spleen Flashcards
what “tickles” the spleen
tail of pancreas
functions of the spleen
-filters abn rbc(not store)
-stores platelets
-produces tuftsin and properdin (opsins)
produces antibodies and site of phagocytosis
delayed splenic rupture
subcapsular hematoma or pseudoaneurysm may rupture some time after blunt trauma, causing delayed splenic supture; rupture classically occurs about 2 wks after injury and presents with shock and abd pain
s/sx ruptured/injured spleen
hemoperitoneum and kehr’s sign; luq abd pain; ballances sign
kehr’s sign
left shoulder pain seen w splenic rupture
ballance’s sign
luq dullness to percussion
seagesser’s sign
phrenic nerve compression causing neck tenderness in splenic rupture
dx spleen injury
abd ct (stable); dpl or fast exam if unstable
tx stable pt w spleen injury
nonop in stable w an isolated splenic injury without hilar involvement/complete rupture
tx pt unstable spleen injury
dpl/fast lap w splenorrhaphy or splenectomy
embolization in select pt
splenorrhaphy
splenic salvage operation:wrapping vicryl mesh, aid of topical hemostatic agents or partial splenectomy, sutures
malignant ds that need splenectomy
hodgkins, splenic tumors, hypersplenism
anemias need splenectomy
medullary fibrosis w myeloid metaplasia, hereditary elliptocytosis, sickle cell, pyruvate kinase def, auto hemolytic anemia, hereditary spherocytosis, thalassemias
thrombocytopenia need splenectomy
ITP, TTP
is g6pd def an indication for splenectomy
no
postsplenectomy complications
thrombocytosis, subphrenic abscess, atelectasis, pancreatitis, gastric dilation, overwhelming postsplenectomy sepsis (OPSS), pancreatic injury of tail
s/sx of overwhelming postsplenectomy sepsis (OPSS)
fever, lethargy, common cold, sore throat, uri followed by confusion, shock, come w death ensuing within 24hr in up to 50%pt
common organisms assoc w opss
encapsulated: strep pneumo, neisseria meningitides, h infl
mc bacteria cause opss
strep pneumo
prevention of opss
vaccines for pneumococcus, h infl, meningococcus; prophylactic penicillin for all minor infx/illness and immediate med care if febrile illness develops
best time to give immunizations to splenectomy pt
preop but if emergent 2 weeks postop
what tests are abn after splenectomy
wbc count inc by 50% over baseline; marked thrombocytosis occurs; rbc smear
findings on postsplenectomy rbc smear
peripheral smear will show pappenheimer bodies, howell jolly bodies and heinz bodies
when and how should thrombocytosis be tx
platelet count >1million, tx w aspirin
mc cause splenic vein thrombosis
pancreatitis
what opsonins does the spleen produce
properdin, teftsin
mc cause of isolated gastric varices
splenic vein thrombosis (usually from pancreatitis)
tx of gastric varices caused by splenic vein thrombosis
splenectomy
which pt develop hyposplenism
pt w ulcerative colitis
what vaccinations should every pt w splenectomy receive
pneumococcus, meningococcus, h inf type B
hypersplenism
hyperfunctioning spleen; doc loss of blood elements; large spleen; hyperactive bone marrow (trying to keep up w loss of blood elements)
define splenomegaly
enlarged spleen
idopathic thrombocytopenic purpure (ITP)
autoimm platelet destruction leading to troublesome bleeding and purpura
mc cause of failure to correct thrombocytopenia after splenectomy for ITP
missed accessory spleen
I’s of ITP
immune etiology (IgG); immunosuppressive tx; immune globulin; improvement w splenectomy
tx TTP
plasmapheresis; splenectomy as last resort
mc pe finding of portal htn
splenomegaly
what arteries and veinous supply the spleen
splenic artery and short gastric arteries; portal vein, splenic vein, left gastroepiploic vein
accessory spleens
result from failure of separate splenic masses in the dorsal mesogastrium to fuse; buds are then carried to various locations
polysplenia
presence of multiple small spleens with no normal spleen
functions of the spleen
hematopoiesis, blood filtering, immune modulation
what raises suspicion of an accessory spleen
after splenectomy, nuclear remnants should be present on peripheral blood smear; if not =accessory spleen
what are opsonins and what ones are produced by the spleen
proteins that bind to particulate and bacterial antigen and facilitate phagocytosis; properdin (complement system), tuftsin (macrophage phagocytosis), fibronectin
the spleen is the body’s largest source of which Ig
IgM
size of a normal adult spleen
12cm long and 7cm wide
axr of spleen
rarely show normal spleen; splenomegaly is suggested when there is displacement of the colon inferiorly, stomach medially, or left diaphragm is elevated; splenic shadow
what can US/ sonography show
splenomegaly, splenic cysts, or splenic abscesses; best way to evaluate trauma pts for presence of blood in the abdomen
CT scan w iv and oral contrast
most useful to determine splenic size and detect splenic injury
radionuclide scans
colloid suspensions of technetium are taken up by the reticuloendothelial system and imaging gives info about size and function; helpful in searching for missed accessory spleens
what has replaced splenic artery catheterization for evaluation of the spleen in stable patients after sonography shows intra-abd fluid in cases of trauma
CT angiography
mc reason for splenectomy
trauma (blunt compressive then penetrating then blunt deceleration)
grade 1 of splenic trauma
hematoma (subcapsular
grade 2 of splenic trauma
hematoma (subcapsular 10-15% sa), parenchymal (
grade 3 of splenic trauma
hematoma (subcap >50% sa), parenchymal (>5cm diameter), any expanding or ruptured laceration (>3cm deep or involving trabecular vessels)
grade 4 splenic trauma
laceration: segmental vessels involved w devascularization
grade 5 splenic trauma
completely shattered spleen or hilar vascular injury w devascularization
what is the scale of splenic trauma used for
predicting which patients will stabilize initially; once they stabilize it has no use
name of signs of peritoneal irritation that include lug tenderness and pain medial to at the top of left shoulder
Kehr’s sign/omalgia
name of percussion dullness of left flank that suggests intraperitoneal bleeding
Ballance’s sign
hemodynamically unstable pts who have signs of blunt abd trauma require
prompt laparotomy
stable pt w signs of abd injury and those neuro status is impaired require
eval w us, ct, and rarely w dx peritoneal lavage
when is a splenectomy performed
spleen is extensively injured (grade 5) or pt is profoundly unstable
how much of the splenic volume needs to be preserved for the immune function of the spleen to remain intact
50%
splenorrhaphy
operative repair of the spleen by debridement of devitalized tissue followed by compression w microcrystalhne collagen, pledgeted suture repair, and creation of polyglycolic acid mesh slings to provide hemostatic compression
what two conditions should splenorrhaphy be abandoned
persistent hypotension or extensive additional intra abd injuries
hyposplenism
diminished splenic function; usually increases susceptibility to infx, particularly w encapsulated bacteria
hypersplenism
excess splenic function manifested by cytopenia which is a dec number of cells and normal/hyperplastic cellular precursors in the bone marrow
3 hematologic disorders of splenic function for which splenectomy may be helpful
hemolytic anemia, immune thrombocytopenic purpure (ITP), and cytopenia assoc w splenomegaly from other ds
hereditary spherocytosis
autosomal dominant trait, is characterized by abnormally shaped, rigid red cells as a result of a deficiency in membrane proteins essential for deformability, such as spectrin, ankyrin, or band 3. These rigid erythrocytes cannot pass through the splenic sinuses and become sequestered in the red pulp. Splenectomy is usually indicated because it allows red cells to survive and hematocrit to reach near-normal values postoperatively
.
sickle cell disease
auto rec, mild hetero, severe homo;hemolytic anemia, sickle cells cause an increase in blood viscosity that leads to stasis and subsequent thrombocytosis. Ischemia occurs as a result and leads to fibrosis in a variety of organs
thalassemias
characterized by deficits in the synthesis of one or more subunits of hemoglobin. There are many varied types. In thalassemia major (homozygous β-thalassemia), splenectomy is beneficial in reducing the requirements for transfusion, the physical discomfort from massive splenomegaly, and the potential for rupture. In thalassemia minor (heterozygous β-thalassemia), splenectomy can decrease the need for transfusion and the problems associated with iron overload. In general, patients who have thalassemia and undergo splenectomy are at the highest risk for OPSI.
positive direct Coomb’s test
Red blood cells from patients with autoimmune hemolytic anemias are coated with immunoglobulin, complement, or both
tx positive coombs
coritcosteroid therapy and tx any underlying disorders; splenectomy if steroids are ineffective or require high does
tx neg coombs
secondary to drugs, toxins, or infectious agents and tx by removing the agent
anemias assoc w warm reactive antibodies (usually IgG)
no complement activation; assoc w splenic sequestration and respond to splenectomy
anemias assoc w cold reactive antibodies (IgM)
complement binding and agglutination; hemolysis occurs inperipheral locations in response to cool environmental temps so splenectomy is not indicated
what are the only types of thrombocytopenias in which a splenectomy is appropriate
idiopathic, immune mediated (another cause can’t be found)
what do pt w thrombocytopenia often have
multiple petechiae
when does acute immune thrombocytopenic purpura (ITP) usually occur
after an acute viral infection
tx ITP
corticosteroids; if don’t respond w an elevated platelet count and are refractory to adv medical therapy such as a gamma globulin or monoclonal antibody, splenectomy is performed ; vincristine and y globulin; gamma globulin
thrombotic TP (TTP)
ds of arteries or capillaries; thrombotic episodes and low platelet counts; fever, purport, hemolytic anemia, neuro manif, signs renal ds
tx ttp
plasma pheresis +/- whole blood exchange transfusions, steroids, and anti platelet therapy
splenectomy is indicated for hypersplenism if
platelet count
tx of choice when there is significant postsplenectomy thrombocytosis
hydroxyurea
congestive splenomegaly
enlargement of the spleen as a result of vascular engorgement (ex portal htn); tx htn > splenectomy; tx splenorenal shunt procedure
felty’s syndrome
leg ulcers or chronic infx assoc w splenomegaly and neutropenia in pt w rheumatoid arthritis
is splenectomy indicated for acute leukemia
no
after splenectomy when does the abc count return to normal from being elevated
5-7days; beyond this may be a sign of infection
absence of howell jolly bodies, nucleated red cells, heinz bodies, pappenheimer bodies, and pitted red cells on peripheral smear after splenectomy suggest
accessory spleen was missed
when does platelet count return to normal after splenectomy
within 2 weeks; if not tx w platelet inhibitors (aspirin, dipyridamole) until returns to normal; avoid anticoag w heparin or warfarin
pt who undergo splenectomy for what reason are at highest risk for OPSI
hematologic disorders
mc causes of infections
strep pneumoniae*, h influ, neisseria meningititdis, beta hemolytic strep, staph aureus, echoli, pseudomonas
what vaccine given after total splenectomy or conservative splenic operation for trauma
polyvalent pneumococcal polysaccharide vaccine
abx prophylaxis for immuno comp, receiving chemo, kids
oral penicillin
mc complication after splenectomy
atelectasis
fever, luq pain, omalgia, left pleural effusion, prolonged atelectasis, pneumonia, prolonged leukocytosis
subphrenic abscess- secondary to bleeding, inflammation, or leakage of pancreatic fluid as result to tail of pancreas
enlarged spleen w lymphadenopathy suggests
mononucleosis, lymphoma, leukemia
what are tender, hard, and rubbery nodes assoc w
tender=acute infx skin/soft tissue;
hard=cancer
rubbery= lymphomas
right supraclavicular adenopathy
cancers of right lung or esophagus
left supraclavicular adenopathy (virchow’s node)
gi and abd malig
axillary lymphadenopathy
cat scratch ds or malignancy (breast)
dx lymphadenopathy
cbc w diff; ct or mri, cxr, FNA, bx
order of bx for generalized lymphadenopathy
cervical, supraclav, axillary, and inguinal
Hodgkin’s ds
malignant lymphoma marked by chronic enlargement of the lymph nodes that is often local at onset and later generalized, together with enlargement of the spleen and often of the liver, no pronounced leukocytosis, and often anemia and continuous or remittent fever; associated with inflammatory infiltration of lymphocytes and eosinophilic leukocytes and fibroses.
non hodgkin’s lymphoma
lymphoma other than Hodgkin’s disease; classified by Rappaport according to pattern (nodular or diffuse) and cell type; a working or international formulation separates lymphomas into low, intermediate, and high grades and into cytologic subtypes that reflect follicular center cell or other origin.
avg age of person with hodgkins
32 (late 20s and mid 70s)
s/sx hodgkins
usually asymp cervical lymphadeno, (fever,night sweats, wl) worse prognosis
dx hodgkins
cxr, excisional bx of enlarged abnormal lymph node, bone marrow bx, evaluation of liver, spleen and retroperioneal nodes w ct
REAL/WHO classification system group of Hodgkins 5 categories
nodular lymphocyte predominate, lymphocyte rich, nodular sclerosis*, mixed cellularity, lymphocyte depleted
large reactive background of lymphocytes, eosinophils, and plasma cells with few malignant mononuclear cells and multinuclear giant cells “Reed stern berg”
hodgkins; owl eye
cotswolds stage 1 hodgkins
Involvement of a single lymph node region or lymphoid structure (e.g., spleen, thymus, Waldeyer’s ring) or a single extralymphatic organ or site
cotswolds stage 2 hodgkins
Involvement of two or more lymph node regions on the same side of the diaphragm (hilar nodes, when involved on both sides, constitute stage II disease); localized contiguous involvement of only one extralymphatic organ or site and lymph node region on the same side of the diaphragm (HE). The number of anatomic regions involved should be indicated by a subscript (e.g., II3)
cotswolds stage 3 hodgkins
Involvement of lymph node regions on both sides of the diaphragm (III), which may be accompanied by involvement of the spleen (Ills), of or by localized contiguous involvement of only one extralymphatic organ site (IIIE), or both (lllSE)
cotswolds stage 3-1 hodgkins
With or without involvement of splenic, hilar, celiac, or portal nodes
cotswolds stage 3-2 hodgkins
with involvement of splenic, hilar, celiac, or portal nodes
cotswolds stage 4 hodgkins
Diffuse or disseminated involvement of one or more extralymphatic organs or tissues, with or without associated lymph node Involvement (Involved organs should be identified by a symbol)
what is used to stage hodgkins
cotswolds: a (asymp) or b (fever, night sweats, wl), x (bulky ds), e (involve extranodal site), cs (clinical stage), ps (pathologic stage)
tx hodgkins
stage 1-2 (radiation- doses of 30-40Gy) other stages is chemo +/- radiation
chemo for hodgkins
nitrogen mustard, vincristine, procarbazine and prednisone (MOPP); and doxorubicin (adriamycin), bleomycin, vinblastine, and dacarbazine (ABVD)
who is at inc risk for nonhodgkins
AIDS and those who undergo organ transplantation
what type of lymphoma is Epstein barr virus assoc w
Burkitts
s/sx nonhodgkins
most asymp; can have fever/night sweats/wl; enlarged node with n/v, bleeding; tends to be disseminated
MALT
lymphomas occur outside the lymph nodes (GI tract, thyroid, breast, or skin)
dx nonhodgkins
cbc, lft, cxr, ct of chest/abd/pelvis, bm bx, (if inter/high bm involvement need lumbar puncture)
what is used in staging nonhodgkins
REAL/WHO, Ann Arbor, or International NHL prognostic factors project
tx nonhodgkins
surgery, radiation, or chemo depending on histologic subtype, stage, and risk relapse
A 27-year-old woman is brought to the emergency department by her husband 16 hours after the onset of fever, malaise, sweats, vague abdominal pain, and increasing confusion. She has no chronic illnesses and takes no medications. Ten years ago, she underwent splenectomy for a ruptured spleen sustained when she was kicked by a horse. She recalls receiving vaccinations at that time when she was discharged from the hospital. Now her temperature is 39°C. Vital signs are pulse—125/mlnute, blood pressure (BP)—85/40 mm Hg, and respirations—30/minute. She Is confused. There are diffuse petechiae over her trunk. Her abdomen Is soft and nontender with a long, well-healed midline incisional scar. Laboratory values are WBC—26,000 mm3, sodium—125 mEq/dL, potassium of 6.0 mEq/dL, and glucose of 60 mg/dL.
After the patient is stabilized, a CT scan Is performed, which shows bilateral adrenal Infarcts with adrenal hemorrhage. Infection with which of the following microorganisms Is the most likely cause for her current infection?
Overwhelming postsplenectomy infection (OPSI) is most often caused by encapsulated organisms such as the Pneumococcus. She received vaccination after splenectomy, and therefore she is still at higher risk for developing OPSI with pneumococcus than someone who was vaccinated prior to splenectomy. Pneumococcal sepsis can lead to adrenal infarction (Waterhouse-Friderichsen syndrome). While the other organisms can cause severe infections, her clinical presentation is most likely due to pneumococcal sepsis.
A 45-year-old woman comes to clinic because of bleeding gums when she brushes her teeth and heavy menstrual bleeding. She has a history of Immune thrombocytopenic purpura that was unresponsive to corticosteroids at that time and underwent splenectomy 15 months ago. Her platelet count 2 months after splenectomy was 175,000/mm3. Her physical exam today reveals scattered petechiae and a few purpuric lesions on her forearms. Platelet count today is 30,000/mm3. A peripheral smear shows normal red cell morphology and no red cell Inclusions. What is the next best step in management?
The correct answer is to obtain a radionuclide spleen scan to look for a missed accessory spleen. Accessory spleens can hypertrophy and sequester platelets just like a normal spleen. For this reason, It is important to look for and remove all accessory splenic tissue at the time of splenectomy. Platelet pheresis has no role at this time. If no accessory splenic tissue is identified on a radionuclide scan, further evaluation with a bone marrow aspirate may be necessary but not at this time. She did not respond initially to steroids so it is unlikely she will respond at this time. Platelet transfusion Is not indicated at this time as she Is not actively bleeding.
A 23-year-old man is brought to the emergency department 30 minutes after a motorcycle crash. He Is awake and complaining of severe abdominal and left chest pain. Oxygen therapy and IV fluids were started at the scene. Blood pressure on admission was 90/60 with a pulse of 110/minute and respirations were 18/minute. A chest tube was placed on the left that yielded only a small amount of bloody fluid. Breath sounds are only slightly diminished at the left base and there is no tracheal deviation. After 2 L of normal saline, his BP is 80/50. A FAST exam shows a large amount of fluid in the abdomen and what appears to be a fractured spleen. In addition to blood transfusion, the most appropriate management Is
The correct answer Is to perform an exploratory laparotomy. This patient Is in shock and appears to have a severe splenic injury with continued hemorrhage. This Is not amenable to no operative treatment. Admission to the intensive care unit is necessary to monitor patients for nonoperative management; however, this patient is too unstable. It takes time to organize an angiography team, and this patient is too unstable. A CT scan is needed before an attempt at angiographic control of splenic hemorrhage in order to rule out other injuries. This patient remains hypotensive because of continued rapid intra-abdominal hemorrhage and needs control of the bleeding, which Is best accomplished at the time of laparotomy. Dopamine will not stop the bleeding.
A 29-year-old woman is seen In clinic with fatigue and weakness. She recently had a urinary tract infection treated for 7 days with trimethoprim/sulfamethoxazole and stopped taking this 2 days ago. She takes no other medications. She has a history of glucose-6-phophate dehydrogenase deficiency. Her pulse is 100. She appears pale. Otherwise her physical exam is normal. Hematocrit Is 22%. What is the most likely mechanism for her anemia?
Glucose-6-phosphate dehydrogenase deficiency is a sex-linked recessive trait. The pentose phosphate shunt is blocked and red cell membranes are Injured by oxidation injury from certain drugs such as sulfamethoxazole, aspirin, phenacetin, or nitrofurantoin. Spectrin deficiency, a membrane component essential for deformabillty, is seen in spherocytosis. Sensitization of red cell membranes by membrane-bound antibody is the result of acquired hemolytic anemia. Conformational change in hemoglobin is seen in sickle cell anemia. Decreased production of ATP leading to membrane destruction Is the mechanism by which pyruvate kinase deficiency causes hemolysis.
A 19-year-old man comes to clinic because of a left neck mass. He first noticed a firm nontender mass just above his clavicle about a month ago. He has not had any recent Infections. He has a cat that has been a pet for 4 years. He has also had nighttime sweats, but he has not taken his temperature. He does not use tobacco products and does not drink alcohol. He is now afebrile. On physical exam, there is a 3-cm, firm, nontender mass in the supraclavicular fossa. The rest of the physical exam is normal. What is the most likely diagnosis?
The correct answer is Hodgkin’s disease. The presence of night sweats and the identification of a large, nontender firm node suggest Hodgkin’s disease as opposed to a benign reactive adenopathy. Cat scratch disease usually presents with painful, suppurative adenopathy. There Is usually generalized mild lymphadenopathy associated with Addison’s disease. He has no risk factors for esophageal cancer, and the node is firm rather than hard, which would be more characteristic of metastatic cancer.
