++

Definitions

++

A finite life span is a distinct characteristic of red cells. Hence, a logical, time-honored classification of anemias is in three groups: (1) decreased production of red cells, (2) increased destruction of red cells, (3) acute blood loss. Decreased production is covered in Chaps. 103, 105, and 107; increased destruction and acute blood loss are covered in this chapter.

++

All patients who are anemic as a result of either increased destruction or acute blood loss have two important elements in common: the anemia results from overconsumption of red cells from the peripheral blood, yet the supply of cells from the bone marrow (in the absence of coexisting marrow disease) is usually increased, as reflected by a reticulocytosis. On the other hand, physical loss of red cells from the bloodstream—which in most cases also means physical loss from the body—is fundamentally different from destruction of red cells within the body. Therefore the clinical aspects and the pathophysiology of anemia in these two groups of patients are quite different, and they will be considered separately.

++

With respect to primary etiology, anemias due to increased destruction of red cells, which we know as hemolytic anemias (HAs), may be inherited or acquired (Table 106–1). From the clinical point of view they may be more acute or more chronic, they may vary from mild to very severe, and the site of hemolysis may be predominantly intravascular or extravascular. With respect to mechanisms, HAs may be due to intracorpuscular causes or to extracorpuscular causes. But before reviewing the individual types of HA it is appropriate to consider what they have in common.

++
Table Graphic Jump Location
Table 106–1 Classification of Hemolytic Anemias* 
++

General Clinical and Laboratory Features

++

The clinical presentation of a patient with anemia is greatly influenced in the first place by whether the onset is abrupt or gradual, and HAs are no exception. A patient with autoimmune HA or with favism may be a medical emergency, whereas a patient with mild hereditary spherocytosis or with cold agglutinin disease may be diagnosed after years. This is due in large measure to ...

Want access to your institution's subscription?

Sign in to your MyAccess Account while you are actively authenticated on this website via your institution (you will be able to tell by looking in the top right corner of any page – if you see your institution’s name, you are authenticated). You will then be able to access your institute’s content/subscription for 90 days from any location, after which you must repeat this process for continued access.

Ok

About MyAccess

If your institution subscribes to this resource, and you don't have a MyAccess account, please contact your library's reference desk for information on how to gain access to this resource from off-campus.

Subscription Options

AccessMedicine Full Site: One-Year Subscription

Connect to the full suite of AccessMedicine content and resources including more than 250 examination and procedural videos, patient safety modules, an extensive drug database, Q&A, Case Files, and more.

$995 USD
Buy Now

Pay Per View: Timed Access to all of AccessMedicine

24 Hour Subscription $34.95

Buy Now

48 Hour Subscription $54.95

Buy Now

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.