Transcript Traumatic rupture of the spleen

Spleen
Splenomegally (Causes)
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Infections
 Salmonella
(bacteria)
 Infectious mononucleosis (viral)
 Schistosomiasis &hydatid (parasite)
 Kala-azar&malaria (protozoa)
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Blood diseases
 Hemolytic
anemia
 Thrombocytopenias
 Leukemias
 Myelofibrosis
 Polycythaemia Vera
Splenomegally (Causes)
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Metabolic diseases
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Collagen diseases
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Felty syndrome
Portal tree occlusion or hypertension
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Gaucher’s disease
Porphyria
Portal hypertension
Splenic vein thrombosis or invasion by pancreatic tumor
Budd-Chiari syndrome
Tumors and cysts
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Hydatid disease
Malignant lymphoma
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
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Traumatic rupture of the spleen
Types of trauma
 Penetrating
 Non-penetrating
 Operative
 Spontaneous rupture
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
Clinically
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Fatal type
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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
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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
Clinically
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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
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
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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
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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
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
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ITP
HS and other types of hemolytic anemia e.g.thalassemia
Lymphoma, cysts, and other tumors
Postsplenectomy complications
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Hemorrhage
 Reactionary
most common due to slipped
ligature
 Intraoperative
 At the site of the drain
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Subphrenic collection
 Due
to improper drainage and bad
hemostasis, with
 excessive use of silk ligatures, and
contamination during operation
Postsplenectomy complications
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Increased suscitibility to infection
 This
is true especially in children where
immunization for late teens is advised to avoid
severe bacterial infections
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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
Postsplenectomy complications
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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)
Postsplenectomy complications
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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
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.
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.
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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
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Idiopathic thrombocytopenic
purpura
Treatment is either by
 steroids or
 azathiprine, and
 splenectomy is last resort if medical
treatment cannot induce and maintain
remissions
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
Hereditary spherocytosis
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Clinically
 Mild
jaundice
 Pallor
 episodes of hemolytic attacks
induced by infections
Hereditary spherocytosis
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Complications
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Pigment stone formation
Bilateral or unilateral leg ulcers
Investigations
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To detect increased fragility of RBC
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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)
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