RUPTURED SPLEEN

RUPTURE OF THE SPLEEN

Rupture of the spleen may occur as a consequence of blunt  injury

of the abdomen or a gunshot wounds.

The  spleen, alone or in combination with other viscera,  is  the

most  frequently  injured  organ following  blunt  trauma to  the

abdomen or the lower thoracic cage. Automobile accidents  provide

the  predominating cause, while falls, and blows incurred  during

contact sports are frequently implicated in children.

Clinical manifestations.

The  signs  and  symptoms produced by trauma to the  spleen  vary

according  to  the  severity  and  rapidity  of   intra-abdominal

hemorrhage. The majority of patients present with some degree  of

hypovolemia and techycardia is almost always present.

The  patient  usually complains of  generalized  upper  abdominal

pain,  which is one third of the cases is localized in  the  left

upper quadrant. Pain at the tip of the shoulder (Kehr's sign)  is

evidence of diaphragmatic irritation but occurs in less than half

the  patients.  If  the patient is placed  in  the  Trendelenburg

position, left shoulder pain may be produced.

Diagnostic Studies

Routine  abdominal  radiographs may  demonstrate  fractured  ribs

which:

1. Elevated immobile left diaphragm

2. An enlarged splenic shadow

3. Medial displacement of the gastric shadow with

4  Widening  of the space between the  splenic  flexure  and  the   

   proportional   fat  pad.  Abdominal  paracentesis   yields   a   

   positive tap.
5 Abdominal CT scan

Treatment

The   great   majority  of  adult   patients   require   surgical

intervention.

Splenectomy  as a life saving procedure is still the  standard  in

many cases.

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Spleen congenital haemolytic anaemia

5. CONGENITIAL HAEMOLYTIC ANAEMIA

Hereditary  spherocytosis is a relatively common  genetic  linked

disorder characterized by :

*  Small dense, spheroid erythrocytes

*  Increased  osmotic  fragility because of a red  cell  membrane

   defect

*  These cells are impeded through the spleen and destroyed

Patients  frequently  present  with a  family  history  and  past

history of attacks of jaundice in childhood and in early life.

Besides anaemia the patients:

*  In acute crisis have accompanied fever and chills

*  In later life may have bilirubin gallstones

*  Show splenomegaly as a characteristic feature

*  Spherocytes can be demonstrated in the peripheral blood smear

*  Osmotic fragility of the R.B.C. is readily demonstrable

TREATMENT

Patients  are benefitted by splenectomy and is recommended  after

the age of six.

Basic  cellular defect persists after splenectomy; but the  cells

survive normally.

Cholecystectomy  is  recommended when stones are present  in  the

gallbladder

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SPLEEN FUNCTION 3 hypersplenism hyposplenism

3. HYPERSPLENISM

The  term hypersplenism is used when there is a reduction in  the

circulation of :

*  Red cells

*  White cells or platelets

*  Any combination of these elements

*  There is in addition bone marrow hyperplasia and splenomegaly

Some  of  the case that may be causes responsive  to  splenectomy

are;

-  Lymphcoma

-  Chronic lymphatic leukemia

-  Hairy cell leukemia

Hyersplenism also occurs in;

-  Portal hypertension

-  Malaria, Kala-azar

-  Sarcoid

-  Lipid storage desease

These  patients  present with symptoms related to  the  deficient

cellular component i.e. anaemia or ecchymosis

Some patients do well after splenectomy

4. HYPOSPLENISM

Hyposlenism  occur  in cases of congenital absence of  spleen  or

splenic infarcts (sickle cell anemia)

This  complication  results in sepsis due to  deminished  splenic

function

It is sometimes seen after splenectomy

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SPLEEN FUNCTIONS 2 RBC Life CYCLE

Blood Cell Cycle

The normal red blood cell is a biconcave disk approximately to 7.5µ in diameter. It is the major component of the cellular compartment of the blood, with a circulating life of about 100 to 120 days.

The primary role of RBC is to deliver oxygen to the tissues for metabolism and carry dissolved carbon dioxide to the lungs for release into the air. The red cell depends on the hemoglobin molecule to for transport of these gases.

The number of erythrocytes in the blood ranges form 3.8 to 5.9 million cells per microliter of blood, with a hemoglobin concentration ranging form 17 to 17g/dl and a hematocrit of 35% to 52%.

This normal range is broad for it cover men and women young and old, and with people living at altitude. Induced erythropeiesis, leading to the expansion of red cell mass, occurs in response to hypoxia, blood loss, and a variety of hormones and diease states.

The most potent stimulator of erythropoiesis is erythropoietin.

Erythropoietin is a hormone produced by the kidney in response to hypoxia. This hormone stimulates the pluripotent stem cells in the bone marrow to become mature.

The bone marrow is capable of increasing the production of red cells by 5 to 10 times normal under the influence of erythropoietin. However, because of the limiting factor of iron in diet the increase is only two to three times normal.

In patients with chronic renal failure or after a nephrectomy, the ability to generate a erythropoietin response is slower.

Red Blood Cell Life and death

The red blood cell does not possess the structures required for DNA synthesis nor, for transcription and translation of proteins. Cellular life depends the cells ability to generate ATP through the utilization of glucose. Without the pathway for ATP generation, the cell would not be able to maintain its membrane integrity, and ionic gradients. The ability to maintain hemoglobin in its reduced form for the transport and delivery of oxygen would also be limited.

Glucose is the primary fuel of the erythrocyte. It enters the cell through diffusion from the plasma, and through glycolysis ultimately is converted to lactate and pyruvate.

This process uses 2 moles of ATP and produce 4 moles of ATP, for a net gain of 2 ATP molecules. The rate limiting step is controlled by the activity of phosphofructokinase, which converts fructose 6-phosphate to fructose 1,6 phosphate. This enzyme is inhibited by high concentrations of ATP, which signal the “fed” state.

Conversely, high concentrations of AMP signal an “energy starved” state favouring continued glycolysis.

The energy generated by glycolysis is utilized by the Na+ -K+ ATPase pump to regulate cell membrance potentials.

Maintenance of the appropriate redox potential is essential for the red blood cell to complete its function of oxygen delivery.

The red cell ultimately dies as its enzyme systema burn out.

The inability to continue glycolysis to maintain membrane gradients leads to changes in membrane permability and ultimately to cell destruction. More than 90% of red cells with altered membrane are destroyed by the macrophages of the reticuloendothelial system (spleen, liver and marrow).

As the cells are destroyed, the hemoglobin molecule is further degraded. The iron is largely conserved, redistributed to the marrow, and incorporated into new hemoglobin

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