1. Spleen

2. Splenomegally (Causes)
Infections
Salmonella (bacteria)
Infectious mononucleosis (viral)
Schistosomiasis &hydatid (parasite)
Kala-azar&malaria (protozoa)
Blood diseases
Hemolytic anemia
Thrombocytopenias
Leukemias
Myelofibrosis
Polycythaemia Vera

3. Splenomegally (Causes)
Metabolic diseases
Gaucher’s disease
Porphyria
Collagen diseases
Felty syndrome
Portal tree occlusion or hypertension
Portal hypertension
Splenic vein thrombosis or invasion by pancreatic tumor
Budd-Chiari syndrome
Tumors and cysts
Hydatid disease
Malignant lymphoma

4. Differential diagnosis of a huge splenic enlargement
Portal hypertension
Chronic myeloid leukemia
Myelofibrosis
Kala –azar in endemic areas
Thalassemia in children
Gaucher disease in children

5. Traumatic rupture of the spleen
Types of trauma
Penetrating
Non-penetrating
Operative
Spontaneous rupture

6. Traumatic rupture of the spleen
Pathology
Subcapsular hematoma
Small superficial tears
Deep tears
Avulsion of a pole of the spleen
Complete pulping of the spleen
Injury of the vascular pedicle

8. Clinically Fatal type The classical type
If the hemorrhage is so severe, the patient may not reach the hospital due to avulsion of the pedicle
The classical type
The patient presents with shock, and internal bleeding (severe pallor)
The patient’s BP is restored temporarily by infusion of crystalloids, and drops back rapidly once the infusion is stopped (a sign of in internal hemorrhage)
The abdomen shows guarding and tenderness in the upper left abdomen with shifting dullness

9. Clinically
Special signs may be present but they are not essential for diagnosis
Balance sign shifting dullness on the right side and no shifting on the left side (hematoma)
Kehr’s sign pain referred tothe left shoulder region due to diaphragmatic irritation
Cullen sign bluish discoloration around the umbilicus

10. Clinically Delayed rupture
About two weeks after the trauma, which is usually, pass unnoticed patient presents with manifestations of internal hemorrhage.
The causes of delay are
Subcapsular hematoma that may rupture later
Sealing with blood clot that may dislodge or dissolve
Sealing with omentum which may retract

11. Investigations
U/S is of utmost importance to visualize the free peritoneal fluid and diagnose perisplenic hematomata
DPL (diagnostic peritoneal lavage), before the U/S it was the main way of investigation
CT, can diagnose other associated retroperitoneal traumatized organs

12. Treatment
After correction of the general condition with blood and crystalloid transfusions
Exploration is done and in the majority of cases splenectomy is done
In children it is advised to try to keep the spleen as much as possible by
splenorrhaphy or
partial splenectomy with postoperative meticulous observation with frequent U/S to monitor any further bleeding.
In case splenectomy was done immunization with penumococcal vaccine is given to protect against future overwhelming infections

13. Indications of splenectomy
The most commonly used indication is splenectomy as part of devascularisation procedures in portal hypertension
The second common is trauma
The third as part of radicality in other operations (stomach, pancreas and esophagus)
Other indications
ITP
HS and other types of hemolytic anemia e.g.thalassemia
Lymphoma, cysts, and other tumors

23. Postsplenectomy complications
Hemorrhage
Reactionary most common due to slipped ligature
Intraoperative
At the site of the drain
Subphrenic collection
Due to improper drainage and bad hemostasis, with
excessive use of silk ligatures, and contamination during operation

24. Postsplenectomy complications
Increased suscitibility to infection
This is true especially in children where immunization for late teens is advised to avoid severe bacterial infections
Hematemesis
This is due to faulty design of the devascularisation procedure
specially if used in patients with abundant splenic collaterals, which were draining the portal tree

25. Postsplenectomy complications
Portal vein thrombosis
This is now believed to reach as high rate as 80%, with splenic vein thrombosis occurring in almost all cases.
This is due to thrombocytosis and elimination of splenic flow .
If partial it cause only unexplained fever,
if complete it can be fatal (shock, bloody diarrhea and flooding ascites)

26. Postsplenectomy complications
Nearby organ injury
Pancreatic tail leading to pancreatitis or pancreatic fistula which can be further complicated by wound dehiscence and left pleural effusion and pancreatic ascites
Splenic flexure of the colon. This will lead to a fecal fistula usually through the drain exit

27. Postsplenectomy complications
Stomach
Due to vitalization of the gastric wall at the site of ligature of the short gastric vessels, which can be very short allowing no space to put a sound ligature
Left copula of the diaphragm
This will cause left basal atalectasis with pleural effusion.

28. Idiopathic thrombocytopenic purpura
The disease is of unknown etiology and all other causes of thrombocytopenia are to be excluded before diagnosing the common disease of ITP
It affects females more and is usually episodic in nature with remission and relapses.

29. Idiopathic thrombocytopenic purpura
The hemorrhage can be under the skin, from urinary or GIT, or more commonly menorrhagia
Blood picture shows thrombocytopenia, while bone marrow shows normal megakaryocyte features

30. Idiopathic thrombocytopenic purpura
Treatment is either by
steroids or
azathiprine, and
splenectomy is last resort if medical treatment cannot induce and maintain remissions

31. Hereditary spherocytosis
Pathology
RBC cell membrane is deficient in a protein known as spectrins,
thus causing more permeability to Na, causing the Na pump to work more needing more glycolysis.
This will lead to spherocytosis.
Spherical cells are trapped in the spleen and became with short half life
The disease is autosomal dominant with equal affection of males and females

32. Hereditary spherocytosis
Clinically
Mild jaundice
Pallor
episodes of hemolytic attacks induced by infections

33. Hereditary spherocytosis
Complications
Pigment stone formation
Bilateral or unilateral leg ulcers
Investigations
To detect increased fragility of RBC
Fragility test
Increased reticulocytes in peripheral blood
The shape of the RBC
Radioactive Cr51 labeled patient’s own RBC to detect shortened half life
To detect size of spleen and gall stones (U/S)

34. Hereditary spherocytosis
Treatment
Splenectomy, will increase the half life of RBC although the original defect is not corrected
The best age is 6-7 years, if before, the immunologic function of spleen may cause problems, if after the gallstones may develop
Search for splenules to avoid recurrence