosteroids, which improve
platelet counts after 3 to 7 days of therapy. Initial
doses are 1 mg/kg orally until the platelet count is
normal, followed by a 4- to 6-week taper. High-dose
dexamethasone or methylprednisolone is also an
option. Intravenous immunoglobulin can be used
to support the platelet count, as can anti-Rh(D) if
patients have Rh(D) positive platelets. For prolonged
active bleeding, platelet transfusions should be
administered to achieve hemostasis. If patients are
asymptomatic, platelet counts of
30,000 can be tol-
erated. Once patients become symptomatic or the
platelet count decreases to
10,000, therapy should
be considered. Patients with chronic refractory ITP
may benefit from rituximab or thrombopoiesis-
stimulating agents, but these are considered experi-
mental at this time.
Few patients enjoy complete and sustained remis-
sion with corticosteroid treatment alone. Patients typ-
ically become refractory to medical treatment, and
thrombocytopenia recurs. Splenectomy is then indi-
cated. After splenectomy, normal platelet counts
develop in approximately 80% of patients because
the organ of both significant antiplatelet antibody
production and platelet destruction is removed.
Hypersplenism
Hypersplenism describes a state of increased splenic
function that results in various hematologic abnor-
malities, which can be normalized by splenectomy.
Elevated splenic function causes a depression of the
formed blood elements, leading to a compensatory
hyperplasia of the bone marrow.
Hypersplenism: History
As in ITP, most patients are women who present with
signs of anemia, recurrent infections, or easy bruising.
Hypersplenism: Physical Examination
Abdominal examination reveals splenomegaly.
Hypersplenism: Diagnostic Evaluation
Peripheral-blood smear may reveal leukopenia, ane-
mia, thrombocytopenia, or pancytopenia. Bone mar-
row biopsy shows pancellular hyperplasia.
Hypersplenism: Treatment
Splenectomy may produce hematologic improvement.
Hemolytic Anemias
Hemolytic anemias are characterized by an elevated
rate of red blood cell destruction from either a
congenital or acquired etiology. Congenital hemolytic
anemias result from basic defects of the cell membrane
(hereditary spherocytosis), hemoglobin synthesis
(thalassemia), hemoglobin structure (sickle cell anemia), or
cellular metabolism (glucose-6-phosphate dehydroge-
nase deficiency). Acquired autoimmune hemolytic
anemias result when antibodies are produced that are
directed against the body’s own red blood cells.
Hemolytic Anemias: Diagnostic Evaluation
A positive direct Coombs test demonstrates com-
plexed antibodies on the red blood cell membrane.
Warm-reactive antibodies are IgG, and cold-reactive
antibodies are IgM.
Hemolytic Anemias: Treatment
The role of splenectomy in treating hemolytic anemias
depends on the particular disease process. For example,
red blood cell survival normalizes after splenectomy for
hereditary spherocytosis, whereas operative interven-
tion has no role in the treatment of anemia of glucose-
6-phosphate dehydrogenase deficiency that is second-
ary to a defect of metabolism, not cellular structure.
Occasionally, splenectomy may be useful in selected
patients with sickle cell anemia and thalassemia.
Patients with autoimmune hemolytic anemias undergo
nitial corticosteroid treatment and progress to splenec-
tomy only after medical treatment failure.
Hodgkin Disease Staging
Because of a greater reliance on CT scans and the favor-
able success of salvage chemotherapy in the treatment
of Hodgkin lymphoma, the need for determining
whether disease is present across the diaphragm by
means of laparotomy and splenectomy has sharply
declined. Treatment with salvage chemotherapy after
local radiation failure still carries a highly favorable out-
come in most cases. Therefore, splenectomy for staging
Hodgkin disease is now rarely performed.
Overwhelming Postsplenectomy Sepsis
Asplenic individuals are at greater risk for developing
fulminant bacteremia because of decreased opsonic
activity, decreased levels of IgM, and decreased clearance
of bacteria from the blood after splenectomy. As a rule,
children are at greater risk for development of sepsis
than are adults, and fatal sepsis is more common after
splenectomy for hematologic disorders than after
trauma. The risk of sepsis is higher in the first postoper-
ative year, and, for adults, each subsequent year carries
approximately a 1% chance of developing sepsis. Other
data show a mortality of less than one per 1,000 patient-
years. The clinical picture of overwhelming postsplenec-
tomy sepsis is the onset of high fever followed by
circulatory collapse from septic shock. Disseminated
intravascular coagulation often occurs. The offending
pathogens are the encapsulated bacteria
Streptococcus
pneumoniae, Haemophilus influenzae,
and
Neisseria
meningitidis.
Splenectomy Considerations
Any patient scheduled to undergo splenectomy
should receive immunization against Steptococcus
pneumoniae, Haemophilus influenzae, and Neisseria
meningitidis, preferably at least 2 weeks before surgery.
Straightforward splenectomy can be performed laparo-
scopically, whereas complicated splenectomy in patients
with massive spleens or severe thrombocytopenia are
more likely to require laparotomy. During surgery, the
spleen is mobilized from the splenorenal, phrenosplenic,
and lienocolic ligaments. The main artery is found on
the superior border of the pancreas and should generally
be taken early. Care must be taken to control the short
gastric arteries entering the greater curve of the stom-
ach. The tail of the pancreas nestles into the splenic
hilum and can be damaged, causing a pancreatic leak
or fistula. Patients generally have nasogastric decom-
pression to prevent the stomach from distending and
hemorrhage along the greater curve. Patients with com-
promised immune systems, including young children
and transplant recipients, should be considered for long-
term oral penicillin prophylaxis.
Splenic Abscess
Splenic abscesses most commonly occur as a conse-
quence of other intra-abdominal infection. They can
also occur after arterial embolization of either the
liver or spleen. Diabetes seems to be a risk factor.
Patients generally present with left upper quadrant
pain, fever, and leucocytosis. Antibiotics, catheter-
based drainage, and splenectomy are all appropriate
management options.
Key Points: Spleen
The spleen is a lymphatic organ that plays roles in
antigen recognition and blood filtering.
•
Accessory spleens occur in 25% of patients and are
most commonly found in the splenic hilum.
•
Arterial blood is supplied via the splenic artery, the
short gastric arteries, and branches of the left gas-
troepiploic artery.
•
Hemorrhage secondary to trauma is the most com-
mon indication for splenectomy.
•
Nonoperative management or organ-sparing splen-
orrhaphy can be attempted to avoid the risk of
overwhelming postsplenectomy sepsis, especially
in children.
•
Hemodynamically stable patients with splenic
injury can be managed nonoperatively.
•
Immune thrombocytopenic purpura, hypersplenism,
and specific hemolytic anemias are disease states for
which splenectomy may be indicated.
•
Splenectomy for staging Hodgkin disease is now
rarely performed, because of improved imaging
modalities (computed tomography scan) and the
success of chemotherapy.
•
The risk of overwhelming postsplenectomy sepsis
is greater in children than in adults. High fever and
septic shock are often accompanied by dissemi-
nated intravascular coagulation.
•
Vaccination against
Streptococcus pneumoniae,
Haemophilus influenzae,
and
Neisseria meningitidis
should be administered to all surgically and func-
tionally asplenic patients, because these encapsu-
lated organisms are responsible for causing over-
whelming postsplenectomy sepsis.
