Endocrine System

Chapter 9

Hematopoietic System

Radiographer Notes

Although the hematopoietic system cannot be directly imaged, many blood disorders result in abnormalities that can be demonstrated radiographically. It may be necessary to increase or decrease exposure factors when imaging patients who manifest advanced stages of these diseases (see Box 1-1). The radiographer must be aware of the severe pain experienced by patients undergoing a sickle cell crisis. Patients with advanced leukemia or lymphoma who have an altered immune status may require protective isolation. Because many hematopoietic system diseases cause significant demineralization of bone, the radiographer must be alert to the possibility of pathologic fracture and thus must exercise caution when moving and positioning patients with these diseases.

Radiographers need to be aware of the importance of using proper radiation safety shielding, pelvic shielding for patients, and aprons for technologists to prevent possible lack of blood cell formation in the pelvis, which could ultimately result in anemia.

Physiology of the blood

Blood and the cells within it are vital to life. An adequate blood supply to all body tissues is necessary to bring oxygen, nutrients, salts, and hormones to the cells and to carry away the waste products of cellular metabolism. The components of blood are also a major defense against infection, toxic substances, and foreign antigens.

Red bone marrow (found in vertebrae, proximal femurs, and flat bones such as the sternum, ribs, skull, and pelvis) and lymph nodes are the blood-forming tissues of the body. Red blood cells (erythrocytes) and platelets (thrombocytes) (Figure 9-1) are made in red bone marrow, whereas white blood cells (leukocytes) (Figure 9-2) are produced in both red marrow and lymphoid tissue. If a bone marrow puncture is necessary for diagnostic testing, the iliac rim and sternum are good sites.

Erythrocytes are biconcave disks without a nucleus that contain hemoglobin, an iron-based protein that carries oxygen from the respiratory tract to the body’s tissues. In a normal person, there are 4.5 to 6 million red blood cells in each cubic millimeter of blood. The amount of hemoglobin per deciliter is approximately 14 g in women and 15 g in men.

Leukocytes, or white blood cells, normally number from 5000 to 10,000/mm3 of blood (see Figure 9-2). Unlike erythrocytes, there are several types of white blood cells. Neutrophils (polymorphonuclear leukocytes), which make up 55% to 75% of white blood cells, defend the body against bacteria by ingesting these foreign organisms and destroying them (phagocytosis). The number of polymorphonuclear leukocytes in the blood increases enormously in acute infections because the bone marrow rapidly releases into the bloodstream the large numbers of these cells kept in reserve. Eosinophils (1% to 4%) are red-staining cells whose number greatly increases in allergic and parasitic conditions. The third type of leukocyte is the basophil (0% to 1%), which contains granules that stain blue. These three types of cells are formed in the sinusoids of bone marrow, and they, like red blood cells, go through immature stages before reaching the adult form.

Lymphocytes represent about 25% to 40% of white blood cells. They play a major role in the immune system and aid in the synthesis of antibodies and the production of immunoglobulins.

The final type of white blood cell is the monocyte, which is actively phagocytic and plays an important part in the inflammatory process. Monocytes are formed in the bone marrow and represent about 2% to 8% of white blood cells.

Platelets, the smallest blood cells, are essential for blood clotting (see Figure 9-1). Normally there are about 150,000 to 400,000 platelets in every cubic millimeter of blood.

Diseases of red blood cells


Anemia refers to a decrease in the amount of oxygen-carrying hemoglobin in the peripheral blood. This reduction can be attributable to improper formation of new red blood cells, an increased rate of red blood cell destruction, or a loss of red blood cells as a result of prolonged bleeding. Regardless of the cause, a hemoglobin deficiency causes the anemic person to appear pale. This is best appreciated in the mucous membranes of the mouth and conjunctiva, and in the nail beds. A decrease in the oxygen-carrying hemoglobin impairs the delivery of an adequate oxygen supply to the cells and tissues, leading to fatigue and muscular weakness and often to shortness of breath on exertion (dyspnea). To meet the body’s need for more oxygen, the respiratory rate increases and the heart beats more rapidly.

Hemolytic Anemia

The underlying abnormality in hemolytic anemia is a shortened life span of the red blood cells with resulting hemolysis and the release of hemoglobin into the plasma. Most hemolytic anemias are caused by a hereditary defect that may produce abnormal red blood cells or abnormal hemoglobin. Less commonly, hemolytic anemia is acquired and related to circulating antibodies from autoimmune or allergic reactions (e.g., drugs such as sulfonamide) or the malarial parasite.

Spherocytosis, sickle cell anemia, and thalassemia are the major hereditary hemolytic anemias. In spherocytosis the erythrocytes have a circular rather than a biconcave shape, making them fragile and susceptible to rupture. In sickle cell anemia, which is generally confined to African Americans, the hemoglobin molecule is abnormal and the red blood cells are crescentic or sickle shaped and tend to rupture. A defect in hemoglobin formation is also responsible for thalassemia, which occurs predominantly in persons living near the Mediterranean Sea, especially those of Italian, Greek, or Sicilian descent.

The breakdown of hemoglobin produces bilirubin, a pigmented substance that is normally detoxified by the liver and converted into bile. The accumulation of large amounts of this orange pigment in plasma causes the tissues to have a yellow appearance (jaundice).

Hemolytic anemia of the newborn (erythroblastosis fetalis) can result when the mother is Rh negative and the fetus has Rh-positive blood inherited from the father. Although the fetal and maternal circulations are separate, fetal blood can enter the mother’s blood through ruptures in the placenta that occur at delivery. The mother thus becomes sensitized to the Rh factor of the fetus and makes antibodies against it. Any antibodies reaching the fetal blood through the placenta in future pregnancies cause hemolysis of the fetal red blood cells. The severity of the disease ranges from mild anemia with jaundice to fetal death.

Radiographic Appearance: The hemolytic anemias produce a variety of radiographic abnormalities. Although the radiographic findings are similar in the various types of hemolytic anemia, they tend to be most severe in thalassemia and least prominent in spherocytosis. Extensive marrow hyperplasia, the result of ineffective erythropoiesis and rapid destruction of newly formed red blood cells, causes generalized osteoporosis with pronounced widening of the medullary spaces and thinning of the cortices in long and tubular bones (Figure 9-3). As the fine secondary trabeculae are resorbed, new bone is laid down on the surviving trabeculae, thickening them and producing a coarsened pattern. Normal modeling of long bones does not occur because the expanding marrow flattens or even bulges the normally concave surfaces of the shafts.

In the skull, there is widening of the diploic space and thinning or complete obliteration of the outer table. When the hyperplastic marrow perforates or destroys the outer table, it proliferates under the invisible periosteum, and new bone spicules are laid down perpendicular to the inner table. This produces the characteristic hair-on-end appearance of vertical striations in a radial pattern (Figure 9-4).

Extramedullary hematopoiesis is a compensatory mechanism of the reticuloendothelial system (liver, spleen, lymph nodes) in patients with prolonged erythrocyte deficiency resulting from the destruction of red blood cells or the inability of normal blood-forming organs to produce them. Paravertebral collections of hematopoietic tissue may appear on chest radiographs as single or multiple, smooth or lobulated, posterior mediastinal masses that are usually located at the lower thoracic levels (Figure 9-5).

In sickle cell anemia, expansile pressure of the adjacent intervertebral disks produces characteristic biconcave indentations on both the superior and inferior margins of the softened vertebral bodies, giving the appearance of fish vertebrae (Figure 9-6, A). Another typical appearance is the result of the development of localized steplike central depressions of multiple vertebral end plates (Figure 9-6, B). This is most often caused by circulatory stasis and ischemia, which retard growth in the central portion of the vertebral cartilaginous growth plate. The periphery of the growth plate, which has a different blood supply, continues to grow at a more normal rate.

Bulging of the abnormally shaped red blood cells in sickle cell anemia typically causes focal ischemia and infarction in multiple tissues. Bone infarcts commonly occur in infants and children. They most frequently involve the small bones of the hands and feet, producing an irregular area of bone destruction with overlying periosteal calcification, which may be indistinguishable from osteomyelitis. In older children and adults, bone infarction may initially appear as an ill-defined lucent area that becomes irregularly calcified.

Acute osteomyelitis, often caused by Salmonella infection, is a common complication in sickle cell disease. The resulting lytic destruction and periosteal reaction may be extensive, often involving the entire shaft and multiple bones (Figure 9-7). Radiographically, it may be impossible to distinguish between osteomyelitis and bone infarction without infection (Figure 9-8).

Throughout their lives, patients with sickle cell anemia are plagued by recurrent painful crises. These episodes are attributable to recurrent vasoocclusive phenomena and may appear with explosive suddenness and attack various parts of the body, especially the abdomen, chest, and joints. It is often difficult to distinguish between a painful sickle cell crisis and some other type of acute process, such as biliary colic, appendicitis, or a perforated viscus. In the extremities, a sickle cell crisis may mimic osteomyelitis or an acute arthritis, such as gout or rheumatoid arthritis.

The most common extraskeletal abnormality in the hemolytic anemias is cardiomegaly caused by severe anemia and increased cardiac output. The heart has a globular configuration, reflecting enlargement of all chambers. Increased pulmonary blood flow produces engorgement of the pulmonary vessels, giving a hypervascular appearance to the lungs. Pulmonary infarction, pulmonary edema with congestive failure, and pneumonia are frequent complications.

Renal abnormalities can be demonstrated by excretory urography in about two thirds of patients with sickle cell disease. A serious complication is renal papillary necrosis (see Figure 6-21), which is probably related to vessel obstruction within the papillae and may produce sinuses or cavity formation within one or more papillae.

Treatment: The cause and type of hemolytic anemia must be determined to successfully begin treatment. For spherocytosis, a splenectomy is curative.

For sickle cell anemia, no cure currently exists. Therefore, treatment consists of management and control of symptoms. The most invasive treatment, bone marrow transplantation, offers a possible cure. During a crisis, bed rest, maintenance of oxygen levels to prevent sickling, folic acid to aid in red blood cell production, maintenance of fluids to keep electrolyte balance stable, and possible blood transfusion (of packed red blood cells) are appropriate. In some cases, prophylactic antibiotics are given. Gene therapy requires removing a defective cell, fixing the gene, and replanting the new cell into the bone marrow. This procedure may help manage and control symptoms and, in some cases, may even provide a cure.

If an Rh-negative mother delivers or aborts an Rh-positive infant, she is given a vaccine of Rh immunoglobulin within 24 hours to prevent the production of antibodies against the Rh factor. Blood testing to determine whether Rh incompatibility exists is now an essential part of prenatal care. An Rh-positive baby born to an Rh-negative mother receives a blood transfusion within 24 hours after birth.

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Apr 10, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Endocrine System

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