The normal red cell content of the spleen is 30-70 mL, or less than about 5% of the total red cell mass. When the spleen is enlarged, expansion of the vascular bed occurs. This results in a considerable pool with a high haematocrit and only a slow exchange of red cells with the general circulation. In myelofibrosis, hairy cell leukaemia and prolymphocytic leukaemia, as much as 40% of the red cell mass may be pooled in the spleen. This pooling will functionally exclude a relatively large volume of red cells from the main arteriovenous circulation, and thus be an important cause of anaemia. In such cases, it should be noted that the red cell mass, as measured by a radionuclide labelling technique, may give a misleadingly normal result, whereas the peripheral blood packed cell volume will give a more reliable measurement of the effectively circulating red cell mass. In splenomegaly due to cellular infiltration, the pool is less prominent. Conversely, in the congestive splenomegaly of portal hypertension, spleen size with an increased red cell pool is a dominant feature.
The normal spleen contains a reservoir of granulocytes, which is in dynamic equilibrium with the circulating granulocytes. It is 30-50% of the body's total marginating pool, with a mean transit time through the spleen of about 10 min. Splenic sequestration of granulocytes is thought to be responsible for the neutropenia that often occurs in patients with splenomegaly. Platelets have also been shown to have a significant reservoir in the spleen, and are rapidly interchangeable with the circulation. In normal subjects, 20-40% of the total platelet mass is pooled in the spleen and the platelets spend up to one-third of their lifespan there. The pool increases when the spleen is enlarged. This pooling and temporary sequestration must be distinguished from destruction of platelets in the spleen, which occurs in many cases of thrombocytopenia.
Plasma volume is controlled by a neurohumoral mechanism which affects distribution of water between intravascular and extracellular fluid compartments across the capillary wall. Under physiological conditions, the red cell volume is fairly constant, while the plasma volume undergoes continual transient vari ations that trigger off the necessary adjustments which ensure that the total blood volume remains constant. There is no evidence that the normal spleen is involved in this mechanism, but when the spleen is enlarged it does play a role; splenomegaly is frequently associated with an increased plasma volume, which may lead to a dilutional pseudo-anaemia. Possible mechanisms that have been suggested to explain expanded plasma volume in splenomegaly include the following:
1 The enlarged organ, acting as a large arteriovenous fistula, requires an expansion of blood volume to fill the additional intravascular space; in conditions where marrow erythropoietic activity is reduced, as in myelofibrosis, it may not be possible to maintain the normal red cell: plasma ratio and the additional volume is provided by plasma alone.
2 As splenomegaly increases, flow-induced portal hypertension may cause activation of the neurohumoral mechanism, augmented renal sympathetic nerve activity and secondary renal sodium retention with consequent fluid imbalance.
3 Protein alterations, especially increased globulin levels with reduced albumin, result in an alteration in colloid cellular osmotic pressure. This has been suggested as a factor in tropical splenomegaly and in cirrhosis.
In blood dyscrasias, the increase in plasma volume is directly proportional to the size of the spleen, less so in cirrhosis.
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