Principles of Splenic Surgery

Content
• Anatomy
• Splenic function
• Hypersplenism
• Splenectomy
• Lap vs open splenectomy
• Outcomes
• Complications
• Splenic trauma
• Splenic repairs
• Conservative treatment
 Anatomy
• The spleen is situated principally in the left
hypochondriac region, but its superior extremity extends
into the epigastric region; it lies between the fundus of
the stomach and the diaphragm.

• It is the largest of the ductless glands, and is of an

oblong, flattened form, soft, of very friable consistency,
highly vascular, and of a dark purplish color.

• The normal size and weight vary somewhat. The approx

size is 12cm(length) x 7cm(width) x 3-4cm(thickness)
with an average weight of 150g (range 80-300g).
 Anatomy

Tail of Pancreas
-Direct contact with
spleen in 30%
-Otherwise within 1 cm
 Relations
• The diaphragmatic surface (facies
diaphragmatica; external or phrenic surface) is
convex, smooth, and is directed upward,
backward, and to the left, except at its upper
end, where it is directed slightly medialward. It is
in relation with the under surface of the
diaphragm, which separates it from the ninth,
tenth, and eleventh ribs of the left side, and the
intervening lower border of the left lung and
pleura.
Drawing - Visceral surface of the spleen illustrating the splenorenal
ligament and the vessels contained within
•   The visceral surface is divided by a ridge into an
anterior or gastric and a
posterior or renal portion.

•   The gastric surface (facies gastrica), which is directed

forward, upward, and medialward, is broad and concave,
and is in contact with the posterior wall of the stomach;
and below this with the tail of the pancreas. It presents
near its medial border a long fissure, termed the hilum.
This is pierced by several irregular apertures, for the
entrance and exit of vessels and nerves. 

•  The renal surface (facies renalis) is directed

medialward and downward. It is somewhat flattened, is
considerably narrower than the gastric surface, and is in
relation with the upper part of the anterior surface of the
left kidney and occasionally with the left suprarenal
gland.
• The superior extremity (extremitas superior) is directed
toward the vertebral column, where it lies on a level with
the eleventh thoracic vertebra.
• The lower extremity or colic surface (extremitas
inferior) is flat, triangular in shape, and rests upon the left
flexure of the colon and the phrenicocolic ligament, and
is generally in contact with the tail of the pancreas.
• The anterior border (margo anterior) is free, sharp, and
thin, and is often notched, especially below; it separates
the diaphragmatic from the gastric surface.
• The posterior border (margo posterior), more rounded
and blunter than the anterior, separates the renal from
the diaphragmatic surface; it corresponds to the lower
border of the eleventh rib and lies between the
diaphragm and left kidney. The intermediate margin is
the ridge which separates the renal and gastric surfaces.
• The inferior border (internal border) separates the
diaphragmatic from the colic surface.
 Ligaments

• The spleen is almost entirely surrounded by peritoneum,

which is firmly adherent to its capsule. It is held in
position by two folds of this membrane.

• The parietal peritoneum adheres firmly to the splenic

capsule, except at the splenic hilum. The peritoneum
extends superiorly, laterally and inferiorly, creating folds
which form the suspensory ligaments of the spleen.

• The splenocolic and the splenophrenic ligaments are

relatively avascular
 Ligaments

• The splenorenal ligament runs from the anterior left

kidney to the hilum of the spleen as a two layered fold in
which the splenic vessels and the tail of the pancreas are
invested.

• The other fold, the gastrosplenic ligament, is also formed

of two layers, derived from the general cavity and the
omental respectively, where they meet between the
spleen and stomach; the short gastric and left
gastroepiploic branches of the splenic artery run
between its two layers. The lower end of the spleen is
supported by the phrenicocolic ligament.
Suspensory Ligaments

Gastrosplenic Ligament
􀂃 Short Gastric Vessels
􀂃 Gastroepiploic Vessels

Splenorenal Ligament
􀂃 Splenic Vessels
􀂃 Tail of Pancreas

Splenocolic Ligament

Phrenicocolic Ligament
􀂃 Phrenicosplenic ligament
 Blood supply
• The celiac axis – largest but shortest branch
of the abdominal aorta: 15-20mm long.
• Arises above the body of the pancreas, and
in 82% of specimens divides into three
primary branches
􀂃 The left gastric artery
􀂃 The hepatic artery
􀂃 The splenic artery
 Splenic Artery
• In rare instances the splenic artery originates directly
from the aorta, and even less often a second splenic
artery arises from the celiac axis.
• Other variations include the splenic artery originating
from the Superior mesenteric artery, the middle colic
artery, the left gastric artery, the hepatic artery, or the
accessory right hepatic artery
• As a rule the splenic artery arises from the celiac axis to
the right or the midline, which means that the aorta must
be crossed to reach the spleen and that selective
angiography is likely to be difficult at times
• Acounts for approximately 5% of cardiac output
• It courses along the superior border of the
pancreas and the branches include numerous
pancreatic branches, the short gastric branches,
the left gastroepiploic artery and the terminal
splenic branches

• Splenic arterial geography can be divided into 2

types – Distributed or Magistral (Michels NA The
variational anatomy of the spleen and splenic
artery . Am J Anat 70: 21, 1942)
30% - Magistral

-Branches originate 3-13cm from

hilum

-Transverse Anastomoses – why

embolization / clipping may fail

-Pancreatica Magna – embolic

debris from angio may cause
pancreatitis
70% - Distributed

-Branches originate within 3.5 cm

of hilum

-L Gastroepiploic artery– Most

varied of splenic branches (72%
arise several cm from splenic artery
proximal to terminal branching
 Histology
• The spleen is invested in a fibroelastic capsule from which
trabeculae pass into the parenchyma, branching to form a
trabecular network that subdivides the gland into small
compartments.

• Parenchyma has 2 main elements : - red pulp ( 75%) and white pulp

• A narrow marginal zone exists at the interface of the red and white
pulps
 Pseudo-Segmental Blood Supply

‘White pulp’ contains end arterioles

surrounded by sheaths of densely packed
small lymphocytes subdivided into central,
intermediate and peripheral marginal zones
Central zone -> CD4+T- helper lymphocytes
Intermediate follicular zone is the B- lymphocyte zone

‘Red pulp’ consists of large thin walled

sinuses that are filled with blood and
separated by thin plates / cords of lymphoid
tissue, the Cords of Billroth
macrophages, lymphocytes, plasma
cells, granulocytes, red blood cells and
platelets
White Pulp
-Opsonins – IgM, IgG, tuftsin, properdin
-T-Cells

Red Pulp (75% of parenchyma)

-Phagocytosis
-“Pitting” damaged RBCs, WBCs
-Opsonized Pathogen Clearance
Splenic Function
 Hypersplenism
• “Hematologic effects of splenomegaly”
• Hypersplenism is a disorder which causes the spleen to
rapidly and prematurely destroy blood cells.
• Enhanced capacity of the enlarged spleen:
􀂃 Pooling,
􀂃 Sequestering, and
􀂃 Destroying blood cells
• Results in reduction of blood cell counts
􀂃 Bone marrow function usually normal
􀂃 Sometimes by sequestration alone
􀂃 Cytopenia corrected following splenectomy
 Causes and symptoms
• Primary hypersplenism – caused by problem with the
spleen itself.
• Secondary hypersplenism results from another disease
such as chronic malaria, rheumatoid arthritis,
tuberculosis, or polycythemia vera
• Symptoms of hypersplenism include easy bruising, easy
contracting of bacterial diseases, fever, weakness, heart
palpitations, and ulcerations of the mouth, legs and feet.
Individuals may also bleed unexpectedly and heavily
from the nose or other mucous membranes, and from
the gastrointestinal or urinary tracts.
Hypersplenism–Many Etiologies
 Hypersplenism
Platelet Sequestration

Healthy Hypersplenism

Palpable spleen is at least twice its normal size

 Hypersplenism
• Why Splenectomy in Hypersplenism?

􀂃 Treat Splenomegaly
• Compressive symptoms
• Risk for splenic injury if active

􀂃 Improve blood counts – RBC’s, Platelets

􀂃 Temporize underlying condition

• Rarely curative, but an adjunctive therapy
• Failed medical management
• Reduce number of required transfusions
• Pain or abscess secondary to splenic infarction (sickle cell, thalassemia)

􀂃 Staging Procedure
 Splenectomy
1549 – First reported by
Zacarello in Italy

1816 – First in North America,

O’Brien
􀂃 Victim stabbed in LUQ while
committing a rape

1826 - Quittenbaum,
1st elective splenectomy
􀂃 Portal HTN
• 1866 – Bryant, 1st splenectomy for leukemia

• 1908 – Johnson reports mortality of 87.7% in

49 patients with leukemia

• 1916 – Kaznelson reports good results for

thrombocytopenic purpura

• 1952 – OPSS reported

• 1962 – Christo in Brazil: Splenic salvage prevents

OPSS

• 1991 – Laparoscopic splenectomy reported by

four different groups
 Patient preparation
• Counseled
• Vaccination - at least 7-14 days prior
• Transfusion if needed to achieve Hb >10g/dl
• Cross match - 2 – 4 units
• ? Platelet transfusion
• Parental corticosteroids periopratively if on
steroids.
▪ DVT prophylaxis
▪ Antibiotics - 1st generation cephalosporin
▪ NGT after intubation
 Splenectomy techniques
• Although laparoscopic surgery (LS) is recognized as the
standard approach for normosplenic patients requiring
surgery, open splenectomy (OS) is still widely practiced.
• The most common indication for OS is traumatic rupture of
the spleen.
• Other situations where OS may be favored include massive
splenomegaly, ascites, portal hypertension, multiple prior
operations, extensive splenic radiation, and possibly splenic
abscess.
 Laparoscopic Splenectomy
• LS has steadily surpassed OS as the approach
of choice for most elective splenectomies .

• Several large series have shown the benefits of

LS to patients with normal sized spleens

• Recent literature supports LS in expert hands in

situations that were previously reserved for OS
e.g. morbid obesity, splenomegaly, multiple prior
surgeries, and even pregnancy.
 Laparoscopic Splenectomy -
Indications
• ITP 􀃆 Most Common • Splenic Abcess
• Hereditary Spherocytosis • Splenic Cyst
• TTP • Gaucher’s Dz (storage)
• Autoimmune Hemolytic Anemia • Felty’s Syndrome
• Lymphoma 􀂃 RA neutropenia
􀂃 Hodgkin’s Dz (Staging) 􀂃 Splenomegaly
􀂃 Non-Hodgkin’s • Myelofibrosis
(hypersplenism) 􀂃 Extramedullary
• Leukemia (hypersplenism) hematopoiesis
• Hemoglobinopathies • Splenic Infarct
􀂃 Thalassemia, Sickle Cell • AIDS Thrombocytopenia
• Hypersplenism
􀂃 Portal HTN, SLE, or
Sarcoid
Lap vs Open Splenectomy
Laparoscopic Splenectomy
 Laparoscopic Splenectomy
• Patient Positioning
􀂃 Usually right lateral decubitus position
􀂃 Anterior approach for large spleens(>25-30cm)
• Trocar placement
lateral – 3 or 4 ports
anterior – 5-6 ports
 Laparoscopic Splenectomy
Procedure:
The stomach is retracted medially to expose the spleen.
• A thorough search is made for accessory spleens. Any accessory
spleens found should be removed immediately as they are considerably
harder to locate once the spleen is removed and the field is stained with
blood.
• Splenocolic ligament divided as are the lateral peritoneal attachments,
resulting in medial mobilization of the spleen. Short gastrics divided by
individual application of clips, endovascular stapler or haemostatic
energy sources.
• After retracting the lower pole of the spleen, the splenic hilum is then
accessible to clips or stapling device.
• Once excised, the spleen is placed in a nylon or freezer bag, the neck of
which is pulled through one of the trocar sites.
• The spleen is then morcellated and extracted piecemeal
 Splenic Trauma
• Most common indication for laparotomy following blunt
trauma
• MVA’s most common source

• Other mechanisms include: motorcycle crashes, falls,

RTA’s, bicycle crashes, and sports.
• Splenic injuries are produced by rapid deceleration,
compression, energy transmission through the posterior
lateral chest wall over the spleen, or puncture from
adjacent rib fractures
• Rapid deceleration results in the spleen continuing to
move forward while tethered at the point of attachment
 Splenic Trauma cont’d
• Injuries produced by decelerating forces result in capsular
avulsion along the various ligamentous attachments and
linear or stellate fractures of varying depths.
• Because of the solid structural characteristics and density,
energy transfer is relatively efficient.
• Injuries cause by assaults or falls are usually the result of
direct blows over the lower chest wall, with transmission of
energy resulting in splenic lacerations.
• The spleen receives about 5% of the cardiac output. The
splenic artery divide into several segmental vessel supplying
the poles and midportion, and these vessels divide into 2nd
and 3rd order vessels that course transversely within the
spleen.
• Because of this extensive supply, even small lacerations or
capsular avulsions yield substantial hemorrhage.
 Splenic Trauma

• Most frequently injured

intraabdominal organ in
blunt trauma

• Fractured left ribs and

pulmonary contusion
most common associated
Injuries

• Hematuria most common

nonspecific finding
􀂃 Renal injury
 Splenic Trauma - Diagnosis
• Old: Peritoneal Lavage
􀂃 >100,000 RBC’s/HPF
􀂃 Food Particles
􀂃 Very Sensitive
􀂃 Many False +’s
• Intermediate: CT Scan
• New: FAST
􀂃 Looking for Blood only
􀂃 NOT looking for organ detail!
􀂃 Wait for foley: may get
more detail if bladder full
 American Association for the Surgery of Trauma
(AAST) splenic injury scale (1994)
Grade Injury description Score
I Hematoma Subcapsular <10% surface area 2
Laceration Capsular tear <1cm parenchymal depth 2
II Hematoma Subcapsular 10-50% surface area; 2
intraparenchymal <5 cm in diameter
Laceration Capsular tears, 1-3cm parenchymal depth, does
not involve a trabecular vessel
III Hematoma Subcapsular, >50% surface area or expanding: 3
ruptured subcapsular or parenchymal hematoma; 3
intraparenchymal hematoma >5cm or expanding
Laceration >3cm parenchymal depth or involving trabecular
vessels
IV Laceration Laceration involving segmental or hilar vessels 4

producing major devascularisation (>25% of spleen)

V Laceration Completely shattered spleen 5
5
Vascular Hilar vascular injury that devascularises spleen
 Splenic Trauma

• Treatment has come full circle

􀂃 1890’s – Nonoperative Management
􀂃 1900’s – Operative Management
􀂃 1970’s-1990’s – Nonoperative Management
• OPSS – Not as likely following Trauma
􀂃 Partial Splenectomy
􀂃 Accessory Spleens
􀂃 Splenosis
• Spleen Removal (Splenectomy). This exhibit illustrates the splenectomy procedure in
which the spleen is removed. The first image shows the midline incision in the
abdomen through which the damaged spleen is exposed. The second image depicts
the mobilization of the lacerated spleen and ligation (binding) of the splenic vessels
which will be clipped. An enlargement of the removed spleen is pictured off to the
side to highlight the specific injuries.
 Splenic repairs
• Splenic conservation historically
performed in Children:
• - More likely to develop OPSS, saving
splenic function protective
• - Capsule more amenable to repair (adults
tear)
• -Lower arterial pressure in splenic arterial
system – easier hemostasis
 Splenectomy outcomes

Results in characteristic changes to blood composition.

These include :
appearance of Howell Jolly bodies and siderocytes

Leukocytosis – WBC raises within one (1) day and may remain
elevated for several months

Increased platelets occur wihin 2 days (but may not peak for several
weeks)
 Hematologic outcomes
• Divided into initial and long term responses:
• For thrombocyopenia :
Initial response : rise in platelets within several days
Long term response is defined as a platelet count > 150 000/ml more
that 2 months after surgery with out medication
▫ LS long term response obtained in 85%
▫ OS has success rate of 60-90%

• For chronic hemolytic anemias, a rise in hemoglobin levels to above 10g/dl

without the need for transfusion signifies a successful response to
splenectomy
▫ successful in 60-80%of cases

For patients with hereditary spherocytsis the success rate is 90-100%

 Complications
• Classified as :
Pulmonary
Hemorrhagic
Infectious
Pancreatic
Thromboembolic
Functional
Pulmonary :
Left lower lobe atelectasis - Most common (16% of patients)

Pleural effusions and pneumonia (10%)

Hemorrhagic
Usually occurs intra op and corrected then, but may present as a
subphrenic hematoma

Transfusions have become less frequent with LS and depend on the

indication for splenectomy

Across all elective cases – need for transfusion occur in 3-5% of cases
Infectious :
Subphrenic abscess (usually associated with drain placement)
OPSS (see below)

Pancreatic
Pancreatitis
Pseudo cyst formation
Pancreatic fistula
These may all be due to trauma to the pancreas especially to the tail during the
dissection of the splenic hilum
• Thromboembolic:

eg. portal vein thrombosis; deep vein thrombosis

Occurs in 5-10% of patients and DVT prophylaxis is recommended

The risk is even higher in patients with hemolytic anemia,

myeloproliferative disorders and splenomegaly.

Functional:
Persistence of hyperspleenism (unresected accessory spleen)
 Overwhelming Post- Splenectomy Sepsis
a.k.a. OPSS, OPSI

RISK: 
• All post splenectomy patients have an increased risk of
overwhelming bacterial infection.  Certain factors however do
influence the degree of risk:
  Age : Younger patients have greater risk
Underlying disease : Risk with underlying immunodeficiency
> thalassemia > sickle cell anemia > traumatic splenectomy
Time since splenectomy : Recent splenectomy has greater
risk than many years post-operatively with 80% of cases occurring
within 2 years of splenectomy
 Pathogens:
• The most common cause of overwhelming post-splenectomy sepsis
is S. pneumoniae (50-60%), however all of the pathogens listed
below can be a source of serious infection in these patients:

·         Encapsulated bacteria: S. pneumoniae, H. influenza (20-

30%), N. meningitidis (10-20%)
·         S. aureus
·         Numerous gram negatives including E. coli, K. pneumoniae,
Salmonella sp. and Capnotcytophagia sp. (the latter usually
acquired from a dog bite)
·         Malaria
·         Babesia (acquired from ticks in the Eastern seaboard
particularly Cape Cod, Martha’s Vineyard, Nantucket, Block Island)
 Clinical manifestations
• Fever
– Any fever must be viewed as possible PSS
• Bacteremia
• Coagulopathy
– Purpura, petechiae
• Meningitis
– Headache, neck stiffness, seizure
• Respiratory symptoms
– Cough, dyspnea, respiratory failure
• GI symptoms
– Nausea, vomiting, diarrhea, GI bleeding
• Shock
 Labs

• CBC
• Blood smear
• DIC profile
• Lumbar puncture
• CXR
• Blood culture
 Management
• Broad-spectrum antibiotics
– Based on expert opinion
– Must cover:
• penicillin-resistant pneumococcus
• beta-lactamase producing H.influenzae
– General suggestion
• Ceftriaxone + Vancomycin
• Levofloxacin + Vancomycin
• Life-support measures
– H/D or CVVH for ARF
– Ventilator
– Inotropic agents
– Fluid
 Prevention
• Avoid unnecessary splenectomy
􀂃 Splenic salvage highly desirable when safe
Selective nonoperative management (i.e. Trauma)
Operative splenorrhaphy
Intentional splenosis when appropriate

• Immunization
– Timing
• 14 days before splenectomy
• 14 days after splenectomy (not immediately)
– Pneumococcal vaccine
• PPV-23 for adults
• PCPV-7 for children and some adults
– Haemophilus B vaccine
– Meningococcal vaccine
– Re-immunization
– Other vaccines: influenza vaccine
 Vaccinations

• There are currently 2 licensed pneumococcal vaccine:

 
• 1) a 23-valent Pnemococcal Polysaccharide Vaccine, PPV-23 
(Pneumovax®). This vaccine is immunogenic only in those > 2
years of age and provides protection against the greatest number of
clinically relevant serotypes.

2) a 7-valent Protein-Conjugated Vaccine, PCV-7  (Prevnar®),

which is immunogenic and safe beginning at 6 weeks of age. It has
not been well studied in older patients and provides protection
against only 7 serotypes.
 Vaccination: Recommendations

Current recommendations for this use of these vaccines post splenectomy are as
follows:

•       Children less than 2 years of age should receive PCV-7 at the usual ages
recommended for children their age: 2, 4, 6 and 12-15 months of age. These children
should be given PPV-23 at 2 years of age.

•    Children 2 to 5 years of age should receive two doses of PCV-7 given 2 months
apart, followed > 2 months later by a dose of PPV-23.

•      Older children and adults should receive the PPV23.

•        A booster PPV23 should be given approximately 5 years after the initial
vaccine/series.

•       Quadrivalent conjugated meningococcal vaccine should be given to all

asplenic individuals > 2 years of age.

•        Hemophilus influenza vaccine should be given once to all individuals > 2 years
of age and at the time of routine vaccination for younger children.
 Prophylactic Antibiotics
The only regimen which has been studied is penicillin prophylaxis for patients
with functional asplenia from sickle cell anemia.  Resistance to penicillin (and
other antibiotics) is a growing concern, so it’s efficacy is currently presumed to
be lower. In addition, compliance with an indefinite daily regimen is extremely
difficult.

• The patients who are most likely to benefit from prophylaxis are:
   􀂃 Children < 5 years of age,
􀂃 Individuals who have had splenectomy within the past year,
􀂃 Those with an underlying immunodeficiency in addition to splenectomy

• Regimens for children:

Penicillin G : Pediatrics: 250 mg. p.o. b.i.d. (less than 5 years, 125 mg p.o. b.d.) .
Alternatives: Amoxicillin: Pediatrics: 20mg/kg/day divided b.i.d.
       
  As there are currently no ideal second line oral agents, allergy to the penicillins
should be assessed carefully.

No data are available in adults and antibiotic prophylaxis is generally not

recommended this population
 
 Post-Splenectomy Sepsis

* Pre-op for distal pancreatectomy in case splenectomy performed

 Nonoperative management

• With careful patient selection, success rate now

approaches 95% (85-95%)
􀂃 Hemodynamic stability
􀂃 No contrast ‘pooling’ on CT
􀂃 No other intraabdominal injuries requiring laparotomy

• Follow frequent serial vital signs and H/H

􀂃 Treat persistently falling RBC with pRBC’s
􀂃 Rebleeding most likely within 1st 48 hours
􀂃 Likely failure if patient requires ≥ 2 u pRBCs
If still falling after 2u, consider angio for embolization
If hypotension develops, consider angiography
 Nonoperative Management

• Follow-up CT scans rarely necessary

􀂃 Indicated for falling BP or H/H during observation
􀂃 Grade I-II: rarely show progression of lesion or other
complications on CT. No need for repeat CT scan if
H/H and vitals stable
􀂃 Grade III: CT’s on case-by-case basis
􀂃 Consider U/S for monitoring if necessary
􀂃 Contact Sports: Complete resolution on CT required
before can return to activity
• 2-5% of patients treated nonoperatively will develop
parenchymal infarction or infection
Nonoperative Management
 Nonoperative Management

• Delayed Rupture
􀂃 75% occur within 2 weeks in several
series
• Hematoma liquifying?
􀂃 Can occur anytime! (1 month – years)
􀂃 Actual incidence of delayed rupture very
low
􀂃 Need to inform patients of this prior to
Dischage
 Failure of nonoperative management of
Blunt Splenic Injury
• Increasing or persistent fluid requirements to maintain
normal hemodynamic status

• Failed angioembolization of arteriovenous fistula /

pseudoaneurysm

• Transfusion requirement to maintain hematocrit and

hemodynamic stability

• Increasing hemoperitoneum associated with hemodynamic

instability

• Peritoneal signs/rebound tenderness