Property of Prof Dr. Nawel Matar FRCS, Department of General Surgery, Faculty of Medicine. University of Zagazig

1. ‫بسم‬‫هللا‬‫الرحمن‬‫الرحيم‬

2. PROF. Dr.
NAWEL
THE SPLEEN

3. ANATOMY OF SPLEEN
• Weight: Normal adult spleen weighs 100-150
grams.
• Size: Adult spleen measures 3 X 8 X 14 cm,
• The largest single mass of lymphoid tissue in
body & is completely covered by peritoneum
• Relations:
– Site: Beneath left diaphragm separating it from 9,
10, &11 ribs.
– Posterolaterally; Attached to left kidney by the
lienorenal ligament.
– Antero-medially; attached to the stomach by

4. ANATOMY OF SPLEEN
• Blood supply:
– Arterial: Splenic artery from the celiac trunk & run
a tortuous course over the upper border of
pancreas till it reaches the spleen.
– Venous: See portal circulation.
• Open & closed circulation of spleen:
– Closed circulation i.e. The arterioles branch into
capillaries that are contiguous with the venous
sinuses within the red pulp.
– Open circulation i.e.The capillaries drain freely
into splenic parenchyma & the blood cells flow
through the fenestrations in venous sinuses into

5. Functions of spleen
• Cellular Functions:
– Culling Action i.e. removal of aged RBCs & abnormal cells e.g. spherocytes. Because the spleen is not
the only site of RBCs destruction, the life span of RBCs is not affected after splenectomy.
– Pitting Action i.e. Removal of non-deformable structures from deformable cells e.g.→
• Nuclei (Howell jolly bodies).
• Iron granules (Papen heimer bodies).
• Denaturated hemoglobin (Heinz bodies).
• Nuclear remnant & excess membrane (Reticulocytes)
• Parasites & fungi.
– Hemopoiesis:
• Spleen is the site of hemopoiesis during intra uterine fetal life.
• Spleen is one of extra medullary hemopoietic site.
– Storage of Platelets:
• About ¼ of platelets are present inside the spleen.
• In hypersplenism, 80% of platelets are trapped in spleen → thrombocytopenia.
• Immunological Functions***
– Removal of blood borne bacteria in absence of pre-existing antibody against it.
– Phagocytosis of anti-body coated bacteria & phagocytosis of encapsulated organisms e.g.
Pneumococci. & hemophilus influenza.

6. CONGENITAL ANOMALIES OF
SPLEEN
1. CONGENITAL ABSENCE of spleen: Very rare &
occurs in association with cardiac anomalies.
2. WANDERING SPLEEN: the spleen has a long
splenic mesentery → great mobility (may
reach to any part of abdomen). It may
undergo torsion → severe pain & shock. The
condition is more commonly seen in children
& females between 20-40 years.
3. SPLENCULI
Incidence: 10% - 25%.
Sites:

7. ASPLENIC STATE OR
HYPOSPLENISM
• Causes:
– Splenectomy.
– Splenic atrophy.
• Auto splenectomy e.g. sickle cell anemia.
• Chronic illness e.g. celiac disease, hyperthyroidism, ulcerative colitis.
• Splenic arterial or venous thrombosis e.g. Pancreatitis.
• Complications → over whelming post-splenectomy sepsis 
– Explanation: Spleen is capable of phagocytosis of micro organisms (especially
capsulated organism) in absence of pre-existing antibodies to these organisms.
– Post-splenectomy sepsis has a high mortality rate up to 40%.
– Prophylaxis :
• Vaccination: Polyvalent pneumococcal vaccine. (Vaccination against H influenza & meningococci.)
• Penicillin. , Pediatric follow up: For all splenectomized children below 10 years.
• Partial splenectomy instead of total splenectomy or splenic auto transplantation should be
practiced whenever possible.

8. HYPERSPLENISM
• Definition: hypersplenism is a syndrome
characterized by the followings: 
– Splenic enlargement.
– Deficiency of one or more blood cell lines.
– Normal or hyperplasic cellularity of deficient cell
in bone marrow.
– If diagnosis is correct, splenectomy is expected to
correct defect.
• Pathogenesis:
– Deficiency of blood cell elements may be due to:
→

9. HYPERSPLENISM
• Types:
– Primary Hypersplenism : very rare
– Secondary Hypersplenism : due to →
• Congestive splenomegally e.g. Portal hypertension.
• Neoplastic diseases e.g. Lymphomas, leukemia’s,
myeloid metaplasia.
• Inflammatory diseases, sarcoidosis, SLE, Felty’s
syndrome.
• Infections e.g. acute septicemia, chronic TB infection,
brucellosis, malaria.
• Storage diseases e.g. Gaucher’s disease, amyloidosis.
• Myelo-proliferative disorders e.g. Myelo-fibrosis.
• Chronic hemolytic anemia.

10. RUPTURE SPLEEN
• Predisposing factors:
– Infectious mononucleosis, malaria, typhoid fever.
– Generalized infection e.g. septicemia, pyaemia.
• Causes:
– Direct trauma: Penetrating or closed trauma
(more common).
– Indirect trauma e.g. falls from height or
compression.
– Spontaneous: Rupture may be due to trivial
trauma overlooked by patient.
– Operative trauma: Common with operations of
esophagus, stomach.

11. RUPTURE SPLEEN
• CLASSICAL RUPTURE
– Initially; the victim develops a shock & then
recovered with signs & symptoms of internal
hemorrhage & peritoneal irritation.
– Internal Hemorrhage:
• General: Pallor, tachycardia, restlessness, sighing
respiration.
• Local (blood in peritoneal cavity) 
• Shifting dullness ……Elicited on right side of abdomen.
• Balance’s sign i.e. fixed dullness on left side due to
hematoma in splenic bed.
• Cullen’s & Gray turner’s signs: Discoloration around
umbilicus & flanks few days after trauma (gravitation of

12. RUPTURE SPLEEN
– Peritoneal Irritation {reflex rigidity & tenderness
& irritation due to presence of blood} →
• Severe abdominal pain marked in flanks & left
hypochondrium.
• Kehr’s sign i.e. hyperthesia in left shoulder on palpation
of left upper abdominal quadrant & on Trendlenberg
position (Elevation of foot bed for ¼ hour, → blood
touches the under surface of diaphragm → irritation →
referred pain to left shoulder).
• P-R: Marked tenderness in rectovesical pouch + soft
boggy swelling (due to accumulation of blood in pelvis).
• Rigidity & tenderness: Early on left side. Later on,
generalized.
• Tenderness over 9th 10th & 11TH ribs.

14. RUPTURE SPLEEN
• DELAYED RUPTURE
– Incidence: 10% of blunt trauma cases.
– Causes:
• Presence of sub capsular hematoma (absorbs more
water, → ↑pressure inside it → burst).
• Dislodgment of blood clot over a tear.
• Associated pancreatic tail injury “enzymes digest any
clot present”.
– Presentation:
• Effects of injury are delayed for hours, days & even
months {Latent period of Boudet}.
• 50% of cases; present in first week after trauma, (25%
in 2nd W).

15. RUPTURE SPLEEN
• SPONTANEOUS RUPTURE
– Causes:
• Malaria, typhoid.
• Infectious mononucleosis (2nd – 4th week).
• Leukemia, hemolytic anemia, polycythemia Vera.
• Congestive splenomegally,
• Pregnancy.
• Anticoagulants.

16. RUPTURE SPLEEN
• Investigations for rupture spleen:
– Plain x-ray:
• Normal out line of spleen is strong evidence against
rupture.
• Signs suggestive of rupture spleen →
– Obliteration of splenic outline.
– Enlarged splenic shadow.
– Obliteration of psoas shadow.
– Indentation of left side of stomach air bubble.
– Fracture one or more of lower ribs on the left side (27%).
– Elevation of left copula of diaphragm.
– Sonogram & CT: advantages →
• DD splenic hematomas from lacerations.
• Diagnosis of associated renal or liver injuries.

17. RUPTURE SPLEEN
• Management of rupture spleen:
– Conservative Treatment : Allowed in 25% of
cases provided that →
• Trauma is blunt.
• No other associated injuries requiring surgical
interference.
• Patient is hemodynamically stable.
• Total transfusion requirement is not > 2 units.
• Regular follow up by radiology, scintiscan & CT.
– Concept: Anatomy of spleen favors spontaneous cessation of
bleeding after trauma as sinuses facilitate platelets
aggregation & clot formation.
– Surgery:
• Small Capsular Tear → Splenorrhaphy.

18. SPLENOMEGALLY
• Introduction:
– 10% of healthy children have a palpable spleen
normally.
– Approximately 3% of healthy young persons have
palpable spleens.
– Normal palpable spleen is soft, smooth, & non
tender.
– A pathologically enlarged spleen is often is firmer,
may abnormal surface or texture.
• Characters of splenic swelling:
– Site :Left hypochondrium

19. SPLENOMEGALLY
• Causes of splenomegaly:
– Infective:
• Bacterial e.g. typhoid, paratyphoid, typhus, anthrax, TB,
septicaemia, splenic abscess.
• Spirochetal e.g. syphilis, Weil’s disease
• Viral e.g. infectious mononucleosis, Psittacosis.
• Protozoal e.g. Bilharsiasis, malaria, Kala azar.
• Parasitic e.g. hydatid disease.
– Blood Diseases e.g.
• Leukaemia (myeloid, lymphatic).
• Pernicious anaemia, polycythaemia, erythroblastosis
foetalis.
• Spherocytosis acquired haemolytic anaemia.

20. SPLENOMEGALLY
• Investigations:
– Complete Blood Cell Count.
– Antinuclear Antibody Titre: To screen for systemic
lupus erythematosus.
– Immunoglobulin Levels, neutrophil function, & T-
cell subclasses (e.g. immuno deficiency).
– Viral Antibody Titres: To detect EBV, CMV,
toxoplasmosis, & HIV.
– Bone Marrow Biopsy: For leukaemia, lymphoma,
storage diseases, & disseminated fungal or
mycobacteria infections).
– Ultrasound: Confirm the presence of the enlarged

21. PORTAL HYPERTENSION
• Physiology
– Hepatic blood flow is 1.5 litre/minute = ¼ cardiac
output;
– 2/3 of hepatic blood flow comes through the
portal vein (50% of O2 supply)
– 1/3 of hepatic blood flow comes through the
hepatic artery (50% O2 supply).
– Normal portal vein pressure is 10-15cmH2O or 7-
10 mmHg.
– Variceal bleeding occurs when pressure rises
above 12 mmHg.

22. PORTAL HYPERTENSION
• Anatomy:
– Portal vein is formed by the confluence of the
superior mesenteric & splenic veins behind the
neck of the pancreas & runs for approximately 6
to 8 cm posterior to CBD & hepatic artery up to
the porta hepatis where it bifurcates.
– IMV drains into splenic vein.
– Right gastroepiploic vein drains into SMV.
– Left gastroepiploic vein & short gastric veins drain
into splenic vein.
– Main tributaries of portal vein include → Right
gastric vein, Left gastric vein & Umbilical vein

23. PORTAL HYPERTENSION
• Pathophysiology:
– Pressure in portal vein (PV) = Flow x Resistance
– Portal hypertension can result from  flow or 
resistance
–  Resistance e.g. Bilharzias fibrosis, cirrhosis,
portal vein obstruction.
–  Flow e.g. arteriovenous fistula which may be
due to 
• Trauma
• Giant splenomegally, tropical splenomegally,
splenomegally due to myeloid dysplasia.
– Portal vein pressure  Pressure in portal vein

24. PORTAL HYPERTENSION
• Pathophysiology:
– The type of collateral development depends on
the cause of portal hypertension e.g.
• In extra hepatic portal vein thrombosis without liver
disease , the collaterals are hepatopetal i.e. transport
the blood to liver around occluded vein e.g.
– Hepatopetal collaterals in diaphragm, hepatocolic & hepato-
gastric ligaments.
– Deep cystic vein, accessory vein of Sappy.
– Vein of suspensory ligament, epiploic vein.
• In presence of liver disease , the collaterals are
hepatofugal i.e. carry blood around the liver into
systemic circulation e.g.
– Collaterals at lower oesophagus (with azygos vein →

25. PORTAL HYPERTENSION
• Etiology of portal hypertension: it may be
presinusoidal, sinusoidal, or post sinusoidal.
– In Presinusoidal Portal Hypertension, liver
functions are normal.
– Cirrhosis is the major cause of sinusoidal portal
hypertension:
• The most common causes are viral hepatitis & alcohol.
• Both portal hypertension & hepato-cellular damage
exist.
• Liver functions are markedly affected.
– Post sinusoidal Portal Hypertension is rare &
caused by a hepatic venous outflow obstruction.

26. BLEEDING OESOPHAGEAL VARICES
• Causes: Either due to explosion from within or
erosion from without (e.g. Hcl & trauma by
food).
– Explosion from within: Occurs when expanding
force exceeds that of venous wall tension
(Pressure more than 250-300 cm H2O).
– In 30% of cases, the bleeding is due to associated
other causes e.g. peptic ulcer.

27. BLEEDING OESOPHAGEAL VARICES
• Investigations:
– Barium Swallow: Grape like filling defects in lower
oesophagus.
– Endoscopy: Diagnosis & management of bleeding
varices. Risk of rebleeding is high in big varices &
in presence of red whale markings (Long. dilated
venules).
– Duplex ultrasound : →
• Diagnosis of portal hypertension & varices (PV> 13mm).
• Diagnosis of ascites (sensitive up to300ml).
• Diagnosis of the cause of portal hypertension.
• Direction of blood in portal vein (hepatopetal or

28. BLEEDING OESOPHAGEAL VARICES
• Investigations:
– Measurement of Portal Venous Pressure:
• Measurement of Sinusoid or Post sinusoid Pressure:
The pressure can be obtained by getting the wedge
hepatic venous pressure through trans-jugular trans-
hepatic catheterization of hepatic vein.
• Measurement of Pre sinusoid Pressure : The pressure
can be obtained by one of following methods →
– Percutaneous catheterisation of splenic sinusoids.
– Percutaneous transhepatic catheterisetion of intra hepatic
branches of portal veins.
– Measurement of intra variceal pressure (through endoscopy)
using either micro needle introduced into varices or
pneumatic cuffs compressing varices at certain pressure.

29. BLEEDING OESOPHAGEAL VARICES
• CHILD'S-PUGH CLASSIFICATION:
• Grades: A, 5 to 6 points; B, 7 to 9 points; C,
10 to 15 points.
• The operative mortalities after shunt
determined by child- Pugh classification are 
• For type A: 5 %......For type B: 10%.............For type C:
40%.
• Liver Biopsy: The severity of histological
changes in liver is correlating with immediate
death rate after shunt. The most ominous
findings are; the presence of hepatocellular

30. CHILD'S-PUGH CLASSIFICATION
Three points Two points One point Parameter
> 3.0 2.0-3.0 < 2.0 Bilirubin (mg/dl)
< 2.8 2.8-3.5 > 3.5 Albumin (g/dl)
> 6 4-6 1-3 Prothrombin time
(seconds above
control value)
Moderate slight None Ascites
3-4 (severe) 1-2 (mild) None Encephalopathy

31. BLEEDING OESOPHAGEAL VARICES
• MANAGEMENT OF BLEEDING VARICES:
– General resuscitative measures {fresh blood transfusion, antacids, VK
injection & repeated enemata to decrease absorption of ammonia, fluids}.
– Pharmacotherapy: To reduce portal pressure by 20% either in acute or chronic
setting → Vasopressin & somatostatin: Vasopressin is infused at 0.2 to 0.4 units/min..
– Inderal or propranolol.
– Endoscopic Sclerotherapy, endoscopic Banding Ligation or both:
• Intra variceal injection of one of the following sclerosants e.g. Sod. Marrhuate,
ethmoline, ethanolamine oleate, tetradecylsulphate…etc
• Complications of Sclerotherapy:
– Fever, retrosternal chest pain, septicaemia
– Pulmonary complications e.g. pneumonia, ARDS, pleural effusion, infiltration on chest
X ray.
– Oesophageal complications:
• Mucosal ulceration & bleeding.
• Oesophageal perforation, acute injection dysphagia.
• Oesophageal stricture.
– Technical difficulties:
• Poor results in fundic varices.
• Difficulties in visualization in 25% of cases.

32. BLEEDING OESOPHAGEAL VARICES
• Trans-jugular Intra-hepatic Portal Systemic
Shunt (TIPS)
– Technique: TIPS are introduced through the right
internal jugular vein → catheterisation of a main
hepatic vein → trans-parenchymal catheterisation
of portal vein, & serial dilation of track until large
enough to insert a stent. Technical success rate is
92 %.
– Complications:
• The rebleeding rate is 20 % at 1-year follow-up.
• Shunt dysfunction in 50-60% of cases at 6 months e.g.
thrombosis, migration, stenosis & obstruction.

33. BLEEDING OESOPHAGEAL VARICES
– Percutaneous Transhepatic Obliteration of
Varices: It is indicated in case of failure of
endoscopic sclerotherapy & the patient is unfit for
shunt surgery}.
– Angiographic Embolization of mid splenic, left
gastric & left gastro epiploic arteries.
– Emergency Operations:
• Tanner’s trans-gastric resection & anastomosis.
• Trans-thoracic trans-esophageal ligation of varices.
• Devascularisation procedure (Hassab’s operation):
This procedure consists of splenectomy, gastric &
oesophageal devascularisation by ligation of left
gastric, left gastroepiploic & phrenic veins.
• Emergency Shunt Operations e.g. portocaval shunts

34. BLEEDING OESOPHAGEAL VARICES
• Balloon Tamponade: types include →
– Sengestaken Black more Tube: Three luminal tube;
gastric (200 cc air), oesophageal (40 mmHg) &
central luminal tubes). The most important is
gastric tube; traction against cardia → obstruction
of collaterals at cardia.
– Minnesota Tube: This tube has an additional
lumen to aspirate saliva.
– Complications of Balloon Tamponade;
• Renewing of haemorrhage after removal
• Aspiration of saliva (use four lumen tubes )
• Necrosis of mucosa due to prolonged pressure (tube

35. MINNESOTA TUBE

36. BLEEDING OESOPHAGEAL VARICES
• SURGICAL SHUNTS
• Shunts can be total, partial or selective
• Role of shunts is to:
– Emergency control of variceal bleeding if TIPS is
not available or contraindicated.
– Reduce portal hypertension in patients awaiting
transplantation
– Relieve intractable ascites
– Reduce bleeding from rectal, colonic or stomal
varices
– All types of shunt will correct hypersplenism if

37. BLEEDING OESOPHAGEAL VARICES
• TOTAL SHUNTS
– End-to-Side Porto-caval Shunt: End of PV to side
of IVC.
– Side-to-side porto-caval shunt: Side-of PV to side
of IVC.
– Meso-caval Shunt: Prosthetic or internal jugular
vein graft is interposed between IVC & SMV.
– Central Spleno-renal Shunt : Splenic vein is
anastomosed to centre of renal vein after removal
of spleen )

40. BLEEDING OESOPHAGEAL VARICES
• PARTIAL OR SELECTIVE SHUNTS
• Introduction: The portal vein carries 50% of
oxygen supply to liver; hepatic oxygenation is
impaired by 50% in case of total shunt →
progressive hepatocellular damage & hepatic
encephalopathy. In partial shunt, still some
blood reaches the liver → ↓incidence of
hepatic encephalopathy.
• Definition: Selective drainage of variceal area
only while the rest of portal circulation

41. BLEEDING OESOPHAGEAL VARICES
• Types of Selective Shunts:
– Distal splenorenal shunt (Warren): The splenic
vein is inserted into the left renal vein.
Oesophageal varices is selectively decompressed
through the short gastric veins into the splenic &
then into renal veins.
– Left gastric vena caval shunt (Inokuchi): The left
gastric vein is anastomosed to IVC
• Advantages of selective shunt:
– Selective decompression of variceal area.
– Low incidence of hepatic encephalopathy

43. BLEEDING OESOPHAGEAL VARICES
• Sugiura Operation: The operation is formed of
two stages;
– Thoracotomy (The first stage): All dilated venous
collaterals between oesophagus & adjacent
structures are divided & ligated. The oesophagus
at the level of diaphragm is transected &
reanastomosed.
– Laparotomy is done in the second stage (this stage
can be done with the first stage if there is active
bleeding): Upper 2/3 of stomach is devascularized.
Splenectomy, selective vagotomy & pyloroplasty
are carried out.

44. ASCITES
• Causes:
– Lymphatic ooze from liver surface
– Hypoalbuminemia
– Salt & water retention
– Portal hypertension ( ↑filtration force )
– 2% of cases, TB
• Investigations:
– Paracentesis:
• WBCs ( > 250 /µL i.e. silent bacterial peritonitis)
• Cytological examination to exclude malignancy
• Amylase level: the level is high in pancreatic sources.
– Ultrasound: Sensitive to detect up to 300 ml of

45. ASCITES
• Treatment:
• Medical Treatment:
– Sodium intake is restriction; Diuretics (see medical
side).
– Albumin transfusion
– Paracentesis: If above measures failed,
paracentesis can be used or more recently TIPS
has been shown to alleviate refractory ascites.

46. PARACENTESIS

47. ASCITES
• Surgical Treatment:
• Portocaval Shunt.
• Peritoneal Jugular Shunt (Le Veen shunt):
– Procedure: Silastic catheter with unidirectional
valve is kept subcutaneous under between
internal jugular vein & peritoneal cavity.
– Indications:
• Refractory ascites failing to respond to high doses of
diuretics.
• Ascites due to Budd Chiarri syndrome
• Malignant ascites esp. if malignant cells are not present
in ascitic fluid.

48. LE VEEN SHUNT

49. 1. Acute abscess: This is a rare condition
occurring as a sequel of specific fever, e.g.
typhoid fever, it can also be blood borne from
a distant septic lesion or during systemic
pyaemia. The treatment is splenectomy if
possible, but if there are dense adhesions,
drainage of the abscess is only performed.
2. Chronic abscess: This is also rare and can
result form a neglected acute abscess or an
infected cyst. Treatment is splenectomy.
3. Tuberculosis: The disease is usually a
INFECTIONS OF THE SPLEEN

50. This category includes a wide spectrum of
disorders in which there is accelerated
destruction of mature red blood cells.
Haemolytic anaemias are generally classified to
congenital or acquired:
Congenital anaemias: are due to an intrinsic
abnormality of the red blood cells like hereditary
spherocytosis , thalassaemia and sickle-cell
anaemia.
Acquired anaemias: are related to extra-
corpuscular factors acting on normal red blood
CHRONIC HAEMOLYTIC ANAEMIAS

51. Hereditary spherocytosis
Aetiology:
There is a defect in the red-cell membrane due to
deficiency of certain proteins known as spectrins. As a
result, there is excessive permeability to sodium ions
and the red cell integrity can only be .maintained by
increasing the glycolytic activity to provide the energy
required to pump out the sodium ions.
1. The increased metabolic activity leads to the
development of microspherocytosis in the red – pulp
of spleen where the available glucose is diminished.
2. Microspherocytes are trapped in the red pulp
because they lack deformability and so they are
CHRONIC HAEMOLYTIC ANAEMIAS

52. Hereditary spherocytosis
Pathology:
1. Blood: Abnormal fragility; haemolysis occurs at
higher concentrations of saline than in the
normal .Normal haemolysis starts at 0.45%
saline solution. In spherocytosis ,haemolysis
starts at o.6%. In spherocytosis, the R.B.Cs are
biconvex instead of being biconcave.there is
anaemia with reticulocytosis.
2. Liver: Slightly enlarged, Pigment stones may form
in the biliary system, Biliary cirrhosis may occur
in late cases.
CHRONIC HAEMOLYTIC ANAEMIAS

53. Hereditary spherocytosis
Clinical features:
Usual course:
Jaundice is associated with anaemia.
Life span is not greatly affected.
Icterus index is usually not more than 50.
Severe cases: These are rare and are characterized by:
 Haemolytic crisis; fever, severe anaemia and depth of
jaundice increases.
 Striation of cranial bones may be detected in X-ray.
CHRONIC HAEMOLYTIC ANAEMIAS

54. Hereditary spherocytosis
Complications:
A. Pigment gall stones may occur in up to 60% of
patients.
B. Chronic leg ulcers may occur in long standing cases.
Treatment:
Splenectomy relieves jaundice and anaemia (as spleen is
the site of destruction of the RBCs), but it does not
affect the spherocytosis. The best timing for
splenectomy is at the age of 6-7 years. Before this age
there is a risk of increased liability to infection due to
loss of the immune functions of the spleen. If there are
any biliary stones, cholecystectomy should be done
CHRONIC HAEMOLYTIC ANAEMIAS

55. Idiopathic Thrombocytopenic purpura
Aetiology
This disease was formerly though to be idiopathic . But it
is now known to be an auto-immune disease. Platelets
are sensitized with an auto-antibody that results is their
early sequestration by the reticuloendothelial cells
(mainly in the spleen and liver).
Pathology
The term ITP should be reserved for the haemorrhagic
disorder characterized by:
1. Subnormal platelets count.
2. Bone marrow contains normal or increased
megakaryocytes.
CHRONIC HAEMOLYTIC ANAEMIAS

56. Idiopathic Thrombocytopenic
purpura
Clinical features
Symptoms
1. The disease occurs most commonly in children and
young adult females.
2. The course of the disease runs in remissions and
relapses.
3. It may present by an attack of bleeding under the skin
(ecchymosis) or mucous membrane or from an
orifice, as the nose, urinary or gastrointestinal tract.
Menorrhagia is a common complaint in affected
CHRONIC HAEMOLYTIC ANAEMIAS

57. Idiopathic Thrombocytopenic
purpura
Investigations
The red and white cells are diminished due to
repeated haemorrhages.
Platelets are diminished in number. Their count
may drop to 30.000/ul.
Bleeding time is prolonged up to 20 minutes
(normally 2-5 min). Coagulation time is
normal. The blood clot is soft, friable and fails to
retract.
CHRONIC HAEMOLYTIC ANAEMIAS

58. THANK YOU