Spleen Flashcards

1
Q

What is the Fx of the spleen

A

Red pulp:
- MOs capture and break down defective RBCs/platelets via phagocytosis
- Fetalerythropoiesis
- Sequestration ofplatelets: up to⅓ of body’splateletsare stored in spleen

While Pulp
Lymphatic tissue of spleen → mounts immune response toblood-borneantigensand infections
- After maturation in primary lymphatic organs, LOsmigrate into spleen and lie dormant until activation → after differentiation to effector cells, activated B and T LOs reenter bloodstream via red pulp to mount immune responsein inflamed tissue
- MOs and otherAPCsin PALS and marginal zone trapAgfrom circulation and present it to LOs of spleen
- SplenicMOs capture opsonised encapsulated bacteria→ opsonisation body’s primary defence againstencapsulated bacteria
- B LOs in follicles differentiate into plasma cells which produce antibodies (e.g., IgM) and for memory cells
- Spleen = major site ofIgM productionin body

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2
Q

How does splenectomy increase pt susceptibility to certain organisms and which ones

A

Encapsulated organisms e.g., haemophilus influenza, neisseria meningiditis, streptococcal pneumonia

Reduced IgM production –> reduced complement activation and C3b opsonisation of encapsulated organisms

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3
Q

What are some common causes of splenomegaly

A

Infection
1. Acute e.g., septic shock, infectious endocarditis, EBV, typhoid, CMV
2. Chronic e.g., TB, brucellosis, HIV
3. Parasitic e.g., malaria, schistosomiasis
Inflammation
1. Rheumatoid arthritis (Felty syndrome)
2. SLE
3. Sarcoidosis
4. Serum sickness
Haematological
1. Haemolytic anaemia
2. Haemoglobinopathies
3. Myeloproliferative disorders
4. Leukaemia
5. Lymphomas
Congestion
1. Splenic vein thrombosis/obstruction
2. Portal vein obstruction e.g., hepatic cirrhosis
3. Constrictive pericarditis
4. Congestive heart failure
5. Hepatic vein obstruction
Infiltrative
1. Amyloidosis
2. Sarcoidosis
3. Gaucher’s disease
Neoplasia
1. Primary and secondary neoplasia
NB. Massive splenomegaly  chronic myeloid leukaemia, myelofibrosis, chronic malaria and rarely Gaucher’s disease

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4
Q

What are the results of hypersplenism

A

Overactive spleen → cells removed from blood faster thannormal →↓ ofa single or combination of cell lines, including possiblecytopenia (pancytopenia, leukopenia, anaemia, thrombocytopaenia) → reactive bone marrow hyperpalsia (unless defective BM is cause of splenomegaly)

→ increased risk of bleeding, infection, pallor, fatigue, signs of haemolysis
→ splenomegaly

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5
Q

What is a splenectomy

A

A surgical procedure (laparoscopic or open) consisting of partial or total removal of spleen.

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6
Q

What are the indications for splenectomy

A

Indications include spleen rupture, significant splenomegaly or hypersplenism, and certain hematologic disorders and malignancies.

  • Trauma resulting from an accident or during a surgical procedure e.g., during mobilisation of oesophagus, stomach, distal pancreas or splenic flexure of colon
  • Removal en bloc with stomach as part of a radical gastrectomy or with pancreas as part of a distal or total pancreatectomy
  • To reduce anaemia or thrombocytopenia in spherocytosis, ITP, or hypersplenism
  • In association with shunt or variceal surgery for portal HTN
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7
Q

What are the complications of splenectomy

A

Immediate

  • Haemorrhage from slipped ligature
  • Haematemesis from gastric mucosal damage and gastric dilatation (uncommon)
  • Left basal atelectasis (common) and possible pleural effusion
  • Adjacent stomach and pancreas at risk during procedure
    • Damage to greater curvature during ligation of short gastric vessels → fistula formation
    • Damage to tail of pancreas → pancreatitis, localised abscess or pancreatic fistula
  • Postoperative thrombocytosis may arise → if platelet count exceeds 1 x 10^6/mL, prophylactic aspirin recommended to prevent axillary or other venous thrombosis
  • Post-splenectomy septicaemia may result from streptococcus pneumoniae, neisseria meningitides, haemophilus influenzae and escherichia coli
    • Higher risk: young pts, pts Tx with chemoradiotherapy, pts who have undergone splenectomy for thalassaemia, sickle cell disease and autoimmune anaemia or thrombocytopenia

Opportunistic Post-Splenectomy Infection (OPSI)

Subphrenic abscess

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8
Q

What is post-splenectomy OPSI and what is the risk

A

Opportunistic Post-Splenectomy Infection (OPSI) = a bacterial infection that rapidly progresses to fulminant, overwhelmingsepsisin the setting of anatomic orfunctional asplenia

  • Risk of overwhelming asplenic sepsis greatest within first 2-3yrs post-splenectomy but increased risk of fulminant andlife-threateninginfections and sepsis for up to30 yearsor longer aftersplenectomy

Prognosis → mortality 70% w/out Tx but reduced to ~10-40% with early Tx

Most infections could be avoided through appropriate and timely immunisation, antibiotic prophylaxis, education and prompt treatment of infection

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9
Q

How does OPSI present

A

Clinical:initially flu-like Sx → rapid deterioration within hourswithfever, severemalaise, signs of sepsis, and meningitis

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10
Q

What is the cause and pathophysiology of OPSI

A

Aetiology: Encapsulated bacteria e.g., strep pneumoniae, neisseria meningiditis, haemophilus influenzae
- Also increased risk of severe malaria if travelling to countries where malaria is present, and overwhelming post-splenectomy sepsis due to capnocytophaga canimorsus from dog, cat or other animal bites.

Pathophysiology: Splenectomy→↓IgM production →↓ complementactivation →↓ C3bopsonisation→↓ clearanceofopsonised bacteria →↑ susceptibilityto infection by encapsulated bacteria
- Normally,encapsulated pathogensareopsonisedwithantibodiesand thenphagocytosed by specialised MOs in spleen
- Individuals with asplenia lack these specialisedMOs so pathogens are able to spread → sepsis

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11
Q

What is a subphrenic abscess

A

Subphrenic abscess: accumulation of pus located directly under diaphragm (~2% pts post-abdominal surgery) due to polymicrobial infection (e.g., due to enterococcus spp.,e/ coli and clostridiumspp.) followingintraperitonealperforation
- Develops ~3-6wks post-surgery

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12
Q

How does a subphrenic abscess present and what are potential complications

A

Clinical: fever, pain over ribs 8-11 on affected side, cough, increased RR, pleural effusion
Complications: empyema, sepsis, high mortality

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13
Q

How is a subphrenic abscess Dx and Tx

A

Diagnostics: leukocytosis, abscess visualised on USS, air below diaphragm on CXR

Tx: drainage and antibiotics

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14
Q

What are the haematological changes that occur in an asplenic patient

A

Peripheral blood smear: Howell-Jolly bodies (basophilicspots within RBCs; if not → accessory spleen), target cells

Labs: lymphocytosis due to loss of sequestration of LOs in spleen, neutrophilia, decreased production of Ig (IgG, IgM) → decreased complement activation and C3b opsonisation, reactive thrombocytosis usually for the first weeks to months aftersplenectomy (spleenstores~ ⅓of circulatingplatelets filters oldplatelets from bloodstream)
- Transient elevation of platelet and white cell count after splenectomy may mimic sepsis

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15
Q

Describe the aetiology of a traumatically ruptured spleen

A

MC = Direct blunt abdominal trauma (MC MVA; also contact sports, physical altercations, falls from great heights)

  • Consider splenic rupture in any case of blunt abdominal trauma, esp. when LUQ injury

Iatrogenic injury to the spleen remains a frequent complication of any surgical procedure, esp. those in LUQ when adhesions are present

NB. Splenic rupture can also be atraumatic

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16
Q

What are the mechanisms of splenic rupture

A

Acute rupture: injury of splenic capsule and possibly the splenicparenchymaltissue → acuteintra-abdominalbleeding

Delayed rupture: injury of splenicparenchymaltissue in an initiallyintact splenic capsule→ central orsubcapsular haematoma→asymptomatic interval(days to weeks) ashaematomadistends inside capsule → subsequentcapsular rupturewithintra-abdominalbleeding

17
Q

What is the presentation of a ruptured spleen

A

Diffuse abdominal pain esp. in LUQ

  • Possible abdominal guarding
  • Kehr’s sign = referred pain in left shoulder d trauma or damage within peritoneal cavity when free fluid irritates diaphragm and nerve roots
    • Pain transferred to left shoulder and may be aggravated when pt lies down with feet elevated

Ballance’s sign = dullness on LUQ percussion

Haemorrhagic and hypovolaemic shock (often delayed): tachycardia, hypotension etc.

In delayed splenic rupture, symptoms may not present until days to weeks after trauma

Important to identify signs of other majorlife-threateninginjury in polytrauma pt

Pancreaticinjury(tail)

18
Q

What Ix are performed in splenic rupture

A

Labs: low Hb, leukocytosis, thrombocytosis, crossmatch for blood transfusion if needed

  • Hb and Hct often normal in early stages of bleeding due to ~ equal amounts of cell and plasma loss. Dilution (a decrease inHb and Hct) more noticeable in later stages of rupture

Haemodynamically unstable

USS → screen for central or subcapsular haematoma, free intra-abdominal fluid (Koller pouch = splenorenal recess, Morrison’s pouch = hepatorenal recess, Pouch of Douglas = rectouterine/rectovesical pouch)

If free intraabdominal fluid →diagnostic laparoscopy/laparotomy

RepeatedUSS is crucial esp. inconservative managementof splenic rupture

Hemodynamically stable

CT abdomen with contrast (alternatives = MRI or angiography if impaired renal function or contrast allergy; sometimes CXR or AXR)

19
Q

Mx for ruptured spleen

A

Tx depends on severity and aetiology of rupture, and hemodynamic stability of pt

  • Most (60-90%) isolated blunt traumatic splenic injuries, esp. in children, can be managed non-operatively
    • hospital observation with frequent USS Ex
    • Large/small vessel injuries with bleeding in stable trauma pt or pt who fails conservative Mx → angiographic embolisation of injured BVs
  • Exploratory laparotomy indicated if continuing haemodynamic instability or pt has required 4 units of blood in 48hrs
  • Surgery
    • Spleen can be packed, repaired or placed in mesh bag
    • Initial choice in surgical management → repair capsular lacerations (splenorrhaphy)/if only peripheral rupture: trial of splenic salvage → suturing, coagulation, or ligation of injured BV
    • Partial splenic resection
    • If extensive injury, hilar rupture or uncontrolled hemorrhage → splenectomy
      • Splenectomy may be a safer option esp. in unstable > 55 yo patient with multiple potential sites of bleeding due to risk of rebleed
  • Post-splenectomy vaccinations for encapsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae,andNeisseria meningitides)
20
Q

Infection Prevention in Asplenic Pt

A

Antibiotic prophylaxis (daily amoxicillin or 2x daily phenoxymethylpenicillin) usually indicated for:

  • children 5 years or younger with asplenia or hyposplenism
  • patients who have had a splenectomy → prophylaxis is started as soon as oral therapy is tolerated postoperatively and continued for at least 3 years

Consider lifelong prophylaxis for patients who:

  • have survived overwhelming postsplenectomy infection esp. invasive pneumococcal infection
  • are significantly immunocompromised (e.g., coexisting hypogammaglobulinaemia, advanced liver disease, solid organ transplant recipients, primary immunodeficiency disorder, HIV infection, haematological malignancy)
  • have had a splenectomy for haematological malignancy esp. those with GVHD or receiving immunosuppressive therapy

Vaccination (give prior if elective or post-op in trauma victim → antibody levels > 50% of those achieved if vaccination is given in presence of an intact spleen and protection not guaranteed)

  • Pneumococcus, meningococcus, Hib
  • Yearly influenza vaccination

Unexplained fever → seek urgent medical attention and emergency supply of antibiotics (immediate amoxicillin)

Lifestyle: Specific advice regarding travel and animal handling

21
Q

Investigations for splenomegaly

A
  • FBC + blood film/smear, UEC, CRP/ESR, LFT
  • USS (confirm splenomegaly, size and analyse portal pessures)
  • CT
  • Infection suspected, consider blood cultures, monospot, serologies (EBV, CMV, HIV), antibodies for SLE/RA etc.
  • Bone marrow biopsy, LN biopsy, laparotomies etc. may be required