splenectomy

CC Huevos || CC Gerra
Indications for
splenectomy
1 Benign 3 Others
o RBC disorders o Cysts and tumors
o Hemoglobinopathies o Infections and abscesses
o Platelet disorders o Splenic rupture
o Trauma, etc.
2 Malignant
o WBC disorders
o Bone marrow disorders
Fast facts
Most common indication for splenectomy is
trauma to the spleen
§ External trauma
Ø Blunt or penetrating
§ Iatrogenic injury

Most common indication for elective splenectomy

is Immune Thrombocytopenic Purpura (ITP)
RBC disorders
Hereditary Spherocytosis
Pathophysiology
• Inherited (autosomal dominant) dysfunction or
deficiency in one of the erythrocyte membrane
proteins (spectrin, ankyrin, etc.) à destabilization
of membrane lipid layer à pathologic release of
membrane lipids
• RBC becomes more spherical and less
deformable à sequestered and destroyed in
spleen à hemolytic anemia
RBC disorders
Hereditary Spherocytosis
Presentation
• Mild jaundice • Elevated erythrocyte distribution width (RDW)
• Splenomegaly • Elevated reticulocyte count
• Varying degrees of anemia • Elevated LDH
• Elevated mean corpuscular hemoglobin • Elevated unconjugated bilirubin
concentration (MCHC) • Spherocytes on PBS
RBC disorders
Hereditary Spherocytosis
Management
Main indications for splenectomy: Near total splenectomy in children
ü Symptomatic hemolytic anemia Ø dramatic clinical improvement despite hemolysis
ü Growth retardation Ø Timing of splenectomy should be delayed until
ü Skeletal changes child is between 4-6 yo
ü Leg ulcer Ø To reduce the possibility of overwhelming
ü Extramedullary hematopoietic tumors postsplenectomy sepsis/infection (OPSI)

If gallstones coexist, gallbladder should be removed.

Ø Prophylactic cholecystectomy without stones
not recommended
 RBC disorders
Pyruvate Kinase Deficiency

Most common RBC enzyme deficiency to cause congenital chronic homolytic anemia.

Pathophysiology: Unclear

Presentation: mild anemia to transfusion-dependent anemia, splenomegaly

Splenectomy: done to alleviate transfusion requirements in severe cases

Children: delay to at least 4 y/o

 RBC disorders
Warm-antibody Autoimmune
Hemolytic Anemia (WAIHA)

Pathophysiology: Autoantibodies attack antigens on the RBC leading to destruction of the RBCs.

Presentation: mild jaundice, mild anemia, splenomegaly

Diagnosis: hemolysis (anemia, reticulocytosis), products of RBC destruction (bilirubin), positive

direct Coomb’s test

Management: blood transfusion, corticosteroids continued for 3 weeks (mainstay therapy)

Splenectomy: considered after failure of steroids or anti-CD20 antibody administration

Hemoglobinopathies
Sickle Cell Disease
An inherited (autosomal codominant) chronic hemolytic
anemia resulting from the mutant sickle cell hemoglobin
(HbS) within the RBC.

Pathophysiology
Mutation of adenine to thymine in sixth codon of the B-globin
gene à substitution of valine for glutamic acid à HbS

Deoxygenated HbS is insoluble and becomes polymerized and

sickled à lack of deformability of the RBC à microvascular
congestion à thrombosis, ischemia, and tissue necrosis
Hemoglobinopathies
Sickle Cell Disease
Presentation: splenomegaly (due to sequestration), painful intermittent episodes (due to
splenomegaly, infarction of the spleen, and autosplenectomy); patients often have a
functional asplenia

Splenectomy: recurrent acute sequestration crises, hypersplenism, massive splenomegaly,

and splenic abscess;
Ø occurrence of even one major acute sequestration crisis is generally already
considered sufficient grounds for splenectomy
ü rapid painful enlargement of the spleen
ü circulatory collapse
Hemoglobinopathies
Sickle Cell Disease
Management:
ü Adequate hydration ü Hydroxyurea- oral chemotherapeutic agent that
ü Avoidance of hypothermia upregulates fetal hemoglobin, interfering with the
polymerization of HbS and thus reducing the
ü Transfusion
sickling process
Ø Anemia
Ø Moderately severe episodes of acute
Splenectomy does NOT affect the
chest syndrome (new infiltrate on
sickling process, and is therefore just a
CXR, fever, cough, sputum production,
PALLIATIVE procedure
or hypoxia)
 Hemoglobinopathy
Thalassemia
Group of inherited (Mendelian recessive) disorders of hemoglobin synthesis and
classified according to the hemoglobin chain (ɑ, ɓ, or ƴ) affected.

Pathophysiology
The primary defect is absent or reduced production of hemoglobin chains. This leads to:
a) Reduced functioning of hemoglobin tetramers à hypochromic microcytic anemia
b) Unbalanced biosynthesis of individual ɑ and ɓ subunits à insoluble RBCs that
cannot release oxygen normally
 Hemoglobinopathy
Thalassemia
Presentation:
ɑ-thalassemia Thalassemia major (homozygous)
Ø ɑ chains are needed to form both fetal ü Pallor
and adult hemoglobin ü Growth retardation
Ø Symptomatic in utero or at birth ü Jaundice
ü Hepatomegaly
Ɓ-thalassemia ü Splenomegaly
Ø ɓ chains involved only in adult hemoglobin ü Others:
Ø Symptomatic at 4-6 months • Intractable leg ulcers
• Head enlargement
• Frequent infections
Thalassemia minor (heterozygous)
• Need for periodic blood transfusions
ü asymptomatic
 Hemoglobinopathy
Thalassemia
Laboratory findings:
ü Hypochromic microcytic anemia
ü Distorted RBCs and nucleated RBCs
(target cells) on PBS
ü Elevated reticulocyte count
ü Elevated WBC
ü Elevated unconjugated bilirubin
 Hemoglobinopathy
Thalassemia
Management
ü Blood transfusion to maintain hgb >9 mg/dL
ü Intensive parenteral chelation therapy with
deferoxamine
Splenectomy: for patients with excessive
transfusion requirements (>200mL/kg/yr),
discomfort due to splenomegaly, or painful
splenic infarction
CAUTION!
q Thalassemia patients are increased risk for
pulmonary hypertension post-splenectomy
q Increase in infectious complications d/t
coexisting immune deficiency secondary to
iron overload
q Children: delay until after 4 yo d/t OPSI,
consider partial splenectomy
Platelet Disorders
Idiopathic thrombocytopenic purpura
Autoimmune disorder characterized by a low platelet
count and mucocutaneous and petechial bleeding.

Pathophysiology
1 Antiplatelet immunoglobulin G autoantibodies are
produced in the spleen
2 Platelet autoantibodies interact with Fc receptors
expressed on tissue macrophage in spleen and liver
3 Premature removal of platelets à low platelet count
 Platelet Disorders
Idiopathic thrombocytopenic purpura
Presentation
ü Petechia or ecchymoses Children
Ø Present at young age (5 yo)
ü Bleeding from mucosal surface Ø Sudden onset purpura/petechia days
o Gingival bleeding after infectious illness
o Epistaxis Ø Splenomegaly uncommon
o Menorrhagia
o Hematuria Adult
o Melena Ø Chronic, insidious onset
Ø Splenomegaly uncommon
Plt >50 – incidental findings
Plt 30-50 – easy bruising
Plt 10-30 – spontaneous petechiae
Plt <10 – internal bleeding
Platelet Disorders
Idiopathic thrombocytopenic purpura
Diagnosis
ü Based on exclusion of other differentials in the
presence of low platelet and mucocutaneous bleeding
Ø SLE, APAS, HIV, Hepatitis C, etc.
Ø drugs (antimicrobials, anti-inflammatories,
anti-hypertensives, anti-depressants)
ü Low platelet count
ü Large, immature platelets (megakaryocytes) on PBS
 Platelet Disorders
Idiopathic thrombocytopenic purpura
Management
ü First line: Oral prednisolone 1.0-1.5 mg/kg/d for 3 weeks
ü IVIG 1.0g/kg for 2-3 d
Ø Given for internal bleeding when plt remains <5, extensive purpura, or pre-operatively
Ø MOA: impair clearance of igG-coated platelets by competing for binding to tissue macrophage receptors
ü Rituximab
ü Thrombopoietin receptor agonists

Splenectomy: failure of medical therapy, prolonged steroid use (need >10-20mg/d for 3-6 mos to maintain plt >30)

Ø Effective for refractory ITP

Ø Provides permanent response without subsequent need for steroids in 75-80% of patients
Ø Laparoscopy is approach of choice for elective cases
Ø Children: indication is to avoid intracranial hemorrhage
 Platelet Disorders
Thrombotic thrombocytopenic purpura
Serious disorder characterized by thrombocytopenia,
microangiopathic hemolytic anemia, and neurologic
complications.

Pathophysiology
Abnormal platelet clumping in arterioles à reduce lumen
à microvascular thrombotic episodes + shearing stress
to RBCs à deformed RBCs à hemolysis ß sequestration
and destruction in spleen
 Platelet Disorders
Thrombotic thrombocytopenic purpura
Presentation Diagnosis
ü Petechiae in the lower extremities – most common ü Thrombocytopenia
ü Fever ü Schistocytes, nucleated RBCs, and basophilic
ü Flu-like symptoms (malaise, fatigue) stippling on PBS
ü Neurologic symptoms (headaches, altered mental ü Negative Coomb’s test
status, seizures, coma) ü Vs. Evan’s syndrome (ITP + hemolytic anemia)
ü Renal failure ü Vs. SLE
ü Cardiac symptoms (heart failure, arrythmias)
Petechiae and thrombocytopenia is sufficient to
diagnose TTP and consider treatment.
 Platelet Disorders
Thrombotic thrombocytopenic purpura
Management
First line: Plasma exchange
ü Daily removal of a single volume of the patient’s plasma
ü Replacement with fresh-frozen plasma until symptoms are corrected
ü Therapy then tapered over 1-2 wk

Splenectomy: key role in patients in relapse or require multiple plasma exchange

Malignancy
WBC Disorders
Splenectomy for WBC disorders can be effective
therapy for symptomatic splenomegaly and
hypersplenism, improving some clinical parameters,
but generally NOT altering the course of the disease.

Therefore, only PALLIATIVE.

Malignancy
WBC Disorders
HAIRY CELL LEUKEMIA
Presentation: splenomegaly, pancytopenia, marked
increase of abnormal lymphocytes in bone marrow
Ø Lymphocytes show hair-like cytoplasmic
projections on PBS
Splenectomy: does NOT correct dse; but returns cell
counts to normal and alleviate splenomegaly
 Malignancy
WBC Disorders
HODGKIN’S DISEASE
Disorder of the lymphoid system characterized by presence of Reed-Sternberg cells.
Presentation:
ü Lymphadenopathy above the diaphragm
Ø May be bulky in mediastinum leading to SOB, cough, or obstructive pneumonia

Ø Spleen is often an occult site of spread

Splenectomy: historically used for staging, now use CT and 18F-FDG PET scan
Current indications for surgical staging:
Clinical suspicion of lymphoma without evidence of peripheral disease
Restaging for suspicion of failure after chemotherapy
Malignancy
WBC Disorders
NON-HODGKIN’S LYMPHOMA
A proliferation of any one of NK cells, T cells, or B cells. All lymphoid ca that is not HD.
Presentation:
ü Indolent – mild or no symptoms, swollen lymph node
ü Aggressive – pain, swelling d/t vessel obstruction, fever, night sweats
ü Sometimes splenomegaly
Diagnosis and staging
ü Hx, PE, CXR, A/P CT scan, biopsy of involved lymph nodes, bone marrow biopsy

Splenectomy: if diagnosis cannot be established, relief of splenomegaly symptoms,

improvement of cytopenias
Malignancy
WBC Disorders
CHRONIC LYMPHOCYTIC LEUKEMIA
Progressive accumulation of old and non-functional lymphocytes
Presentation
ü Weakness, fatigue, fever, night sweats, frequent infections
ü Lymphadenopathy – most common
ü splenomegaly

Splenectomy: improvement of cytopenias, symptomatic relief of splenomegaly, facilitate

chemotherapy in patients whose counts were prohibitively low
Malignancy
Bone Marrow Disorders
Splenectomy is done due to symptomatic splenomegaly.
Symptoms are early satiety, poor gastric emptying, heaviness
or pain LUQ, diarrhea, and concurrent hypersplenism. It does
not treat underlying dse, therefore is only PALLIATIVE.

Splenomegaly sometimes treated non-surgically by chemo (busulfan,

hydroxyurea, interferon-a) to reduce size but discontinuation may result in
rapid regrowth.
Malignancy
Bone Marrow Disorders
CHRONIC MYELOID LEUKEMIA
Disorder of pluripotent stem cells à increase in progenitors in PBS.
Due to transposition between bcr gene on Chr 9 and abl gene on Chr 22
Presentation
ü Often asymptomatic
ü Fatigue, anorexia, sweating
ü Splenomegaly (LUQ pain and early satiety)

Management: Imatinib or allogenic SC transplantation

Splenectomy: ease pain and early satiety; does not prevent blast crisis
Malignancy
Bone Marrow Disorders
ACUTE MYELOID LEUKEMIA
Rapid proliferation of hematopoetic SCs à inhibit growth and maturation of normal cells
Presentation
ü Viral like illness (fever, malaise)
ü Bone pain d/t expansion of medullary space – common

Management: Induction therapy with daunorubicin, cytarabine, and SC transplantation

Splenectomy: symptomatic relief of splenomegaly

CAUTION! Risk of OPSI in AML pxs immunocompromised d/t neutropenia and chemotherapy
Malignancy
Bone Marrow Disorders
CHRONIC MYELOMONOCYTIC LEUKEMIA
CMML differs from CML in that it is associated with monocytosis in PBS (>1 x 103
monocytes/mm3 and in the bone marrow.

Presentation
ü Splenomegaly

Splenectomy: symptomatic relief of splenomegaly

Malignancy
Bone Marrow Disorders
ESSENTIAL THROMBOCYTHEMIA
Abnormal growth of megakaryocyte à increased platelets. Diagnosis of exclusion.
Presentation
ü Vasomotor symptoms, thrombohemorrhagic events, recurrent fetal loss
ü Malignant transformation
ü Splenomegaly

Management: hydroxyurea to reduce thrombotic events, does not alter dse

Splenectomy: reserved for later stages, when myeloid metaplasia develops

 Malignancy
Bone Marrow Disorders
POLYCYTHEMIA VERA
Increase in RBC mass, accompanied by leukocytosis,
thrombocytosis, splenomegaly.
Presentation
ü Ruddy cyanosis, conjunctival plethora, HPN
ü hepatosplenomegaly

Management: phlebotomy, aspirin, chemotherapy

Splenectomy: reserved for later stages, when myeloid

metaplasia develops
 Malignancy
Bone Marrow Disorders
MYELOFIBROSIS (AGNOGENIC MYELOID METAPLASIA)
Generic condition of fibrosis of the bone marrow.
Presentation
ü Splenomegaly, blood progenitors in bloodstream, marrow
fibrosis, EM hematopoiesis
ü Nucleated RBCs, immature myeloid elements in blood
ü Teardrop poikolocytosis in PBS

Management:
ü allogenic BM transplant – only cure
ü Supportive therapy for anemia – steroids, danazol, EPO,
blood transfusion
Malignancy
Bone Marrow Disorders
Preoperative:
ü Acceptable cardiac, pulmonary, hepatic, and renal reserve
ü Coagulation system – factors V. VIII, fibrin split products, platelet, bleeding time

Splenectomy: For splenomegaly, but sometimes chemo (discontinuation causes rapid

regrowth)
Ø Provides durable, effective palliation for nearly all AMM patients
Ø Alleviate mechanical symptoms if splenomegaly
Ø Manage anemia, thrombocytopenia, or portal hypertension

Complications
Ø Thrombosis, hemorrhage, and infection
Others
Infection and abscess
Primary infections of the spleen are not common but are dangerous because of the
potential risk of spontaneous splenic rupture.
ü Infectious mononucleosis due to Epstein-Barr virus
ü Cytomegalovirus infection
ü Others (malaria, Listeria, fungal infections, dengue, Q fever, etc.)

Pathophysiology
Infiltration of the splenic parenchyma with inflammatory cells à distortion of architecture and fibrous
support à thinning of the splenic capsule à spontaneous rupture after minor trauma or even a Valsalva
maneuver
Others
Infection and abscess
Abscesses of the spleen are also uncommon. Pathophysiology
Occurs more frequently in the tropics, 1. Hematogenous infection
associated with thrombosed splenic vessels 2. Contiguous infection
and infarction in patients with sickle cell 3. Hemoglobinopathy
anemia. 4. Immunosuppression
5. Trauma
Others
Infection and abscess
Presentation Management
ü Fever • Broad-spectrum antibiotics
ü LUQ pain
ü Leukocytosis - Adjust accordingly based on culture
ü Splenomegaly - Continue for 14 d
• Splenectomy
Diagnosis
ü UTZ or CT scan – confirmatory - Operation of choice
ü Culture of abscess - Percutaneous and open drainage are options
- streptococci, E. coli mostly
- others MTB, salmonella
 Others
Splenic Cysts
Splenic cysts can be either parasitic or non parasitic. Diagnosis:
Parasitic infection is the most common cause of splenic ü UTZ can establish presence of cystic lesion
cyst. Majority is due to Echinococcus sp. ü Serologic testing for echinococcal antibodies
- can confirm or exclude cystic lesion as parasitic
Presentation: - Important for preoperative planning
ü Mass lesion in LUQ
ü Lesion that impinges on stomach Splenectomy: for symptomatic parasitic cysts
CAUTION! Avoid spillage of cyst contents to peritoneal
cavity; may result to anaphylactic shock
 Others
Tumors and metastasis
Most common primary tumor of spleen is sarcoma.
Approximately 0.6% rate of tumor metastasize to the spleen; often are carcinomas.
Lung cancer is the most common tumor that spreads to the spleen.
Spleen is an infrequent site of metastatic deposits, and usually appears in cases of widely
disseminated disease.

Management: if isolated splenic metastasis is confirmed, do laparoscopic splenectomy with intact

spleen retrieval
 Others
Storage diseases
GAUCHER’S DISEASE
An inherited lipid storage disorder characterized by Presentation:

deposition of glucocerebroside in cells of the ü Splenomegaly – early satiety, abdominal discomfort

macrophage-monocyte system ü Hypersplenism – thrombocytopenia, normocytic

anemia, mild leukopenia

Pathophysiology: ü Bone pain, pathologic fractures, jaundice

Deficiency in activity of a lysosomal hydrolase à

Abnormal glycolipid storage à Organomegaly Splenectomy: to alleviate hematologic abnormalities,
does not alter disease
• Partial splenectomy for children to avoid OPSI
Others
Infiltrative disorders
AMYLOIDOSS
Abnormal extracellular protein deposition.
Primary amyloidosis, associated with plasma cell dyscrasia, have splenic
involvement in 5% of cases.
Secondary amyloidosis, associated with chronic inflammatory conditions,
present with splenomegaly.

Splenectomy done to relieve splenomegaly symptoms.

Others
Infiltrative disorders
SARCOIDOSIS
Disease characterized by noncaseating granuloma in affected tissues. May involve
any organ system, but commonly involve the lung, then the spleen.

Presentation: fatigue and malaise, splenomegaly

Splenectomy: for splenomegaly or hypersplenism symptoms
- Effectively relieves symptoms
- Corrects hematologic abnormalities
Others
Splenic artery aneurysm
Splenic artery aneurysm is rare but is the most common visceral artery aneurysm.
Usually arises in the middle to distal portion of the splenic artery.
Indications for treatment: symptomatic, pregnant, intention to get pregnant,
pseudoaneurysms associated with inflammatory process
Management:
ü Aneurysm resection or ligation alone – for amenable lesions in mid-splenic artery
ü Splenectomy – distal lesions in close proximity to splenic hilum
ü Splenic artery embolization – option but painful abscess may follow
Others
Portal Hypertension
Portal HPN has many causes but commonly due to cirrhosis.

Presentation: Splenomegaly and splenic congestion à hypersplenism

Splenectomy:
ü Done to reduce bleeding from esophageal varices exacerbated by thrombocytopenia
Ø NOT for hypersplenism per se
Ø Splenorenal shunt – performed to decompress portal system
ü Curable in portal HPN secondary to splenic vein thrombosis
 Others
Felty’s Syndrome
Triad of RH arthritis, splenomegaly, and
neutropenia.
Pathophysiology:
Immune complexes coat the surface of WBC à
sequestration and clearance in spleen à
neutropenia (<2000/mm3) à increased risk for
recurrent infections à splenectomy
Presentation: Spleen is 4x heavier than normal
Management: Corticosteroids, hematopoietic
growth factors, methotrexate
Splenectomy: for symptomatic neutropenia,
transfusion-dependent anemia, profound
thrombocytopenia
Others
Wandering Spleen
The spleen “floats” inside the abdominal cavity due to an anomaly of embryogenesis.
The wandering spleen is not normally attached to adjacent viscera in the splenic fossa
à splenic torsion and infarction.

Management: Splenectomy or splenopexy

Preoperative
considerations
Vaccination
And Patient Education
Vaccinations against encapsulated pathogens
Ø Infection is the most common complication, i.e. OPSI/OPSS
Ø Risk is greatest in the first 2 years after splenectomy
Ø Asplenic patients remain at lifelong risk
- Spleen is the site for special adaptation of macrophages that target
encapsulated organisms
- S. pneumoniae, H. influenzae type b, N. meningitidis, capnocytophaga
canimorsis (transmitted by dog bites)
Vaccination
And Patient Education
Ø In elective splenectomy, patients should be vaccinated 2 weeks prior to surgery
Ø In emergency splenectomy, vaccinations administered postoperatively
- Delay administration for 2 wks to avoid the transient immunosuppression
- Antibody levels decline steadily within 5-10 yrs, revaccination is
recommended
Ø Patient education of OPSI/OPSS is very important because patients may rapidly
progress from a febrile illness to circulatory collapse and death within hours
- Teach them to watch out for fever, flu-like symptoms post-splenectomy
DVT prophylaxis
Ø Risk of deep vein thrombosis (DVT) and portal vein thrombosis (PVT) after
splenectomy especially in cases involving splenomegaly and myeloproliferative dse.
Ø DVT prophylaxis
Ø Know risk factors (obesity, history of DVT, hypercoagulable state, elderly)
Ø Compression devices
Ø Subcutaneous administration of heparin (5000 U)
Ø Post-splenectomy PVT
Ø Presentation: anorexia, abdominal pain, leukocytosis, thrombocytosis
Ø Diagnosis: high index of suspicion, contrast enhanced CT
Ø Treatment: anticoagulation immediately
Splenectomy
techniques
Patient Preparation
• Polyvalent pneumococcal, meningococcal, Haemophilus vaccines
• Blood clotting parameters
• CBC, plt, blood type, antibody screening tests
Ø Anemic – blood transfusion prior to surgery, maintain hgb 10 g/dL
Ø At least 2-4 units of cross-matched blood available
Ø Thrombocytopenia – correct with platelet transfusion
• Pxs on corticosteroid therapy preop – receive parenteral corticosteroid periop
• DVT prophylaxis
• Endotracheal intubation
• Nasogastric tube
Open Splenectomy

LEFT SUBSCOSTAL INCISION

• Parallel to left costal margin, 2 fingerbreadths below
• For elective cases
MIDLINE INCISION
• For ruptured or enlarged spleen
Open Splenectomy
2. Mobilize spleen by dividing ligamentous attachments
(splenocolic, gastrosplenic, gastrohepatic) to gain
access to the lesser sac.
3. Ligate the splenic artery along the superior border of
the pancreas
4. Further mobilization of spleen by incising lateral
peritoneal attachments, splenophrenic ligament
5. Individual ligation and division of the short gastric
vessels
6. Splenic hilar dissection. Dissect and individually
ligate the splenic artery and vein in order before
dividing them. Great care must be taken to avoid
injuring the pancreas (within 1cm of the splenic
hilum)
7. Excision of spleen. Hemostasis secured by
irrigating, suctioning, and through inspection of the
bed of dissection
8. Thorough search for accessory spleens.
Laparoscopic Splenectomy
• Gold standard for elective cases in patients
with normal-sized spleens

RIGHT LATERAL DECUBITUS

MIDWAY “DOUBLE ACCESS”
- 45º Right lateral decubitus
- Allows concomitant lap. chole.
https://www.youtube.com/watch?v=Gy1dH0QDSck&t=439s

Jump to 3:40– 6:00 for procedure!

Hand-Assisted Splenectomy
Single-Incision LS
Robotic Splenectomy
Partial Splenectomy
Intraoperative Splenic Injury
Causes significant short-term morbidity
ü Increased blood loss
ü Need for transfusion
ü Prolonged hospital stay
Pathophysiology
• Improper traction on the spleen against its peritoneal
attachments (most common mechanism)
• Capsular tears (most common type of injury), parenchymal
lacerations, subscapular hematoma
• Lower pole is more commonly injured due to its location
and greater concentration of ligaments
Intraoperative Splenic Injury
Management for hemorrhage
• Direct compression of spleen
• Packing of LUQ
• Compression of vessels at splenic hilum
• Pressure on the splenic artery at the superior pancreatic margin

Management for splenic injury

• Splenic salvage
• Splenectomy

Management for capsular tears

• Splenorrhapy techniques: topical hemostatics, suture plication of
disrupted parenchyma with or without omental buttress, and use of
bioabsorbable mesh sheets
Splenectomy
Outcomes
Changes in blood
• Appearance of Howell-Jolly bodies and
siderocytes
• Increased platelet (within 2 days usually)
• Increased WBC (within 1 day, persists for
several months)
• Hemorrhage intra- and postoperatively,
presenting as subphrenic hematoma
• Transfusions
• Subphrenic wound infections/abscess
• Pancreatitis, pseudocyst, pancreatic fistula

Complications Hematologic outcomes

• Left lower lobe atelectasis (most common) • For thrombocytopenia- rise in plt within days
• Pleural effusion • For chronic hemolytic anemia- rise in hgb to
• Pneumonia >10g/dL without the need for transfusions
Overwhelming postsplenectomy
infection
OPSI demand lifelong vigilance and intimate knowledge of the appropriate precautions and
preventive measures. Asplenic patients are high risk for infections for the rest of their lives.

Sepsis in asplenic patients is a medical emergency! Any clinical suggestion of infection, like
isolated fevers, must be view ed with a high index of suspicion and treated empirically as
investigation proceeds.
OPSI/OPSS
Pathogenesis
Presentation:
• Loss of splenic macrophage
Prodrome
• Diminished tuftsin production
• Fever, malaise, myalgia, headache
• Loss of spleens screening function
• Vomiting, diarrhea, abdominal pain
Normally, these three work to eliminate
Fulminant bacteremic shock
encapsulated bacteria. In asplenia, elimination
• Hypotension, anuria, DIC
of these pathogens falls solely to the liver,
which is less effective.
A high index of suspicion, prompt action, and
aggressive education of the patient and folks
are needed. Overall lifetime risk is low.
OPSI/OPSS
Antibiotics in asplenic patients considered for: Ø Lifelong daily antibiotic prophylaxis
• Established or presumed infections recommended only for those whose
• Prophylaxis in anticipation of invasive antibody titers fail to respond to
procedures vaccination
• General prophylaxis
Asplenic patients advised to carry at all times a
Chemoprophylaxis in children reserve supply of antibiotics to be self-
Ø Daily doses of antibiotics until 5 y or at administered at the earliest signs of infection
least 5 y after splenectomy
Ø Some advocate continuation until young
adulthood
OPSI/OPSS
Risk factors: Risk management strategies:
• Reason for splenectomy – most important ü Wearing a medical bracelet
• Hematologic disease higher risk ü Carrying a laminated medical alert card
• Age <5 y or >50 y ü Medical letter with specific empiric
therapy instructions (drug names,
dosages)
ü Keeping a 5-day supply of standby
antibiotics, especially if travelling
thank
you!