An RBC’s life span is approximately 120 days, and an important waste product of RBC death is bilirubin. Bilirubin binds with albumin for transport to the liver cells to conjugate with glucuronide, forming direct bilirubin. Because unconjugated bilirubin is fat-soluble and can’t be excreted in urine or bile, it may escape to extravascular tissue, especially fatty tissue and the brain, resulting in hyperbilirubinemia and skin that appears icteric (or jaundiced). Too much bilirubin may result in brain damage—a condition known as kernicterus. In newborns, the normal range of bilirubin levels are determined by the baby’s age in hours. For instance, an infant who is 48 hours old will have a different range of acceptable levels than does an infant who is 96 hours old. Other things that may place a newborn at risk for hyperbilirubinemia are being born premature, having a sibling who has had hyperbilirubinemia, or having a blood group incompatibility with the mother (such as the mother having an O+ blood type and the baby having an A+ blood type).

Oxygen is carried in the cell in a protein (globin) and iron (heme) structure known as hemoglobin. If adequate amounts of iron aren’t available, the protein structure can’t be formed and RBCs can’t carry their normal amount of oxygen. Lead can also replace iron in the molecule, causing toxicity.

Granulocytes include:

Agranulocytes include:

Lymph nodes filter foreign invaders, such as viruses and bacteria, and can serve as waiting stations for lymphocytes that might be needed in that area to fight infection.

In children, the lymphatic system grows rapidly between ages 3 and 6 years. At this age, slightly swollen (less than 0.5 cm) lymph nodes in the neck and groin areas are common. Lymph nodes that should cause concern are:

Parents of a 3- to 6-year-old child will commonly report that he snores. Snoring at this age is usually due to the enlarged tonsils partially obstructing the airway during sleep.

These antibodies then travel in the blood and lymph, which circulate throughout the body. When the antibodies find the antigen, they bind to it to tag it so other immune system cells can destroy it.

Some antibodies are proteins that perform special functions and are called immunoglobulins. There are five types of immunoglobulins (Igs) produced by B cells:

IgA defends external body surfaces and is present in colostrum, saliva, tears, and nasal fluids as well as respiratory, gastrointestinal (GI), and genitourinary secretions (neonates have small amounts of this Ig and are more susceptible to an overgrowth of organisms in mucous membranes such as oral Candida).

IgD is found on the surface of B cells and functions in controlling lymphocyte activation or suppression.

IgE is the antibody responsible for hypersensitivity reactions; it has an immediate response to an antigen and stimulates the release of heparin and histamine from mast cells.

IgG makes up the majority of plasma antibodies and is the main antibacterial and antiviral antibody; transfusions of IgG specific for viral diseases, such as varicella (chickenpox), are useful in treating children who are exposed but have decreased immune function (such as those on chemotherapy).

IgM is the first Ig produced during an immune response; because it’s very large, IgM is usually seen only in the blood and can’t pass into tissues to fight infections.

Different types of T cells work together to create the best immune response possible. Helper T cells (CD4⁺ cells) stimulate B cells to mature into plasma cells that produce Igs to fight antigens and to also remember them if they occur again in the future.

The helper T cells also help the killer T cells (CD8⁺ cells) to more readily recognize the antigen and attack directly. Killer T cells bind to the surface of the invading antigen and disrupt the cell membrane, causing the antigen’s destruction.

IgE is produced in sufficient quantities only with repeated exposure and, therefore, may have little effect with occasional allergic reactions. Because severe reactions may not occur with the first exposure to a drug or allergen, the body may only produce antibodies, which will react with the second exposure. In severe reactions, anaphylaxis may occur, resulting in respiratory and cardiac arrest. Someone may not react to an antibiotic the first time—even if they are allergic—but react the second or third time.

Binding of an antigen and an antibody activates the complement system, which ultimately disrupts the cellular membranes, causing cell death. Cytotoxic T cells and NK cells also contribute to tissue death in type II hypersensitivity. Examples of type II hypersensitivity include transfusion reactions and hemolytic disease in the neonate.

Autoimmune disorders are caused by type III reactions in which the immune complexes have difficulty distinguishing between normal and abnormal tissue and may attack both. These disorders include systemic lupus erythematosus (SLE), juvenile rheumatoid arthritis, and glomerulonephritis.

T cells function by releasing lymphokines, which recruit and activate other lymphocytes, monocytes, macrophages, and polymorphonuclear leukocytes. The coagulation (kinin) and complement pathways also contribute to tissue damage in this type of reaction. The most serious reactions occur with transplantation when the transplanted tissue is perceived as foreign and attacked. Type IV reactions also occur with exposure to plants or substances that trigger a response resulting in contact dermatitis.

Allergy shots run the risk of causing an anaphylactic reaction, and the nurse should be prepared to provide emergency care. The child should remain in the facility for at least 15 minutes after the shot to be monitored for an injection site reaction and signs of an impending anaphylactic reaction.

Bone marrow aspiration or biopsy can be performed under light general anesthesia or with a local injection to numb the area. An oral or intravenous (I.V.) sedative may be given before the procedure. Prepare the child for the test with an age-appropriate explanation, and monitor for sedation or adverse effects of anesthesia. Tell the child that a parent may stay with him during the test.

In addition, follow these steps:

Prepare the child for venipuncture and allow the parent to be present to comfort the child. After the venipuncture, monitor the site for signs of continued bleeding.

Prepare the child and his parents for the procedure. Reassure the parents (and the child, if old enough) about the measures that are taken to ensure the safety of transfused blood products.

In addition, follow these steps:

The donor and the recipient should be prepared for the procedure with age-appropriate explanations. In addition, follow these steps:

Because HIV becomes part of the cell, the body’s normal defense mechanisms (from the immune system) don’t recognize it as foreign, and the virus goes unchallenged.

From the first single cell, the virus replicates and then enters other cells, eventually infecting several cells and rendering them nonfunctional. When a large number of cells become infected, the normal ability to control common organisms is compromised, and the person develops AIDS.

The mode of transmission in children has always been different from that in adults. Although transmission in adolescents may occur from sexual contact or I.V. drug use, these issues aren’t common factors in transmission to the younger child. Potential sources of infection in children include:

HIV has a particular affinity for the CD4⁺ helper T cell as well as monocytes and macrophages. The virus invades these cells and renders them nonfunctional, resulting in suppressed cell-mediated and humoral immunity. The degree of immunosuppression will progress and, eventually, result in opportunistic infection and even death.