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SPLENIC
INFARCT,
CVC SPLEEN
CVC LUNG
PRACTICAL
CLASS
Dr Meenu E V
MBBS MD DNB
Spleen
A lymphoreticular organ
Weight : 150gm
Blood supply : splenic artery  central arterioles ->
vascular sinuses -> splenic venules -> splenic vein
Gross : capsulated, homogeneous, soft, dark
red mass [ red pulp] with grey white nodules
[ white pulp / malpighian bodies]
Microscoscopy :
capsule , extend to form trabeculae
Red pulp consist of network of thin
walled venous sinuses which contain
rbc, wbc, & macrophages - blood
spaces are arranged in cords called
cords of Billroth
White pulp – lymphoid follicle with
eccentrically placed arteriole
Function
– Maintain immunity , where B & T cells multiply
– Sequesterate & remove, normal & abnormal blood cells
– Regulate portal blood flow
– A site of extramedullary hematopoiesis
Disorders of spleen
– Splenic infarct
– Splenomegaly
– Hypersplenism
– Splenic rupture
– Tumours
– Cvc
Case 1
60yr / female
 c/o abdominal pain x 4 days,
breathlessness & Palpitation x 2 weeks
 H/o hypertension , smoking , dyslipidemia
 O/E - HR – 180/mt, BP – 140/90 mm Hg,
 Abdominal exam - epigastric & left upper quadrant tenderness
 ECG : Atrial fibrillation
 Ultrasonography - hypodense lesion in spleen with decreased vascular supply
 CT angiography - investigation of choice
Infarct
Splenic infarct
2 types : segmental / global
arterial / venous
Etiology :
 Splenic artery occlusion [ secondary to cardiac emboli]  white infarcts
 Thrombosis of splenic vein , secondary to pancreatitis
 Wegners granulomatosis / vasculitis
 Sickle cell disease -> autoinfarction
 Leukemia / lymphoma / myelofibrosis
 Blunt trauma – long vascular pedicle
Gross
– Wedge shaped, white grey infarct
involving capsule
– Infarct heals as large depressed scars
– Recent infarct – haemorrhagic
– Old infarct – fibrotic, pale yellow-
grey
Microscopy
– Necrotic areas – homogenous
pink
– Hematoidin crystals +
– Hemosiderin laden
macrophages, Inflammatory cells
around margin of infarct
Complication
– Hemorrhage
– Rupture
– Abscess
– Pseudocyst formation
Treatment : depends on etiology
Conservative treatment / splenectomy
Case 2
80 yr male
 c/o progressive dyspnea x 2 weeks [ worsens with exercise and sleeping /
orthopnea]
H/O MI x 4 yrs back, hypertension +, hyperlipidemia+
O/E – PR – 100/mt, feeble, RR – 30/mt, SpO2 – 80 %
 cyanosis +, mild pedal edema, BP - 150/100 mmHg
Respiratory system - wheeze +, bilateral crepitation,+
CVS - Cardiomegaly +
Chest X ray - cardiomegaly, prominent bronchial marking
Organs affected
by congestion
Lungs – heart failure
cells
Liver - nutmeg liver
Spleen – Gamna
Gandy Bodies
Kidney
HEART
FAILURE
LEFT HF
Pressure into Pumonary
Vein
CVC LUNGS
RIGHT HF
Pressure into Systemic Venous system
CVC LIVER CVC SPLEEN CVC KIDNEY
Hyperaemia Congestion
Localised increase in volume of blood
within organ
Due to increased inflow – arterial /
arteriolar dilatation
Active process
Tissue ll b red - more oxygenated
blood
Tissue will be warm
Localised increase in volume of blood
within organ
Due to diminished outflow – impaired
venous drainage
Passive process
Red- blue in colour – deoxygenated
blood
Cold & clammy
CHRONIC VENOUS CONGESTION OF
LUNG
Long standing accumulation of deoxygenated blood along with damage to the
tissue
ETIOLOGY
Left heart failure – back pressure
Obstruction of veins due to thrombi
Gross
 Lungs are heavy, firm
 C/S – dark, rusty brown – brown
induration
Microscopy
 Alveolar septa widened & thickened - due to
interstitial odema & dilated, congested
capillaries in septal wall & fibrosis
 Rupture of dilated capillaries - intra-alveolar
haemorrhages, hemosiderin laden
macrophages [ heart failure cells] in alveolar
lumen
 Brown induration on gross – due to
pigmentation & fibrosis
Cvc spleen
– Causes :
– Right heart failure
– Portal hypertension in liver cirrhosis
GROSS : enlarged, congested, capsule
tensed, C/S – grey tan, FIRM
Microscopy
– Red pulp enlarged due to marked
sinusoidal dilatation & congestion.
– Old & new haemorrages.
– Splenic macrophages increased
– Within haemorrhage : hemosiderin
pigment + Calcium salts + Fibrosis
organised to form GAMNA GANDY
BODIES / SIDEROFIBROTIC
NODULES.
Cvc liver
THANK YOU

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SPLENIC INFARCT, CVC SPLEEN & LUNGS PATHOLOGY PRACTICAL CLASS FOR MBBS

  • 2. Spleen A lymphoreticular organ Weight : 150gm Blood supply : splenic artery  central arterioles -> vascular sinuses -> splenic venules -> splenic vein
  • 3. Gross : capsulated, homogeneous, soft, dark red mass [ red pulp] with grey white nodules [ white pulp / malpighian bodies]
  • 4. Microscoscopy : capsule , extend to form trabeculae Red pulp consist of network of thin walled venous sinuses which contain rbc, wbc, & macrophages - blood spaces are arranged in cords called cords of Billroth White pulp – lymphoid follicle with eccentrically placed arteriole
  • 5. Function – Maintain immunity , where B & T cells multiply – Sequesterate & remove, normal & abnormal blood cells – Regulate portal blood flow – A site of extramedullary hematopoiesis
  • 6. Disorders of spleen – Splenic infarct – Splenomegaly – Hypersplenism – Splenic rupture – Tumours – Cvc
  • 7. Case 1 60yr / female  c/o abdominal pain x 4 days, breathlessness & Palpitation x 2 weeks  H/o hypertension , smoking , dyslipidemia  O/E - HR – 180/mt, BP – 140/90 mm Hg,  Abdominal exam - epigastric & left upper quadrant tenderness  ECG : Atrial fibrillation  Ultrasonography - hypodense lesion in spleen with decreased vascular supply  CT angiography - investigation of choice
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  • 11. Splenic infarct 2 types : segmental / global arterial / venous Etiology :  Splenic artery occlusion [ secondary to cardiac emboli]  white infarcts  Thrombosis of splenic vein , secondary to pancreatitis  Wegners granulomatosis / vasculitis  Sickle cell disease -> autoinfarction  Leukemia / lymphoma / myelofibrosis  Blunt trauma – long vascular pedicle
  • 12. Gross – Wedge shaped, white grey infarct involving capsule – Infarct heals as large depressed scars – Recent infarct – haemorrhagic – Old infarct – fibrotic, pale yellow- grey
  • 13. Microscopy – Necrotic areas – homogenous pink – Hematoidin crystals + – Hemosiderin laden macrophages, Inflammatory cells around margin of infarct
  • 14. Complication – Hemorrhage – Rupture – Abscess – Pseudocyst formation Treatment : depends on etiology Conservative treatment / splenectomy
  • 15. Case 2 80 yr male  c/o progressive dyspnea x 2 weeks [ worsens with exercise and sleeping / orthopnea] H/O MI x 4 yrs back, hypertension +, hyperlipidemia+ O/E – PR – 100/mt, feeble, RR – 30/mt, SpO2 – 80 %  cyanosis +, mild pedal edema, BP - 150/100 mmHg Respiratory system - wheeze +, bilateral crepitation,+ CVS - Cardiomegaly + Chest X ray - cardiomegaly, prominent bronchial marking
  • 16. Organs affected by congestion Lungs – heart failure cells Liver - nutmeg liver Spleen – Gamna Gandy Bodies Kidney HEART FAILURE LEFT HF Pressure into Pumonary Vein CVC LUNGS RIGHT HF Pressure into Systemic Venous system CVC LIVER CVC SPLEEN CVC KIDNEY
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  • 18. Hyperaemia Congestion Localised increase in volume of blood within organ Due to increased inflow – arterial / arteriolar dilatation Active process Tissue ll b red - more oxygenated blood Tissue will be warm Localised increase in volume of blood within organ Due to diminished outflow – impaired venous drainage Passive process Red- blue in colour – deoxygenated blood Cold & clammy
  • 19. CHRONIC VENOUS CONGESTION OF LUNG Long standing accumulation of deoxygenated blood along with damage to the tissue ETIOLOGY Left heart failure – back pressure Obstruction of veins due to thrombi
  • 20. Gross  Lungs are heavy, firm  C/S – dark, rusty brown – brown induration
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  • 22. Microscopy  Alveolar septa widened & thickened - due to interstitial odema & dilated, congested capillaries in septal wall & fibrosis  Rupture of dilated capillaries - intra-alveolar haemorrhages, hemosiderin laden macrophages [ heart failure cells] in alveolar lumen  Brown induration on gross – due to pigmentation & fibrosis
  • 23. Cvc spleen – Causes : – Right heart failure – Portal hypertension in liver cirrhosis GROSS : enlarged, congested, capsule tensed, C/S – grey tan, FIRM
  • 24. Microscopy – Red pulp enlarged due to marked sinusoidal dilatation & congestion. – Old & new haemorrages. – Splenic macrophages increased – Within haemorrhage : hemosiderin pigment + Calcium salts + Fibrosis organised to form GAMNA GANDY BODIES / SIDEROFIBROTIC NODULES.