THE SPLEEN

CHAPTER OUTLINE:
o The Spleen
o Embryology & Anatomy
o Physiology & Pathophysiology
o Splenectomy Techniques
 Px Preparation
 Open Splenectomy
 Laparoscopic Splenectomy
 Partial Splenectomy
 Inadvertent Intraoperative Splenic Injury
o Indications for Splenectomy
 RBC Disorders
• Congenital
• Acquired
 WBC Disorders
• Chronic Lymphocytic Leukemia
• Hairy Cell Leukemia
• Hodgkin's Disease
• Non-Hodgkin's Lymphoma
 Platelet Disorders
• Idiopathic Thrombocytopenic Purpura
• Thrombotic Thrombocytopenic Purpura
 Bone Marrow (Myeloproliferative) Disorders
• Chronic Myeloid Leukemia
• Acute Myeloid Leukemia
• Chronic Myelomonocytic Leukemia
• Essential Thrombocythemia
• Polycythemia Vera
• Myelofibrosis (Agnogenic Myeloid Metaplasia)
 Cysts & Tumors
 Infections & Abscesses
 Storage & Infiltrative Disorders
• Gaucher's Disease
• Niemann-Pick Disease
• Amyloidosis
• Sarcoidosis
 Misc. Disorders & Lesions
• Splenic Artery Aneurysm
• Portal Hypertension
• Felty's Syndrome
o Imaging: Size & Pathology
 Ultrasound
 Computed Tomography
 Plain Radiography
 Magnetic Resonance Imaging
 Angiography
 Nuclear Imaging
 Splenic Index
o Preoperative Considerations
 Vaccination
 Splenic Artery Embolization
 Deep Vein Thrombosis Prophylaxis
o Splenectomy Outcomes
1
  Complications
 Hematologic Outcomes
 Overwhelming Postsplenectomy Infection

INTRODUCTION
Embryology & Anatomy
SPLEEN
A. Embryology of the Spleen
o Arises from the MESODERM between 1-2 Months Gestation
o Becomes evident on the 5th Week of Gestation in an 8mm Embryo

- encapsulated mass + lymphoid tissue

- largest reticuloendothelial organ in the body
- origin: primitive mesoderm (as an outgrowth of the L side of the dorsal mesogastrium)
- 5th wk of gestation: 8mm long

B. Anatomy of the Spleen

o It is a Multifauceted Organ
o It is in Close Association with the Pancreas, Left Kidney, Stomach, Transverse Colon
o Superior to the Spleen is the DIAPHRAGM
o Located in the 9th ICS (L1) – at the level of the Left Mid-Axillary Line
o (+) Anterior Notch

1. Dimensions of the Spleen

 10 cm Long (7-11cm long)
 Weight = 100g (in Filipinos)
 TO be Palpable (Splenomegaly) = Size has to be DOUBLED!
2. Accessory Spleen
 Most Common ANOMALY of Splenic Embryology
 80% are found in the Region of the Splenic Hilum and Vascular Pedicle
3. Splenomegaly (prenotes)
 Spleen weighing 500mg or more and/or 15cm (or more) in Length

- final location: LUQ; smooth, diaphragmatic surface facing posterosuperiorly

- abdominal surface of the diaphragm separates the spleen from the lower left lung and pleura and the 9th-11th ribs
- visceral surface faces the abdominal cavity and contains gastric, colic, renal, and pancreatic impressions
- superior border of the spleen: separates the diaphragmatic surface from the gastric impression of the visceral
surface and often contains 1 or 2 notches (particularly pronounced when the spleen is greatly enlarged)
- ave. audult spleen: 7-11cm in length & weights 150g (70-250g)
- Splenomegaly:
Moderate, massive, hyper
≥500g and/or averaging ≥15cm in lengh
massive: >1kg in mass or >22cm in length
at least 2x the normal size: spleens palpable below left costal margin; est. ≥750g
may result in sequestration of up to 80% of the platelet pool
- most common anomaly: accessory spleen (20% of population; 30% of Px w/ hematological disease)
- locations of accessory spleen in descending order of frequency:
1. region of the splenic hilum & vascular pedicle (80%)
2. gastrocolic ligament
3. pancreas tail
4. greater omentum
5. stomach’s greater curve
6. splenocolic ligament
7. small & large bowel mesentery
8. left broad ligament in women
2
 9. left spermatic cord in men

C. Four Cardinal Ligaments (Suspensory Ligaments that Support the Spleen)

o Stomach = GASTROSPLENIC (it is the ONLY Vascular Ligament of the Spleen)
o Colon = Splenocolic Ligament
o Diaphragm = Phrenosplenic Ligament
o Kidney, Pancreas = Splenorenal Ligament

**NOTE: Gastrosplenic is the ONLY Vascular Ligament

 It contains Short Gastric Vessels
 The others are NOT Vascular

- of particular clinical relevance: the spleen is suspended in position by several ligaments and peritoneal folds:
1. to the colon: Splenocolic ligament
2. to the stomach: Gastrosplenic ligament – contains the short gastric vessels, the remaining ligaments are
avascular, with rare exceptions, such as in patients with portal hypertension
3. to the diaphragm: Phrenosplenic ligament
4. to the kidney, adrenal gland, tail of the pancreas: Splenorenal ligament
**cadaveric normal series: the tail of the pancreas has been demonstrated to lie w/n 1cm of the splenic hilum 75% of the
time and in 30% of patients actually to abut the spleen

D. Vasculature of the Spleen

o Splenic Artery = Comes from the CELIAC AXIS - where the spleen derives most of its blood
o Short Gastric Vessels = from the LEFT GASTROEPIPLOIC ARTERY running w/n the gastrosplenic
ligament
o Splenic Vein = joins the Superior Mesenteric Vein to form the Portal Vein and accommodates the major
venous drainage of the spleen

1. Splenic Artery
 Provides Majority of the Blood Supply
 It is the FIRST Branch of the Celiac Artery
 LARGEST and Most TORTUOUS Branch of the three main branches of the Celiac Artery
 Types according to the pattern of its terminal branches
a) distributed type – most common – 70% - distinguished by a short trunk with many long branches entering over
¾ of the spleen’s medial surface
b) magistral type – 30% - has a long main trunk dividing near the hilum into short terminal branches, and these
enter over 25%-30% of the spleen’s medial surface

 Blood Flow through the Spleen:

Celiac Artery
↓
Splenic Artery
↓
SPLEEN
↓
Splenic Vein
↓
Combines with the Superior Mesenteric Vein
↓

3
 Portal Vein

2. Short Gastric Vessels

 Provides a SMALL amount of Blood to the Spleen

3. Splenic Vein
 Accommodates the Major Venous Drainage of the Spleen
 Runs retropancreatically as it fuses with the Superior Mesenteric Vein to form the Portal Vein
 In Patients with Portal Hypertension = there is ENLARGEMENT of the Splenic Vein and even
the SPLEEN itself (Splenomegaly)
E. Histology of the Splenic Parenchyma
***when a normal, freshly excised spleen is sectioned, the cut surface is finely granular and predominantly dark
red with whitish nodules distributed liberally across its expanse – reflects microstructure
1. Outer Red Pulp
 Contains the Venous Sinuses (drain into tributaries of the Splenic Vein) – surrounded and
separated by the reticulum (a fibrocellular network of collagen fibers and fibroblasts;
appear as splenic cords) – lined by long, narrow endotheial cells that are variably in close
apposition to one another or are separated by intercellular gaps in a configuration unique to the
spleen
 Macrophages – w/n the reticulum – remove microorganisms, cellular debris, antigen-antibody
complexes, and senescent erythrocytes from the circulation
 Comprises ~75% of the Total Splenic Volume
 Serves as a DYNAMIC FILTRATION System

2. Marginal Zone (Interface)

 At the junction of the Red and White Pulp; Intertwines the Red and White Pulp
 Lymphocytes - loosely aggregated in this zone
 Blood is derived from this zone to the Red Pulp, where lymphocytes & locally produced
immunoglobulins ultimately enter the systemic circulation
 Narrow; Contains the Plasma Cells and Macrophages
 Also with FILTERING Function

3. Inner White Pulp

 Has Immunologic Function (for IMMUNOLOGIC Function)
 Consists of Collagen and Malphigian Follicles
 Consists of nodules that are normally ≤ 1mm in size but can increase to several cm when nodules
coalesce (as occurs in certain lymphoproliferative disorders)

**Periarticular Lymphatic Sheath - around the terminal mm of splenic arterioles; replaces the native adventitia of the
vessel; composed of T lymphocytes & intermittent aggregations of B lymphocytes or lymphoid follicles
**Follicles – when stimulated: centers of lymphocyte proliferation  develop germinal centers  regress as the
stimulus/infection subsides
**blood flow: arteriesarterioleswhite pulpmarginal zonered pulp

II. PHYSIOLOGY OF THE SPLEEN: **”Defense Spleen”

• Filtration
• Host Defense
• Storage
• Cytopoiesis

A. Filtration (Capsule of the Spleen: 1-2mm thick; rich in Collagen & Elastin fibers)
o Most IMPORTANT Function, along with providing Immunity, of the Spleen
o It filters the Dead Red Blood Cells (it clears damaged or aged blood cells, removes abnormal WBCs and
Platelets and some Foreign Bodies)

4
 o Mostly via the slower/open circulation – blood percolates through the reticular space and splenic cords,
thus gaining access through gaps/slits in the endothelial cell lining to the sinuses **blood is exposed to
extensive contact with splenic macrophages
o Selective slowing of blood cell flow vs. plasma flow: within the spleen the erythrocte conc. (hematocrit) is
2x that of the general circulation
o Recall: Lifespan of RBC = 120 days (2 days spent sequestered in the spleen)
o It is the “Graveyard of the RBCs” = approximately 20mL of Aged RBCs are removed DAILY

B. Immunologic Function (Host Defense)

o Contribute to BOTH Humoral and Cell-Mediated Immunity
o Antigens – filtered in the white pulp; presented to immunocompetent centers w/n the lymphoid follicles;
elaboration of immunoglobulins (predominantly Immunoglobulin M)
o Antigen challengeacute immunoglobulin M responserelease of Opsonic antibodies from the white
pulpantigen clearance (facilitated by the splenic & hepatic reticuloendothelial systems
o Opsonins, Tuftsins, Properidin are manufactured in the Spleen
o Properidin = Initiator of the Alternate Pathway of Complement Activation
o Site of blood borne antigen presentation and the initiation of T and B lymphocyte activities
involved in humoral and cellular immune responses

C. Storage
o Storage for Cellular Elements such as RBC, WBS, etc

D. Hematopoiesis
o In the Fetal Stage, the Spleen is responsible or Hematopoiesis
o The Spleen plays a MINOR Role in the Human Fetus beginning in the 4th month
o Splenic Hematopoiesis = abnormal RBCs in adults w/ myeloproliferative disorders

**Chronic hemolytic disorders – tissue may become permanently hypertrophiedreticular spaces of the red pulp become
distended w/ macrophages engorged w/ the products of erythrocyte breakdownsplenomegaly
**splenomegaly: abnormal enlargement of the spleen; hypersplenism: presence of one or more cytopenias in the context
of a normally functioning bone marrow
**disorders causing hypersplenism:
1. those w/ destruction of abnormal blood cells (occurs in an intrinsically normal spleen)
2. primary disorders of the spleen = sequestration and destruction of normal blood cells
**hypersplenism = neutropenia through sequestration of normal wbc or the removal of abnormal ones
**platelets: survive in circulation for 10days; normally 1/3 of the platelet pool is sequestered in the spleen
**excessive sequestration of platelets or platelet destruction in the spleen = thrombocytopenia
NOTES from Prenotes:
• 5th to 8th Month = Spleen contributes Actively to the Production of BOTH RBCs and WBCs that enter
the Circulation (does NOT Continue into Adulthood)
• Spleen is the LARGEST Reticuloendothelial Organ in the Body
• Total Splenic Inflow of Blood = 250-300mL/min

III. DIAGNOSTIC TEST FOR SPLENIC EVALUATION

**indications: trauma, LUQ pain, splenic lesions (tumors, cysts, abscesses), guidance for percutaneous procedures
A. Ultranosography
o 2D Ultrasound will suffice to identify Shape, Size, Adjacent Structures
o Advantage = COST EFFECTIVE and Readily Available!
o It is NOT Invasive and does NOT expose the Patient to Ionizing Radiation
o One of the Most Commonly Used
o Often the 1st imaging modality used for eveluation/resuscitation of a trauma px
o Percutaneous UTZ guided procedures for splenic disease (ei cyst aspiration, bipsy)
5
 o detection of textural lesions

B. CT-Scan
o Main Advantage = HIGHER Resolution it gives (gives a more detailed appearance of the Splenic
Parenchyma)
o Automated, less operator dependent
o Evaluation & management of the blunt trauma Px
o It delineates the Adjacent Structures BETTER, compared to an Ultrasound
o It uses Iodinated Contrast Material to add Diagnostic Clarity (small but real risks of renal impairment,
allergic rxns)

**Nontrauma: CT-Scan is useful in:

 Assessment of Splenomegaly
 Identification of Splenic Lesions
 Guidance for Percutaneous Procedures

C. MRI
o Excellent detail and versatility in abdominal imaging
o Cost is also HIGH!
o It is reserved for difficult cases when CT-Scan CANNOT determine the Pathology

D. Radioscintigraphy (Nuclear Imaging)

o Identification of ACCESSORY SPLEEN
o Uses Technetium-99 and Sulfur Colloids which are given IV (then it becomes concentrated in the
Accessory Spleen)

E. Plain Radiography (X-Ray)

o Visualization of ORGAN DISPLACEMENT adjacent to the Spleen
o RARELY used alone for Splenic Imaging
o Can provide an Outline of the Spleen in the LUQ or Suggest Splenomegaly by revealing Displacement of
the Adjacent air-filled Structures
o May Demonstrate Splenic CALCIFICATIONS: a non specific finding; phlebolith, splenic artery
aneurysm, sickle cell changes, tumors, echinococcosis, TB

F. Angiography
o Outlining the Vascular Supply
o Invasive arterial imaging; localization and Tx of hemorrhage in select trauma Px, delivery of a variety of
therapies in Px with cirrhosis or portal and sinistral hypertension, and in transplant Px, adjunct to
splenectomy for tx of hematologic disorders such as ITP or hypersplenism, preoperative or intraoperative
SAE for elective splenectomy

G. Splenic Index
o Obtained by multiplying the spleen’s length, width, and height and using these values in a specific
standard ellipsoid volume and linear regression formula
o Normal values: 120mL-480mL
o Normal ex vivo wt. = 150g

6
IV. GENERAL INDICATIONS FOR SPLENECTOMY (check Table 34-1: page 1250)
• Most Common Indication for Splenectomy = TRAUMA to the Spleen
• Most Common Indication for ELECTIVE Splenectomy = (in the past) staging for Hodgkin’s Disease, (more
recently) ITP

7
>>RED BLOOD DISORDERS
CONGENITAL
Hereditary Sperocytosis
Indications for Splenectomy
- hemolytic anemia
- recurrent transfusions
- intractable leg ulcers
Response
- improves/eliminates anemia
Autosomal dominant
Most common hemolytic anemia for w/c
splenectomy is indicated
Results from an inherited dysfunction or
deficiency in one of the erythrocyte
membrane proteins
- spectin
- ankyrin
- band 3 protein
- protein 4.2
destabilization of the lipid bulayer =
pathologic release of membrane lipids
RBC: more spherical, less deformable
shape
Spherocytic erythrocytes are sequestered
and destroyed in the spleen
- mild jaundice
- splenomegaly
- varying degrees of anemia
(severe: 4-6 g/dL)
- mean corpuscular volume: low to
normal or slightly decreased
- screening: mean corpuscular
hemoglobin concentration +
erythrocyte distribution width
RBC Enzyme Deficiencies
Pyruvate Kinase Deficiency Glucose-6-Phosphate Dehydrogenase
Deficiency
Indications for Splenectomy Indications for Splenectomy
- only in severe cases - None
- recurrent transfusions
Response Response
- transfusion -
requirement
- palliative only
- in severe cases,
splenectomy can
alleviate transfusion
requirements
Involved in glycolytic pathways Needed to maintain a high ratio of reduced to
oxidized glutathione in the RBC, protecting it
from oxidative damage
Most common RBC deficiency to Most common RBC enzyme deficiency overall
cause congenital chronic
hemolytic anemia
Pathophysiology is unclear
- transfusion dependent severe - chronic hemolytic anemia
anemia in early childhood - acute intermittent hemolytic episodes
- well compensated mild anemia - no hemoysis ( depend on the variant of
in adolescents or adults G6PD def.)
- splenomegaly is common
- specific mutations at the
complementary DNA or
genomic level
-
8
 - reticulocyte count
- lactate dehyrogenase level
- level of UNconjugated bilirubin
- (+) spherocytes
- timing of splenectomy: impt; aimed at - splenectomy should be - mainstay of Tx: avoidance of drugs
possibility of overwhelming delayed if possible to at known to precipitate hemolysis in px w/
postsplenectomy sepsis least 4yo to  risk of G6PD deficiency
- delay operation until the px is between postsplenectomy - tranfusions are given in case of
4-6yo (unless the anemia and infection symptomatic anemia
hemolysis accelerate)
- gallstones are more likely to dev. In px
w/ HS
- for children w/ cholelithiasis –
prophylactic cholecystectomy is
recommended at the time of
splenectomy

ACQUIRED
Warm-Antibody Autoimmune Hemolytic
Anemia
Indications for Splenectomy
- failure of medical (steroid) therapy
- (painful enlargement of the spleen,
Response
-
-
60-80% response rate
recurrences common
AIHA is classified as either primary or
secondary; also classified as warm (discussed in
the chapter) or cold (based on the temp. at w/c
the autoantibodies exert their effect)
**cold: Sx are uncommon and splenectomy is
almost never indicated
More common among women, mostly idopathic
Characterized by the destruction of RBCs,
whose erythrocytic life span is diminished by
autoantibodies leveled against antigens
-
-
acute or gradual presentation
mild jaundice
- signs ans sx of anemia
- 1/3- ½ (splenomegaly)
- hemolysis as indicated by anemia
- reticulocytosis
- products of rbc destruction
- bilirubin in the blood, urine and stool
- (+) Coomb’s test = confirms the AIHA
Dx by distinguished autoimmune from
other forms of hemolytic anemia
- tx depends on severity; primary vs
secondary
- prompt attention, rbc transfusion for
Hemoglobinopathies: sickle cell disease Thalassemia: (alpha, beta, gamma)
Indications for Splenectomy Indications for Splenectomy
- Hx of acute sequestration crisis - excessive transfusion requirements
- symptomatic splenomegaly
circulatory collapse) - infarction
- Splenic Sx (hypersplenism, splenic
abscess)
- Infarction (consider concomitant
cholecystectomy)
Response Response
-
-
palliative
variable response
- transfusion requirements
- relief of symptoms
Autosomal codominant (inherited from 1 Mendelian recessive
parent(heterozygous): carriers; both parents
(homozygous):sickle cell anemia)
Inherited schronic hemolytic anemia that results
from the mutant sicle cell hemoglobin (HbS) w/n
the rbc
Most common genetic diseases known to arise
from a single gene defect
The underlying abnormality is the mutation of In all forms thalassemia the primary defect is
adenine to thymine in the 6th codon of the Beta- absent or reduced production of hemoglobin
hemoglobin gene  substitution of valine for chains
glutamic acid as the 6th amino acid of the beta-
globin chain
- microvascular congestion 
thrombosis  ischemia  tissue
necrosis
- early splenomegaly infarction of the
spleen  autosplenectomy
- painful intermittent episodes
- splenectomy doesn’t affect the sickling
process
- therapy largely palliative

9
 severe symptomatic anemia - transfusions indicated for anemia,
- mainstay tx: corticosteroids moderately severe episodes of of
- cont. therapy til hematocrit and acute chest syndrome (new infiltrate
on CXR, new sx like fever, cough,
reticulocyte count (usually w/n sputum production or hypoxia) & pre-
3wks) op before splenectomy
- (+) stroke, severe crisis = hydration,
exchange transfusion(manually or
automated apheresis equipment)
- hydroxyurea – an oral
chemotherapeutic agent that
upregulates fetal hemoglobin, w/c
interferes w polymerization of HbS =
sickling process

>>WHITE BLOOD CELL DISORDERS

Chronic Lymphocytic
Leukemia
Indications for Splenectomy
- cytopenias
- anemia
Response
- 75% response rate
Main characteristic:
progressive accumulation of
long-lived but nonfunctional
lymphocytes
Symptoms
- nonspecific
- weakness
- fatigue
- fever w/o illness
- night sweats
- frequent bacterial and
viral infections
- most frequent finding:
lymphadenopathy
- (+) splenomegaly:
may be massive or
barely palpable below
the costal margin
Splenectomy may facilitate
chemotherapy in px whose cell
counts were prohibitively low
before spleen removal;
Palliative splenectomy also
indicated for symptomatic
Hairy Cell Leukemia
Indications for Splenectomy
- cytopenias
- symptomatic
splenomegaly
Response
- 40-70% response rate
Main characteristic:
(+) splenectomy, pancytopenia,
large numbers of abnormal
lymphocytes in the bone
marrow;
An uncommon blood disorder,
2% of all adult leukemias;
Irregular hair like cytoplasmic
projections identifiable on the
peripheral smear
Few symptoms;
Require no specific therapy
Splenectomy doesn’t correct
the underlying disorder but
does return cell counts to
normal in 40-70% of patients
and alleviates sx of
splenomegaly
Hodgkin’s Disease
Indications for Splenectomy
- surgical staging in select
cases
Response
- -
Main characteristic:
(+) Reed-sternberg cells;
4 major histo types:
- lymphocyte
predominance type
- nodular sclerosis type
- mixed cellularity type
- lymphocyte depletion
type
- >90% of px – (+)
lymphadenopathy
above the diaphragm
- lymph nodes can
become become bulky
in the mediastinum =
shortness of breath,
cough, obstructive
pneumonia,
- spleen: an occult site
of spread; massive
splenomegaly is not
common
Staging information affects tx
because px with early stage
disease who have no splenic
involvement may be candidates
for radiotherapy alone; (+)
splenic involvement:
Non-Hodgkin’s Lymphoma
Indications for Splenectomy
- cytopenias
- symptomatic
splenomegaly
Response
improved cbc values
- relief of symptoms
Encompasses all malignancies
derived from the lymphoid
system except classic HD;
Proliferation of any one of the 3
predominant lymph cell types –
NK cells, T cells, B cells – may
be included in the category of
NHL
Classifications:
- nodal / extranodal
- indolent / aggressive /
very aggressive
- clinical manifestations
vary
1. indolent lymphomas –
mild or no symptoms
and seek medical
attention for a swollen
lymph node
2. aggressive/very
aggressive – pain,
swelling due to
obstruction of vessels,
fever, and night
sweats
Splenectomy is indicated for
management of symptoms
related to an enlarged spleen
as well as for improvement of
cytopenias;
Surgical staging not indicated
10
splenomegaly chemotherapy or multimodality
therapy

**Hodgkin’s Disease
- histologic type, location, symptomatology – influence survival for px with HD
Stage I - limited to 1 anatomic region
Stage II – presence of 2 or more contiguous or noncontiguous regions on the same side of the diaphragm
Stage III – involves disease on both sides of the diaphragm, but limited t lymph nodes, spleen and
Waldeyer’s ring (the ring of lymphoid tissue formed by the lingual, palatine, and nasopharyngeal
tonsils)
Stage IV – involvement of the bone marrow, lung, liver, skin, GI tract, or any organ or tissue other than
the lymph nodes or Waldeyer’s ring
- current indications for surgical staging: clinical stage I or II disease of the nodular sclerosing type and no
symptoms referable to HD
- surgical staging procedure for HD includes a bipsy of the liver, splenectomy, and the removal of representative
nodes and the retroperitoneum, mesentery, and hepatoduodenal ligament; an iliac marrow biopsy is geereally
included

>> PLATELET DISORDERS

Idiopathic Thrombocytopenic Purpura Thrombocytic Thrombocytopenic Purpura
Indications for Splenectomy Indications for Splenectomy
- failure of medical therapy - excessive plasma exchange requirement
- recurrent disease
Response Response
- 75-85% rate of long term response - typically curative
- also called immune thrombocytopenic purpura - a serious disorder characterized by
- an autoimmune disorder characterized by platelet count and thrombocytopenia, microangiopathic hemolytic
anemia, and neurologic complications.
mucocutaneous and petechial bleeding.
- Abnormal platelet clumping occurs in arterioles and
-  platelet count stems from premature removal of platelets opsonized by capillaries, reducing the lumen of these vessels and
antiplatelet IgG autoantibodies produced in the spleen. predisposing the patient to microvascular thrombotic
- Adult onset and childhood onset ITP are strikingly different in their clinical episodes
course and management. -  lumen size = shearing stresses on erythrocytes =
- (+) petechiae or ecchymosis, although some will experience major bleeding
deformed RBCs  hemolysis
from the outset.
- underlying abnormality is likely related to the
- Bleeding may occur from mucosal surfaces in the form of gingival bleeding,
persistence of unusually large multimers of von
epistaxis, menorrhagia, hematuria, or even melena.
Willebrand factor associated w/ platelet clumping int
- >50,000/mm3 ---incidental findings
the Px blood
- between 30,000 and 50,000/mm3 --- easy bruising
- Clinical features of the disorder include petechiae,
- 10,000-30,000/mm3 --- spontaneous petechiae or ecchymoses
fever, neurologic symptoms, renal failure, and
- <10,000/mm3 are at risk for internal bleeding. infrequently cardiac symptoms, such as heart failure
- major intracranial hemorrhage is about 1 %, usually occurring early in the or arrhythmias.
disease course - Petechial hemorrhages in the lower extremities are
- Children: often present at a young age (peak age approx. 5 years) with the most common presenting sign.
sudden onset of petechiae or purpura several days to weeks after an - Fever + flu-like Sx (malaise, fatigue)
infectious illness - Neurologic changes range from generalized
- Adults: more chronic form of disease with an insidious onset headaches to altered mental status, seizures, and
- Splenomegaly with ITP is uncommon in both adults and children, and its even coma.
occurrence should prompt a search for a separate cause of
thrombocytopenia.
- (+) petechiae and thrombocytopenia  diagnosis of
- 10% of children have a palpable spleen tip TTP  consideration of treatment
Diagnosis Diagnosis
- exclusion of other possibilities in the presence of platelet count and -
-
confirmed by peripheral blood smear
(+) schistocytes, nucleated RBCs, basophilc
mucocutaneous bleeding
stippling
- other diseases = secondary forms of ITP: systemic lupus erythemaous, - (-) Coomb’s test (to differentiate from Evan’s
antiphospholipid syndrome, lymphoproliferative disorders, HIV infections syndrome, SLE)
and hepatitis C  should be identified and treated when present
- Hx of drugs known to cause thrombocytopenia
- (+) megathrombocytes on peripheral smear
Therapy Therapy
- usual 1st line therapy: oral prednisone (1.0-1.5mg/kg per day) - first line therapy: plasma exchange (daily removal of
- IV immunoglobulin: (1.0g/kg per day for 2-3 days) – indicated for internal a single volume of the px’s plasma + its replacement
bleeding when platelet counts remain <5,000/mm3 or (+) extensive purpura w/ fresh frozen plasma until the Sx are corrected; 1-
11
 – thought to impair clearance of immunoglobulin G-coated platelets by 2wks
competing for binding to tissue macrophage receptors (immediate response - splenectomy: if (+) relapse; (+) multiple exchanges;
is common, sustained remission is not well tolerated w/o significant morbodity
- Splenectomy – indicated for failure od medical tx, prolonged use of steroids
w undesirable effects, most cases of 1st relapse
- Persistent need for > 10-20 mg/d for 3-6months to maintain a platelet count
of >30,000/mm3  splenectomy
- Children w/ typical ITP  obervation + short term therapy in select cases
- Urgent splenectomy if severe in both children and adults
Outcomes
- splenectomy – permanent response w/o subsequent need for steroids in 75-
85% of px
- responses usuallu occur w/n the first post op wk
- for px w extremely platelet counts (<10,000/mm3), platelets should be
available for surgery but should not be given pre-op
- once the splenic pedicle is ligated  platelets are given if (+) cont. bleeding

>>BONE MARROW (MYELOPROLIFERATIVE) DISORDERS

- characterized by an abnormal growth of cell lines in the bone marrow
- common underlying problems leading to splenectomy: symptomatic splenomegaly
- Splenomegaly Sx: early satiety, poor gastric emptying, heaviness or pain in the LUQ, and even diarrhea
- Hypersplenism in these conditions: usually associated with splenomegaly
- Splenectomy usually performed
- Splenomegaly sometimes treated nonsurgically by chemotherapeutic agents (busulfan, hydroxyurea, interferon-alpha)  mild to moderate
size reductions and some relief of Sx (discontinuation=rapid splenic regrowth)
- Radiation: only used when splenectomy is not an option

Chronic Myeloid
Leukemia
Indications
for
Response
:
- disorder of the primitive pluripotent stem cell in the bone marrow = significant erythroid,
megakaryotic, and pluripotent progenitors in the peripheral blood smear
Splenectomy:
- genetic hallmark: transposition between the bcr gene on chromosome 9 and the abl gene
on chromosome 22
Symptomatic Relief of
- 7-15% of all leukemias
splenomegaly abdominal
- often asymptomatic but can cause fatigue, anorexia, sweating and LUQ pain, early satiety
pain and
early due to splenomegaly
satiety - (+) splenomegaly in 50% of CML Px
- Tx: splenectomy=to ease pain and early satiety
Acute Myeloid Intolerable - abnormal growth of stem cells in the bone marrow
Leukemia symptomatic - unlike CML, has a more rapid and dramatic presentation
splenomegaly - hematopoietic stem cells in the bona marrow = inhibition of growth and maturation of
normal RBCs, WBCs, and plateletsDeath w/n wks-months if left untreated
- 1.2% of all cancer deaths
- viral-like illness w/ fever, malaise, bone pain due to expansion of the meduallry space
- Splenectomy: indicated only in the uncommon circumstance that LUQ pain and early
satiety become unbearable; weight benefits vs. risk in immunocompromised px due to
neutropenia and chemotherapy
Chronic Symptomatic - characterized by a proliferation of hematopoietic elements in the bone marrow and blood
Myelomonocytic splenomegaly - differs from CML in that it is associated w/ monocytosis in the peripheral smear (>1x10^3
Leukemia monocytes/mm3) and in the bone marrow
- (+) splenomegaly in 50% of CMML px
- splenectomy= symptomatic relief
Essential
Thrombocytopenia
Only for
advanced
- abnormal growth in the megakaryocyte cell line = platelets in the blood stream
- Dx made after exclusion of other chronic myeloid disorders w/ thrombocytosis
disease
- Vasomotor sx, thrombohemorrhagic events, recurrent fetal loss, tranformation to
myelofibrosis w/ myeloid metaplasia or AML
- Hydroxyurea=thrombotic events in ET but doesn’t alter transformation to myelofibrosis or
leukemia
12
 - (+) splenomegaly in one third to 50% of ET Px
- splenectomy not useful in early stages; reserved for later stages when myeloid metaplasia
has developed
- select px carefully-significant bleeding reported to complicate splenectomy
Polycythemia Vera - clonal, chronic, progressive myeloproliferative disorder characterized by RBC mass;
(+)leukocytosis, thrombocytosis, splenomegaly
- longer survival but still at risk for transformation to myelofibrosis or AML
- rare; annual occurance of 5-17 cases per million pop
- ruddy cyanosis, conjuctival plethora, hepatomegaly, splenomegaly, hypertension
- Tx: tailored to risk status of px; phlebotomy, aspirin, chemotherapeutic agents
- Splenectomy not helpful in early stages; reserved for later stages when myeloid metaplasia
has developed or if splenomegaly Sx are unbearable
Myelofibrosis Severe 76% - response to a clonal proliferation of hematopoietic stem cells
(Agnostic Myeloid symptomatic clinical - marrow failure is common
Metaplasia) splenomegaly response - true incidence unknown
at 1yr,
high risk of
- excessive radiation may play a role: proximity to Japan bombing and Thorotrast (contrast
hemorrhag agent thorium dioxide) = incidence
ic, - Dx: examination of peripheral blood smear + bone marrow; nucleated RBCs, immature
thrombotic myeloid elements in the blood (96% of the cases); teardrop poikilocytosis; exclude Hx of
, infectious primary neoplasm (lymphoma, adenocarcinoma of other organs) or TB-these px may
complicati develop secondary myelofibrosis
ons (26%) - Tx: asymptomatic(observation); symptomatic (therapeutic intervention); splenomegaly-
related sx (splenectomy); medical Tx also an option
- Thorough pre-op workup must precede splenectomy:
1. acceptable cardiac, pulmonary, hepatic,, renal reserve for the operation
2. examine coagulation system (test factor V and VIII and fibrin split products, platelet
count, bleeding time)
- platelet counts = adrenal steroids and/or platelet transfusion at the time of surgery
- complications post-splenectomy more common compaired to other hematologic indications
- thrombosis, hemorrhage, and infection complications are common

>>INFECTIONS AND ABSCESSES

- potential risk of spontaneous splenic rupture
- infectious mononucleosis due to either Epstein-Barr virus or cytomegalovirus infection = small risk of spontaneous splenic
rupture
- examples of possible causes of spon. Splenic rupture
1. malaria 6. Lymphoma
2. listeria 7. Angiosarcoma
3. fungal 8. Amyloidosis
4. dengue 9. Pregnancy
5. Q fever

- presumed pathophysiologic mechanism: infiltration of the splenic parenchyma w/ inflammatory cells, w/c distorts the
architecture and fibrous support system of the spleen and thins the splenic capsule (in this setting: minor external
trauma/Valsalva maneuver  spontaneous splenic rupture)
- abscesses of the spleen: uncommon (0.14-0.7% based on autopsy findings); occur more frequently in tropical locations, where
they are ssociated w/ thrombosed splenic vessels and infarction in px w/ sicle cell anemia

- 5 distinct mechanisms of splenic abscess formation:

1. hematogenous infection
2. contiguous infection
3. hemoglobinopathy
4. immunosuppression (inc. HIV, chemotherapy)
5. trauma
- presentation frequently delayed; Patients endure Sx for 16-22days before diagnosis
- clinical manifestations
1. fever
2. LUQ pain
3. Leukocytosis
4. Splenomegaly
- Dx confirmed by UTZ or CTscan (95% sensitivity and specificity)
- Tx: broad spectrum antibiotics to more specific therapy (14days)
- Splenectomy is the operation of choice (if cant be tolerated: percutaneous (successful for Px w/ unilocular disease) and open
drainage are options)
13
>>CYSTS AND TUMORS
- Most common primary tumor of the spleen: Sarcoma
- Cancer that most commonly spreads to the spleen: Lung Cancer
- 0.6% rate of tumor metastasis to the spleen, mostly carcinomas (autopsy studies)
- parasitic vs. non parasitic
Parasitic Non Parasitic
- most common cause of splenic cysts worldwide - most common: trauma (“pseudocyst”-because it doesn’t
- majority due to Echinococcus have a cellular lining
- more commonly found in areas where the pathogen is - less common examples:
endemic 1. dermoid
- Sx when present ar usually related to a mass lesion in 2. epidermoid
the LUQ or a lesion that impinges on the stomach 3. epithelial cyst
- may be symptomatic or asymptomatic

Dx:
- ultrasound – can establish presence of cystic lesion; incidental finding of asymptomatic mass lesions
- serologic testing – for echinococcal antibodies; can confirm or exclude the cystic lesion as parasitic (impt in planning operative
therapy)

Tx:
- symptomatic parasitic cysts – splenectomy
- avoidance of spillage of parasitic cyts contents into the
peritoneal cavity to avoid anaphylactic shock
Tx:
- small symptomatic non parasitic cyst – excised with
splenic preservation
- asymptmatic – close observation w/ follow up ultrasound
to exclude significant expansion
- large cyst – risk of cyst rupture with even minor trauma if
nonoperative management is used – may be unroofed
- both operations may be done laparoscopically

>>STORAGE DISEASES AND INFILTRATIVE DISORDERS

Gaucher's Diseas Niemann-Pick Disease Amyloidosis Sarcoidosis

Inherited lipid storage Inherited disorder of Disorder of abnormal Inflammatory disease of

disorder characterized by abnormal lysosomal storage extracellular protein young adults characterized
the deposition of of sphingomyelin and deposition by noncaseating
glucocerebroside in cells of cholesterol in the cells of the granulomas in affected
the macrophage-monocyte macrophage-monocyte tissues
system system
Underlying abnormality: 4 types (A,B,C, D): each w Forms: Any organ system may be
deficiency in the activity of a unique clinical presentations Primary- associated w involved;
lysosomal hydrolase; plasma cell dyscaria-splenic
lysosomal involvement (5% of cases) Other affected tissues:
Abnormal glycolipid hydrolasetypes A and B = lymph nodes, eyes, joints,
storageorganomegaly splenomegaly Secondary-associated w spleen and heart
(hepatomegaly, chronic inflammatory
splenomegaly) conditions-may also present
w large spleen
Sx: Sx: Sx: Sx:
- early satiety - splenomegaly Sx - splenomegaly Sx - nonspecific
- abdominal - maye range from - fatugue
discomfort asymptomatic to - malaise
**due to splenomegaly multiorgan failure - splenomegaly (25%
- thrombocytopenia of px)
- normocytic anemia - massive
- mild leucopenia splenomegaly is
**due to hypersplenism rare (>1kg)
excessive sequestration of - Splenomegaly
formed blood elements in and/or
the spleen hypersplenism Sx
14
Other Sx:
- bone pain
- pathologic fractures
- jaundice
Splenectomy alleviates
hematologic abnormalities in
px w hypersplenism but
does NOT correct
underlying disease process
Partial splenectomy –
effective in children to
correct both hematologic
problems and Sx due to
splenomegaly w/o incurring
risk of overwhelming
postsplenectomy sepsis
>>MISC. DISORDERS AND LESIONS
Splenic Artery Aneurysm
- rare
- most common visceral artery
aneurysm
- women 4x more likely to be
affected
- usually arises in the middle to
distal portion of the splenic
artery
- mortality is higher w/ px w
potal hypertension (>50%)
than those w/o it (17%)
Indications fot Tx:
- presence of Sx
- pregnancy
- intentio to become pregnant
- presence of pseudoaneurysms
associated w the inflammatory
processes
- aneurysm resection/ligation
Splenectomy relieves
splenomegaly Sx
Portal Hypertension
- can result from numerous
causes but usually due to
cirrhosis
- splenomegaly and splenic
cingestion often present 
sequestration and destruction
of circulating cells in the
spleen
Splenectomy not indicated for
hypersplenism per se in Px w portal
hypertension
- if splenectomy is required to
Splenectomy effectively
relieves Sx and corrects
hematologic abnormalities
such as anemia and
thrombocytopenia
Felty’s Syndrome
- triad: rheumatoid arthritis,
splenomegaly, neutropenia
- 3% of all px w/ rheumatoid
arthritis (2/3 are women)
- immature complexes coat the
surface of the WBCs 
sequestration  clearance in
the spleen neutropenia
(<2000 neutrophils/mm3)
- neutropenia = risk for
recurrent infections and often
drives need to splenectomy
- spleen varies in size: from non
palpable in 5-10% of px to
massively enlarged in others
- spleen is 4x heavier than
normal
- symptomatic neutropenia
- transfusion dependent anemia
- profound thrombocytopenia
-
- corticosteroid, hematopoietic
15
 alone – for midsplenic artery
lesions
- concomitant splenectomy –
distal lesions in close proximity
to the splenic hilum
- splenic artery embolization –
but painful splenic infarction
and abscess may follow;
otherwise, excellent prognosis
V. Preoperative Considerations
Vaccination
- imparts a small (<1-5%) but
definite lifetime risk of
fulmitant, potentially life
threatening infection
- vaccinations vs. encapsulated
bacteria should be given at
least 2 wks before surgery to
protect against infections
- most common bacteria to
cause serious infections in
asplenic hosts: Streptococcus
pneumoniae, H. influenzae
type B, meninggococcus
- if spleen is removed
emergentyly – like in trauma –
vaccinations should be given
asap after surgery w/ at least
1-2 days allowed for recovery
- after splenectomy – annual
influenza immunization
VI. Splenectomy Techniques
** Patient Preparation
bleeding from esophageal growth factors, methotrxate
varices exacerbated by - splenectomy
thrombocytopenia  - excellent prognosis
concomitant splenorectal
shunt procedure (to
decompress portal system)
- if secondary to splenic vein
thrombosis – may be curable
w splenectomy
- splenectomy if (+) bleeding
from isolated gastric varices,
normal liver function, hx of
pancreatic disease (examine
splenic vein thrombosis and
treat w splenectomy if positive)
Splenic Artery Embolization Deep Vein Thrombosis Prophylaxis
Advantages - not infrequent after
- operative blood loss from splenectomy esp if (+)
devascularized spleen splenomegaly and
- spleen size = easier myeloproliferative disorders
dissection and removal - post splenectomy PVT:
1. anorexia
Disadvantages 2. abdominal pain
- splenectomy related blood 3. leukocytosis
loss 4. thrombocytosis
- need for more analgesics
effective Tx:
- sometimes an extended
index of suspicion=early Dx w/
hospital stay
contrast enhanced Ct scan=start
- possibility of pancreatitis
anticoagulation immediately
- risk of invasive arteriography
DVT prophylaxis:
**author’s practice: pre-op
- sequencial compression
embolization of spleens ≥20sm –
devices
allowed spleens >30cm to be resected
- SC administration of heparin
laparoscopically w/ excellent
(5000 U)
conversion rate
16
- vaccination
- assess need for transfusions
- optimization of preoperative coagulation status
- blood typing
- antibody screening tests
- anemic px: transfused before surgery to a hemoglobin level of 10g/dL
- thrombocytopenic px: should not undergo transfusion before the day or surgery and not before the intraoperative
ligation of splenic artery
- corticosteroid therapy px: give parenteral corticosteroid therapy perioperatively
- DVT prophylaxis
- after endotracheal intubation, na nasogastric (NG) tube is inserted for stomach decompression

>> LAPAROSCOPIC SPLENECTOMY

• Done in ELECTIVE Cases
• Standard approach for normosplenic px requiring splenectomy
• To come up with SMALLER Scars
• Put patient in the Right Lateral Decubitus (a midway “double” access” technique has also been advocated: px in
45-degree R lat. Decub) – and insert the Camera through the Umbilicus; requires 3-4 trochars; additional
advantage over double access: exposure of vital anatomy in a manner that allows for a more intuitive sequence
of dissection, paralleling that of OS)
• Double access technique:requires the placement of 5-6 trochars
• Angled 30 or 45-degree laparoscope (2mm, 5mm,10m)
• Placement f trochars in the LUQ should be performed under laparoscopic visualization

>> OPEN SPLENECTOMY

• Done in EMERGENCY Cases – Most Commonly Indicated for Traumatic Rupture of the Spleen
• Other scenarios: massive splenomegaly, ascites, portal hypertension, multiple prior operations, extensive
splenic irradiation, possible splenic abscess
• Risk of INFECTIONS!
• Px: supine position w the surgeon ath the patient’s right
• Left subcostal incision paralleling the left costal margin and lying 2 fingerbreadths below it – preffered for most
elective splenectomies
• Midline incision – optimal for exposure when spleen is ruptured/massively enlarged/abdominal abcess is needed
for a staging laparotomy for Hodgkin’s disease
• Thoracoabdominal incision – rarely used – may be necessary for access to a challenging/significantly enlarged
spleen
• Incision of lateral peritoneal attachments (most notably the splenophrenic ligament)– further medial mobilization
of the spleenindividual ligation and sequential division of short gastric vesselssplenic hilar dissection (artery
first then vein; be careful not to injure the pancreas)division
• Once the spleen is excised, hemostasis is secured by irrigating and suctioning and inspecting the bed of
dissection (splenic bed not routinely drained)completion of surgeryremove nasogastric tube
• Spleen is mobilized by dividing ligamentous attachments, usually beginning with the splenocolic ligament
• (+)significant splenomegaly  achieve lesses sac access through gastrosplenic or gastrohepatic attachments 
ligate plenic artery in continuity along the superior border of the pancreas
- allows safer manipulation of the spleen
- safer dissection of the splenic hilum
- facilitates some shrinkage af the spleen
- provides an autotransfusion of erythrocytes and platelets

>> PARTIAL SPLENECTOMY

17
 - indicated o minimize the risk of postsplenectomy sepsis in children
- others: certain lipid storage disorders (Gaucher’s) and some forms of traumatic splenic injury (blunt and
penetrating)
- laparoscopic or open
- spleen must be mobilized and the splenic hilar vessels attached to the targeted segment ligated and divided;
devascularized segment of the spleen=transected along an obvious line of demarcation
- limited bleeding from the cut surface= controlled by cauterization, argon coagulation, or application of direct
hemostatic agents (cellulose gauze, fibrin glue)

>> INADVERTENT INTRAOPERATIVE SPLENIC INJURY

- true incidence is unknown
- risk of death, significant short term morbidity, blood loss, need for transfusion,hospital stay
- linked to gastric fundoplication, colectomy, paraesophageal hernia repair, nephrectomy, abdominal and pelvic
vascular surgery, some reports of colonoscopy
- most common mechnism: improper traction on the spleen against its peritoneal attachments
- most common type of injury: capsular tears
- parenchymal lacerations and subcapsular hematomas may also occur
- lower pole more commonly injured

VII. Splenectomy Outcomes

>> COMPLICATIONS OF SPLENECTOMY
A. Pulmonary Complications
o Atelectasis of Left Lung Lobe = MOST Common Complication (16% of Patients after Open
Splenectomy)
o Pleural Effusion and Pneumonia
B. Hemorrhagic Complications
o Bleeding – usually occurs Intraoperatively
o Occasionally presents as a SUBPHRENIC HEMATOMA Post-Op
o Be careful with the Small Gastric Vessels to avoid Brisk Bleeding
C. Infectious Complications
o Infections = OPSS, Wound Infections, Subphrenic Abscess
o OPSI / OPSS (Overwhelming Post-Splenectomy Infection) = Streptococcus pneumonia
o Other Causes include = H. influenza, Meningococcemia, E.coli
D. Pancreatic Complications
o Because the Tail is abuting to the Spleen, if we may accidentally Cut the Tail of the Pancreas, leading
to Fistula Formation (Intraoperative Trauma to the Pancreas – especially the Tail)
o Others: Pancreatitis, Pseudocyst, Pancreatic Fistula
E. Thromboembolic Complications
o Deep Vein Thrombosis (DVT) = occurs in 5-10% of Patients undergoing Splenectomy
o For DVT Prophylaxis = HEPARIN is recommended routinely

18
>> HEMATOLOGIC OUTCOMES
- discussed =)

VIII. OVERWHELMING POSTSPLENECTOMY INFECTION (OPSI / OPSS)

• The Loss of the Spleen’s Ability to Filter and Phagocytose Bacteria and Parasitized Blood Cells
prediposes the Patient to Infection by Encapsulated Bacteria of Parasites
• Reason for splenectomy – single most influencial determinant of OPSI risk
• 3 factors: 1) loss of splenic macropahges 2)diminished tuftsin production 3)loss of the spleen’s
reticuloendothelial screening function
• It is the MOST POTENTIALLY FULMINANT Complication in Splenectomy
• Most Common Cause = Streptococcus pneumoniae (50-90% of Cases)
• Examples: S. pneumoniae, H. influenzae, Neisseria meningitides (classic examples); others- grp A strep,
enterococcus, bacteroides, salmonella, bartonella
• Infections w protozoa that invade RBCs: Babesia microti (tick bites), Ehlichia Plasmodium – infections
occur more frequently in splenectomized px than normal hosts

A. Clinical Manifestations of OPSI / OPSS

o Fever
o Fatigue
o Head and Body Ache
o Diarrhea
o Abdominal Pain
o Hypotension
o Septic Shock
o Disseminated Intravascular Coagulation

B. Treatment
o POLYVALENT VACCINE
o Antibiotic therapy – considered in 3 contexts: deliberate therapy for established/presumed infections,
prophyaxis in anticipation of invasive procedures, general prophylaxis; daily doses of antibiotics until 5yrs
ar atleast 5 yrs after splenectomy
**IMPORTANT Notes: (jaime’s)
 Elective Case (Scheduled Splenectomy) = give Vaccines TWO WEEKS Before the Schedule
 Emergency Splenectomy = give Vaccines WITHIN 2 DAYS Post-Op (after the Splenectomy)
-------- NOT in the textbook =) or at least not discussed in the same order hehe
V. SPLENECTOMY AS A TREATMENT OF CHOICE (This will come out in the Test)
• Hereditary Spherocytosis
• Splenic Cysts and Tumors
• Splenic Abscess
• Splenic Artery Aneurysm
• Massive Splenic Injury (Grade-IV)

SOME CONDITIONS OF THE SPLEEN

• Splenic Abscess
• Splenic Cysts
• Abdominal Trauma

I. SPLENIC ABSCESS
• Most Cultures will Reveal = Staphylococcus and Streptococcus
• Potential risk of Spontaneous Splenic Rupture (Epstein-Barr Virus or Cytomegalovirus  Infectious
Mononucleosis  increased risk of spontaneious splenic rupture)
• It is a RARE Condition that is commonly Missed (a high index of suspicion is needed)
19
 • Routes of Abscess Formation:
Hematogenous (Most Common) Osteomyelitis, Pyelonephritis, Endocarditis, IV-Drug Abuse
Contiguous Pancreatic Fistulas, Colonic Malignancies invading Colonic Wall
Immunosuppression HIV/AIDS Patients; those undergoing Chemotherapy
Trauma Penetrating Splenic Trauma

A. Clinical Presentation of Splenic Abscess

o High Grade Remittent Fever
o Leukocytosis (increase WBC)
o Splenomegaly
o Left Upper Quadrant Abdominal Pain
o Left Shoulder Pain

**NOTE: A Spleen which is 2-3x of its Normal Size = SPLENOMEGALY (it is PALPABLE)!
 Splenomegaly is usually seen in the first 2-Weeks of the Condition

B. Diagnostics:
1. CT-Scan
 Standard Diagnosis!
 (+) Unilocular Abscess Cavity
 Shows Low Density Lesion (in Contrast CT-Scan)

2. X-Ray
 (+) Left Diaphragmatic Elevation (sometimes as high as 5cm)
 (+) Left Pleural Effusion

C. Treatment
o Broad Spectrum Antibiotics = Cephalosporins (based on the Cultures)
o CT-Scan or Ultrasound Guided Percutaneous Drainage
o Open Drainage
o SPLENECTOMY = Gold Standard

**NOTE: Staphylococcus and Streptococcus = PREDOMINANT Microbes identified

II. SPLENIC CYSTS

A. Two Main Classification = TRUE + PSEUDOCYST
1. Primary Cysts (True)
 Non-Parasitic (Congenital + Neoplastic)
 Parasitic

2. Secondary Cyst
 PSEUDOCYST

B. Cysts and Tumors of the Spleen

Echinococcal Cysts Most Common TRUE PARASITIC Splenic Cyst!

Hemangioma Most Common BENIGN Tumor

Non-Hodgkin’s Lymphoma Most Common PRIMARY MALIGNANT Tumor

Splenic Hematoma Most Common PSEUDOCYST (Secondary Cyst)

20
 Epidermoid Cyst Most Common TRUE NON-PARASITIC Splenic Cyst

**NOTE: Lung Cancer = Most Common Malignancy that Metastasizes to the Spleen!

III. ABDOMINAL TRAUMA

• In BLUNT Abdominal Trauma, the MOST COMMONLY Injured Organ is the SPLEEN
• Trauma to the Spleen = Seen in Vehicular Accidents, Gunshot Wounds, Stab Wounds
A. Splenic Injury Scale (1994)
GRADE DESCRIPTION MANAGEMENT (prenotes)
I Hematoma < 10% Surface Area Non-Operative
Laceration < 1cm Deep

II Hematoma 10-15% Surface Area Non-Operative

Laceration 1-3cm Deep

III Hematoma > 50% or Expanding Operative

Laceration > 3cm Deep

IV Laceration Segmental or Hillar Vessels Operative

V Laceration SHATTERED Spleen Operative

**NOTE: The Gravity of the Injury INCREASES as the Grade Increases

 Grade I = GOOD Prognosis
 Grade V = WORST Prognosis!
B. Clinical Manifestations of Patients with Splenic Injuries
o PALLOR (Pale Looking Patient)
o Vital Signs Deterioration (Tachycardia, Hypotension)
o Abdominal Findings (Silent Abdomen, Abdominal Fullness, Tenderness & Quarding)

**NOTE: To Assess Pallor

 Compare your Palm with the Patient
 Also look at the Palpebral Conjunctiva

C. Diagnostic Tests
o Serial CT-Scan
o Ultrasonography
o Serial Hemoglobin and Hematocrit Determination
o Diagnostic Peritoneal Lavage (DPL)

**NOTE: Mainstay is Serial CT-Scan + Serial Ultrasound

D. Management of Splenic Injuries

o Grade I and II = NON-OPERATIVE Management
o Grade III, IV, and V = ICU Observation; SURGERY!

**Criteria for NON-OPERATIVE Management:

 Stable Vital Signs
 CT-Scan Documenting Exact Injury
21
  Absence of Progressive Bleeding Peritonitis
 Absence of Concomitant Intraabdominal Injuries
 Blood Transfusion (< 2 Units / 24 Hours)

E. Techniques for Splenic Salvage

1. Individual Bleeding Vessel Ligation
 If the Hematoma is SHALLOW
 We can Cauterize the Vessel

2. Cautery or Hemostatic Agent Application

 Burning (with the use of Electricity) the Parenchyma of the Spleen
 Hemostatic Agents = absorbs blood and leads to Coagulation

3. Splenorrhapy
 Repairing / Mesh = Wrap the Spleen (especially if Grade-II or III)
 To affect Hemostasis, we do Tightening of the Mesh to Save the Spleen

4. Partial Splenectomy
 Removal of just the Upper or Lower Pole of the Spleen

5. Splenic Autotransplantation
 Cut a piece of Spleen, and Imbed it in the Omentum
 A fragment of spleen is cut and transplanted into the Greater Omentum
 Vascularization will occur, resulting in a FUNCTIONAL Spleen

22