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ЗмістThe basic theoretical items of information
The child with a problem related to the formed elements of the blood
Origin of formed elements
Characteristics of peripheral blood of children of different age
During visual inspection detect evidence of
Laboratory blood tests
White Blood Cell Differential Count
Semiotics of main syndroms
Schonlein-Henoch disease (hemorrhagic vasculitis)
Syndrome of leucocytosis
Classification based on Hb level.
Pathophysiology and clinical manifestations
Morphology and cytochemical markers.
French-American-British (FAB) system.
Immune system in infancy and in toddlers. embryology of immune system and congenital immunodeficiency. immunologic deficiency di
Bukovinian State Medical University
Department of Developmental Pediatrics
to the practical class for medical students of 3-rd years
Modul 1: Child’s development
Subject: THE ANATOMICAL AND PHYSIOLOGICAL PECULIARITIES OF BLOOD SYSTEM IN CHILDREN OF DIFFERENT AGE GROUPS. SEMIOTICS OF MAIN SYNDROMS.
It is completed by:
MD, MSc, PhD Strynadko Maryna
Chernivtsy – 2007
SUBJECT: Developmental Pediatrics.
BASIC LEVEL: Basic knowledge of pediatrics.
INTEGRATED SKILL ACTIVITY:
1. Care of the children. 2. Anatomy. 3. Histology. 4. Pysiology.
STUDENT’S PRACTICAL SKILLS:
During embryonic development the blood cell formation goes through 4 stages because different organs, such as, liver and spleen, serve as main sites of hematopoiesis (see Fig.1).
Fig.1. Stages of hematopoiesis during embryonic development.
1. On the 16th-20th day since fertilization, first blood cells -primitive megaloblasts - appear in the blood islands of yolk sac. These cells contain primitive Hb P, which very soon is changed by fetal Hb F that is main in fetus. Synthesis of adult Hb A begins on the 3rd week of gestation, but by the end of intrauterine existing its amount reaches only 30-40 % from the total Hb level.
2. By the end of the 6th week first blood cells migrate to the liver - it is the beginning of hepatic stage of hematopoiesis, which gets its maximum on the 5th month of gestation and goes to end by the term of birth. During this period the liver produces:
• megaloblasts - the initial cells of erythrocyte series;
• neutrophyles - granulocytic series;
• megakaryocytes - thrombocytic series.
3. The spleen serves as hemopoietic organ from the 3rd till the end of the 5th month and produces:
4. Starting from the 4th month the red bone marrow begins to function as blood-forming organ. By the end of intrauterine life it remains the only hemopoietic organ for the whole life (except for some pathological conditions).
Disorders related to the blood and blood-forming organs in childhood encompass a wide range of diseases and pathologic states. Since the blood is a multipurpose fluid involved in the functions of so many tissues and organs, either primary or secondary changes in the blood are reflected in the essential functions of these structures.
Disorders of blood and blood-forming organs in childhood include the anemias, defects in hemostasis, and the immunologic deficiency diseases. Neoplastic disorders of the hematopoietic system are also discussed.
Blood is composed of two components:
• a fluid portion called plasma;
• a cellular portion known as the formed elements of the blood.
The two components are approximately equal in volume. Plasma is about 90% water and 10% solutes.
The principal solutes are the proteins: albumins, globulins and fibrinogen.
The cellular elements are red blood cells (erythrocytes), white blood cells (leukocytes), and platelets (thrombocytes).
The major blood-forming (hemopoietic) organs of the body are the red bone marrow (myeloid tissue) and lymphatic system. All of the formed elements of the blood, except to some extent the agranulocytes, are believed to be formed in myeloid tissue during postnatal life. During embryonic development the mesenchyme, spleen, liver, thymus, and yolk sac serve as additional sites of blood cell formation. In certain blood disorders these sites, particularly the spleen, can be stimulated to produce blood cells, and constitute extramedullary hematopoiesis.
In infants and young children all of the bones contain red marrow (so-called because of its color from formation of erythrocytes), but as bone growth ceases near the end of adolescence, only the ribs, sternum, vertebrae, and pelvis continue to produce blood cells. The remainder of the bone marrow becomes yellow from deposition of fat. However, in conditions of increased demand for blood cells, the yellow marrow can revert to red marrow as another hemopoietic source.
Although the progressive development of each blood cell is fairly well delineated, there is considerable controversy regarding the origin of the blood cell. One of the most widely held theories (monophyletic) is that each blood cell originates from a primordial (primitive) cell called a blast, or stem, cell. This hemocytoblast in turn gives rise to the erythroblast, myeloblast, monoblast, lymphoblast, and megakaryoblast.
Another system that is involved in blood cell production is the reticuloendothelial system. Although not a discrete anatomic entity, it refers to widely dispersed cells of mesodermal origin that line the vascular and lymph channels. These cells, called reticular cells because they form a network, are capable of phagocytosis (ingestion and digestion of foreign substances), formation of immune bodies, and differentiation into other cells, such as hemocytoblasts, myeloblasts, or lymphoblasts.
In newborn children:
• Smaller than in adults general volume of blood;
• Higher than in adults relative blood volume;
• Erythrocyte level - 6-7 x 1012/ L;
• Anisocytosis (presence of different forms of RBCs inside vessels);
• Short life of erythrocytes (12-40 days);
• High hemoglobin level - 180-240 g/L;
• Color index (CI) - 1,1-1,3 (degree of saturation of Hb in one erythrocyte);
• Level of HbF- 60-70 %;
• Erythrocyte sedimentation rate - 0-2 mm/hour;
• Leucocytosis - 11-33 x 109/ L;
• Presence of extramedullar sources of hemopoiesis.
• Decreasing of Hb level to 120-110 g/1;
• Erythrocyte level decreases to 4-3.5 x 1012/l;
• Colour index is often less than 1.0 (0.8-0.7);
• Leucocytosis (10-12 x 109/l) appears after adding new food in menu, during crying, after strong emotions;
• First cross of WBC count at 5 days of age;
• Thrombocytes have gigantic forms;
• Monocytosis 9-11 %;
• Reticulocyte count is up to 10 %.
Peculiarities of blood in children older 1 year
• Increasing of Hb level to 130-140 g/1 up to 15 years;
• Erythrocyte level is 4.5-5.0 x 1012/L;
• Reticulocytes are about 0.5-5 %;
• Leucocyte level is 7 - 9 x 109 /L;
• Second white blood cross in 5 years of age.
Patients complaints and methods of physical examination
Disorders of hematological system as a rule give a lot of complaints, hich are common to other systems. But there some weighty clinical gns that directly show on blood disorders. They are:
• hemorrhage (bleeding);
• enlargement of lymph nodes;
• ossalgia (pain in bones).
The other complaints are hyperthermia, often headaches, dizziness, light-headedness, slowed thought processes, decreased attention span, apathy, shortness of breath, easy fatigability. During taking health history detail the information about appearance of all symptoms, their changes, date of last blood count, blood type, recent transfusions; take careful diet history to identify any deficiencies, evidence of pica -eating clay, ice, paste. In young children pay attention to obstetric and perinatal history. Accurate family history taking can give the information about cases of sickle cell disease or hemophilia in relatives.
• prolonged bleeding anywhere from or in the body, its intensity and duration;
• skin color:
— paleness: waxy pallor can be seen in severe anemia, quick development of paleness is evidence of profuse inner bleeding;
— jaundice (yellowish discoloration of skin): bright yellow or orange in case of indirect hyperbilirubinemia, greenish or muddy yellow in conjugated (direct);
— cherry red in polycytemia.
• skin rash (macula, petechia, purpura, teleangiectasis, haemorrhage, ecchymose (bruise), haematoma, and hemarthrosis).
• enlarged lymph nodes;
• protrusion of the abdomen (hepatosplenomegaly);
Palpation and percussion can give the information about sizes, shape, consistency, painfulness and mobility of liver, spleen and lymph nodes.
Complex of diagnostic tests and procedures
1. Common blood analysis (RBC count, Hb level, colour index (CI, mean corpuscular Hb concentration), erythrocyte sedimentation rate (ESR), WBC count, platelet count).
3. Coagulation tests (partial thromboplastin time, prothrombin time (PT), thrombin time, concentration of fibrinogen in plasma).
4. Bleeding time, clotting time (Lee-White, Burker).
5. Tourniquet test (capillary fragility).
6. Type and crossmatch.
7. Concentration serum iron, iron-binding capacity (TIBC).
8. Serum bilirubin levels, Coombs test.
9. Sickle turbidity, Hb electrophoresis.
10. Determination of specific coagulation factors deficiency.
11. Ultrasound investigation of spleen, liver, lymph nodes.
13. Biopsy of red marrow.
Type and Crossmatch
Blood typing determines the ABO and Rh blood groups of a blood sample. A crossmatch tests for agglutination reactions between donor and recipient blood.
Complete Blood Count
The complete blood count consists of the following: red blood cell count, hemoglobin measurement (grams of hemoglobin per 100 ml of blood), hematocrit measurement (percent volume of erythrocytes), and white blood cell count.
The white blood cell differential count determines the percentage of each type of leukocyte.
WBC Differential Count
• Decreasing of Hb level (lower than 100 g per litre).
• Decreasing of erythrocyte level (lower 4 x lO^/L).
• Paleness of the skin and mucous membranes.
• Often headaches.
• In the area of the heart - systolic murmur is often found during auscultation.
• Children of the first 3 years of life, as a rule, have iron deficiency anaemias.
Hemorrhagic spots on surface of the skin, petechiae, purpura, teleangiectasis, and hemorrhages. These signs are present not only on the skin, but in subcutaneous fat, muscles, brain, too. The hemorrhagic syndrome is usual in case of inherited thrombocytopenic purpuras, neonatal thrombocytopenic purpuras. The other sings of this syndrome are bleeding, hematuria, upper and lower gastrointestinal tract hemorrhage, prolonged bleeding from the umbilical stump or from veni punctures, intracranial hemorrhage.
Initial investigation should include a platelet count, blood smear, routine blood count, detection of antibodies of platelets.
The examples of this syndrome are present in such diseases as haemophilia, thrombocytopenias (congenital and acquired), and Schonlein-Henoch disease.
This disease is connected with enlarged coagulation of blood in the small vessels due to their inflammation. The main clinical signs are:
• Abdominal pain (colicky and quite severe), vomiting and melena;
• Palpable purpuric rash. more often localized on the lower extremities;
• Increase of coagulation in blood;
• All these symptoms appear after 1 or 2 weeks after the provocation factor (throat infection, influenza, vaccinations).
The main course of this syndrome is enlarged ruining of red blood cells inside vessels. This leads to increasing of free hemoglobin in plasma.
Transferring of hemoglobin usually takes place in the liver. But in case of hemolytic syndrome in children 2 factors - immature ferment systems of liver and significantly increased level of free hemoglobin - result in further metabolism of hemoglobin in plasma that leads to increasing of bilirubin and developing of jaundice (yellowish discoloration of mucous membranes and skin). Another signs are: fever, decreasing of red blood cells, leucocytosis, microspherocytes, anisocytosis, enlargement of liver and spleen.
It is increasing of leucocyte level more than 10 x 109 per litre. Neutrophile leucocytosis develops during inflammation processes
(sepsis, meningitis, pyelonephritis). Very high level of leucocytes we
have in children with leucosis.
Anemia is defined as reduction of red cell volume or hemoglobin concentration to levels below normal. It is an indication or manifestation of an underlying pathologic process or disease. The anemias are the most common hematological disorders of infancy and childhood. This discussion is primarily concerned with an overview of the classification of anemia. Specific anemic conditions such as iron-deficiency anemia and aplastic anemia are discussed elsewhere. Later in this chapter the hemoglobinopathies sickle cell anemia and thalassemia are discussed.
Laboratory criteria of anemia in neonatal period:
• 0 - 14 days - Hb level less than 145 g/1;
• 15-28 days - Hb level less than 120 g/1.
The basic physiologic defect caused by anemia is a decrease in the oxygen-carrying capacity of blood and consequently a reduction in the amount of oxygen available to the tissues. Most of the clinical manifestations are directly attributable to tissue hypoxia. Muscle weakness and easy fatigability are common, although children seem to have a remarkable ability to function q uite well despite low levels of hemoglobin.
The skin is usually pale to a waxy pallor in severe anemia. Cyanosis is typically not evident, because it is the result of the quantity of deoxygenated hemoglobin in arterial blood. Hemoglobin levels generally must exceed 5 g/dl before cyanosis is evident. Anemia is caused by decreased hemoglobin and/or red blood cells, not inadequate oxygen saturation of existing hemoglobin. The doctor should also keep in mind that skin pigmentation can alter one's assessment of skin pallor.
Central nervous system manifestations include headache, dizziness, light-headedness, irritability, slowed thought processes, decreased attention span, apathy, and depression. Growth retardation resulting from decreased cellular metabolism and coexisting anorexia is a common finding in chronic severe anemia. It is frequently accompanied by delayed sexual maturation in the older child.
The effects of anemia on the circulatory system can be profound. A reduction in hemoglobin concentration that results in decreased oxygen-carrying capacity of the blood is associated with a compensatory increase in heart rate and cardiac output. Initially this greater cardiac output compensates for the lower oxygen-carrying capacity of the blood, since blood replenished with oxygen returns to the tissues at a faster than normal rate.
Several tests can be used to estimate the levels of RBC and hemoglobin. These are routine hematological laboratory procedures.
Leukemia, cancer of the blood-forming tissues, is the most common form of childhood cancer. However, even for the child with the most favorable prognosis, leukemia presents innumerable physical, emotional, financial, and familial stresses. Nurses in the hospital, clinic, physician's office, and community can do much to prevent some problems and lessen others.
"Leukemia" is a broad term given to a group of malignant diseases of the bone marrow and lymphatic system. Current research has revealed that it is a complex disease of varying heterogenity. Consequently classification has become increasingly more sophisticated and essential, since identification of the subtype of leukemia has therapeutic and prognostic implications. The following is an overview of the morphologic, cytochemical, and immunologic characteristics of the leukemias.
^ Leukemia is classified according to its predominant cell type and level of maturity, as described by the following:
Lympho - for leukemias involving the lymphoid or lymphatic system. Myelo - for those of myeloid (bone marrow) origin Blastic and acute - for those involving immature cells Cytic and chronic - for those involving mature cells .In children two forms are generally recognized: acute lymphoid leukemia (ALL) and acute nonlymphoid (myelogenous) leukemia (ANLL or AML). Synonyms for ALL include lymphatic, lymphocytic, lymphoblastic, and lympho-blastoid leukemia. Usually the term "stem cell" or "blast cell leukemia" also refers to the lymphoid type of leukemia. Synonyms for the ANLL type include granulocytic, myelo-cytic, monocytic, myelogenous, monoblastic, and mono-myeloblastic. There are also much rarer forms of leukemia that are named for the specific cell involved, such as basophilic or eosinophilic leukemia.
Because of the confusion and inconsistency in classifying the leukemias, acute lymphoblastic and acute nonlymphoblastic leukemias are further subdivided according to another system known as the ^ In the FAB system the subtypes are determined after a thorough study of the morphology (structure) and cytochemical reactivity of the leukemic cells. Accordingly, ALL is subdivided into 3 types. Li stands for lymphoblastic leukemia, child type, which accounts for 80% to 85% of all childhood leukemias and has the best prognosis. ANLL is classified into 7 types and comprises 10% to 20% of the leukemias in children. The types with the best prognoses are Mi, acute myelocytic leukemia without differentiation, and Mz, acute myelocytic leukemia with differentiation (Kobrinsky, Robinson, and Nesbit, 1980).
The various cells also demonstrate different reactions when they are exposed to certain chemicals. For example, lymphoblasts show no reactivity to Sudan black stain and perioxidase, whereas myeloblasts demonstrate reactivity to both.
Another important differentiation between the cell types is the absence or presence of Auer rods, granules containing RNA that appear in the cytoplasm of affected myeloblasts and promyelocytes. Their presence is a strong diagnostic indicator for certain types of ANLL and is associated with improved prognosis.
1. Nursing care of Infants and Children / editor Lucille F. Whaley and I. Wong. Donna L. - 2nd ed. - The C.V. Mosby Company. - 1983. - 1680 p.
2. Nelson Textbook of Pediatrics / edited by Richard E. Behrman, Robert M. Kliegman, Ann M. Arvin; senior editor, Waldo E. Nelson - 15th ed. -W.B.Saunders Company, 1996. - 2200 p.
Immunologic deficiency disorders
To understand immunologic deficiency disorders and their serious, often life-threatening consequences, it is helpful to review the normal functioning of the immune system. In simple terms the function of the immune system is to recognize "self" from "non-self" and to initiate responses to eliminate the "non-self" or the foreign substance known as antigen. However, the specific processes involved in this function are complex and interrelated. The following is a review of the major responses.
The immune system includes the primary lymphoid organs (thymus, bone marrow, and probably liver) and the secondary lymphoid organs (lymph nodes, spleen, and gut-associated lymphoid tissue). The functions of the immune system are basically two types:
nonspecific and specific. Nonspecific immune defenses are activated on exposure to any foreign substance but react similarly regardless of the type of antigen; they are unable to identify the antigen. The principal component of this system is phagocytosis, the process of ingesting and digesting foreign substances. Phagocytic cells are composed of neutrophils and monocytes.
Specific defenses are those that have the ability to recognize the antigen and respond selectively. The components of adaptive immunity are humoral immunity and cell-mediated immunity. The cells responsible for these two forms of immunity are the lymphocytes, specifically B-lymphocytes and T-lymphocytes.
Humoral immunity is involved with antibody production and complement. The principal cell involved in antibody production is the B-lymphocyte. In humans the exact site of production of the B-lymphocyte is speculative, although it is probably the bone marrow. In chickens the site is clearly identified as a hind-gut organ known as the bursa of Fabricius, hence the term "B-lymphocyte," or "B-cell." When challenged with an antigen, B-cells divide and differentiate into plasma cells. The plasma cells produce and secrete large quantities of antibodies specific to the antigen. Five classes of antibodies or immunoglobulins (Ig) have been identified: G, M. A, D, and E, each serving a specific function .
On initial exposure to an antigen, the B-lymphocyte system begins to produce antibody, predominantly IgM. which appears in 2 to 3 days. This process is referred to as the primary antibody response.
With subsequent exposure to the antigen, a secondary antibody response occurs. Antibody, chiefly IgG, is produced in much greater quantities within 1 to 2 days. An example of the secondary response is consecutive administration of immunizations, often called boosters. Memory B-cells allow the immune system to recognize the same antigen for months or years.
When antibody reacts with antigen, they bind to form an antigen-antibody complex. This binding serves several functions. Antibody aids in the phagocytosis of antigen by sensitizing it in such a manner that it is more readily destroyed by phagocytes, a process known as opsonization.
Antibody also activates or fixes complement, the second component of humoral immunity. The complement system is a series of nine major factors (Cl and C9) present in serum that results in a cascade of enzymatic actions and death of a viable antigen. It also serves to bridge cellular and humoral immunity. After being activated by antibody, complement produces a chemotactic factor that summons T-lymphocytes and macrophages to the antigen site.
Cell-mediated immunity is involved in a variety of specific functions mediated by the T-lymphocyte. The T-lymphocyte is so named because it passes through the thymus during the differentiation process, which leads to the mature T-cell. T-lymphocytes do not carry typical immunoglobulins on their surfaces as do the B-cells. However, they are functionally heterogenous in that several subsets have been identified, including cytotoxic T-cells, memory T-cells. helper T-lymphocytes. and regulator T-lymphocytes.
Specific functions of T-lymphocytes include: protection against most viral, fungal, and protozoan infections and slow-growing bacterial infections, such as tuberculosis, rejection of histoincompatible grafts, mediation of cutaneous delayed hypersensitivity reactions, such as in tuberculin testing, and probably immune surveillance for malignant cells. In addition, they also have regulatory functions within the immune system. For example, helper T-lymphocytes assist B-lymphocytes and other types of T-cells to mount an optimum immune response.
The cellular immune response is initiated when a T-lymphocyte is sensitized by antigen. In response to this contact the T-cell releases numerous humoral factors called lymphokines, which eventually bring about death of the antigen. For example, chemotactic factor promotes the migration of phagocytes and other T-lymphocytes to the antigenic area, migratory inhibitor factor prevents their leaving the site, transfer factor transforms nonsensitized T-cells into sensitized T-lymphocytes, blastogenic factor initiates the rapid mitosis of sensitized T-cells, and macrophage activation factor transforms local macrophages to highly phagocytic cells. Another lymphokine is interferon, which nonspecifi-cally inhibits viral replication, promotes phagocytosis, and stimulates the killer activity of sensitized lymphocytes.
The immunologic properties of the mucosal lining of the gastrointestinal tract are immature, which predisposes this system, like the respiratory system, to increased risk of infection and inflammation.
The immunologic system undergoes numerous changes during the first year. The newborn receives significant amounts of maternal IgG, which confers immunity for about 3 months against antigens to which the mother was exposed. During this time the infant begins to synthesize his own IgG, and about 40% of adult levels are reached by 1 year of age. Significant amounts of IgM are produced at birth, and adult levels are reached by 9 months of age. The production of IgA, IgD, and IgE is much more gradual, and maximum levels are not attained until early childhood.
The defense mechanisms of the tissues and blood, particularly phagocytosis, are much more efficient in the toddler than in the infant. The production of antibodies is well-established. Immunoglobulin G (IgG), which neutralizes microbial toxins, reaches adult levels by the end of the second year of life. Passive immunity from maternal transfer disappears by the beginning of toddlerhood, necessitating the use of artificial immunizations. Immunoglobulin M (IgM), which responds to artificial immunizing techniques and combats serious infection, attains adult levels during late infancy. Immunoglobulins A, D, and E increase gradually, not reaching eventual adult levels until later childhood. Many young children demonstrate a sudden increase in colds and minor infections when entering nursery school or kindergarten because of the exposure to new antigens.
The Wiskott-Aldrich syndrome is an X-linked recessive disorder characterized by a triad of abnormalities: thrombocytopenia, eczema, and immunodeficiency of selective functions ofB- and T-lymphocytes.
The exact defect is unknown, although recent evidence suggests a basic hematopoietic cell abnormality specifically elated to cell energy metabolism. A variety of pathologic findings are evident. The platelets are abnormally small in size and have a shortened life span, possibly because of a metabolic defect in their synthesis. The primary immunologic defect consists of the inability of phagocytes (macrophages) to process foreign antigens, particularly polysaccharides such as pneumococcus. As a result, immunologically competent cells fail to produce normal immunoglobulin patterns. Early in life the immuno-globulin levels may be normal, but later low levels of IgM are observed. Typically isohemagglutinins (anti-A and anti-B agglutinins in the blood) are decreased or absent.
The thymus and lymph nodes are normal at birth but become progressively dysfunctional with age until a profound cellular immunodeficiency results. Consequently these children are highly susceptible to iniection and malignancy, especially of the lymphoreticular system.
At birth the major effect of the disorder is bleeding because of the thrombocytopenia. As the child grows older, recurrent infection and eczema become more severe and the bleeding becomes less frequent.
Eczema is typical of the allergic type and readily becomes superinfected. Chronic infection with herpes simplex is a frequent problem and may lead to chronic keratitis of the eye with loss of vision. From infection, chronic pulmonary disease, sinusitis, and otitis media result. In those children who survive the bleeding episodes and overwhelming infections, malignancy presents an additional risk to survival.
Diagnosis can usually be made during the neonatal period because of the thrombocytopenia. Specific tests for immunologic function confirm the diagnosis. Carrier detection is also possible.
Medical treatment mainly involves (1) counteracting the bleeding tendencies with platelet transfusions, (2) using immune globulin to provide passive immunity, and (3) administering prophylactic antibiotics to prevent and control infection. Bone marrow transplants have been attempted but, even if successful, do not reverse all the defects of this disorder. Overall median survival is only to 6.5 years of age, with death most often resulting from infection (pneumonia or sepsis) or bleeding.
Because of the grave prognosis for these children, the main nursing consideration is supporting the family in the care of a fatally ill child. Physical care is directed at controlling the problems imposed by the disorder - control bleeding, preventing or controlling infection, treat eczema.
The genetic implications of this X-linked recessive disorder differ little from those of hemophilia. However, because of the multiplicity of defects, the emotional adjustment and physical care required for these children are greater than those of many other conditions. The nurse can be especially supportive by providing short-term goals during periods of hospitalization and by focusing on long-range needs through coordinated efforts with a public health nurse.
One of the most dramatic advances in pediatrics has been the decline of infectious diseases over the past 30 years because of the widespread use of immunization for preventable diseases. Although many of the presently available immunizations can be given to individuals of any age, the recommended primary schedule begins during infancy and, with the exception of boosters, is completed during early childhood. Therefore, the discussion of childhood immunizations for diptheria, tetanus, pertussis, polio, measles, mumps, and rubella is included under health promotion during the first year.
In order to facilitate one*s understanding of immunization, the following terms are defined for reference throughout the next section:
• immunity: an inherited or acquired status in which an individual is resistant to the occurrence or the eiiects ol a specific disease, particularly an infectious agent.
• natural immunity Innate immunity or resistance to infection or toxicity.
• acquired immunity: immunity from exposure to the invading agent, either bacteria, virus, or toxins.
• active immunity: individual actively forms immune bodies against specific antigens, either naturally by his having had the disease clinically or subclinically or articifically by the introduction of an antigen (vaccine) into the individual.
• passive immunity: temporary immunity by transfusing plasma proteins either artificially from another human or an animal that has been actively immunized against an antigen or naturally from the mother to the fetus via the placenta.
• antibody: a protein found mostly in serum that is formed in response to exposure to a specific antigen.
• antigen: a variety of foreign substances, including bacteria, viruses, toxins, and foreign proteins that stimulate the formation of antibodies.
• antitoxin: antibody formed in response to a toxin (antigen).
• toxin: a poisonous substance usually produced by the invading microorganism.
• toxoid: a toxin that has been treated to destroy its toxic properties but retain its antigenic quality.
• vaccine: collectively a term to denote any type of active immunization, such as toxoids or attenuated live viruses;
specifically a suspension of disease-causing bacteria or viruses that acts like an antigen, stimulates antibody production, and produces active acquired immunity.
• attenuate: reduction of the virulence (infectiousness) of a pathogenic microorganism by such measures as treating it with heat, chemicals, or cultivating it on a certain media. Immunodeficient conditions, or deficiency of immune response, include a wide group of independent diseases (nosologic forms) and concomitant syndromes with such common signs as deficiency of the immune system, inability of an organism to resist an alien antigens* agression.
AIDS is caused by human immunodeficiency virus (HIV) of type 1 (HIV-1). HIV-1 infects CD4+ T-lymphocytes predominantly. Depletion of CD4+ lymphocytes results in immunodeficiency.
The clinical picture of AIDS is the final phase of HIV infection and its manifestation, with a wide spectrum of clinical disorders. The majority of them is nonspecific.
Children with HIV infection present to the ED with a wide spectrum of initial presentations and associated complications. Many who live in chaotic social environments use the ED as their primary source of medical care. The typical case of pediatric HIV infection is a child born to a mother at risk who develops recurrent bacterial infections, thrush, failure to thrive, lymphadenopathy, and hepatosplenomegaly in the first few years of life. However, both those who acquire HIV perinatally and those who acquire infection by transfusion may not present with symptoms until several years of age.
The types of infections are similar to those in patients with hypogammaglobulinemia. Infections with the encapsulated organisms, Haemophilus influenzae type B, Streptococcus pneumoniae, and enteric gram-negative rods are common and can cause chronic or recurrent otitis media, pneumonia, lymphadenitis, bacteremia, mastoiditis. and meningitis. Malignant external otitis, a disease usually seen in older patients, also occurs. Other common conditions include dermatitis, particularly eczema; in those patients Staphylococcus aureusts also an important pathogen. Salmonella infections can be q uite severe and may cause prolonged gastroenteritis or bacteremia; freq uent relapses may occur.
Many of the usual childhood infections are seen in HIV-infected patients, but they may present in a more severe form. Oral candidiasis (thrush) is extremely common, particularly in infancy. HIV-infected patients often have extensive thrush, in the absence of previous antibiotic therapy. Infection may extend to the esophagus or the larynx and is resistant to the " usual forms of therapy. Viral diseases such-as herpes simplex, varicella, and measles can be quite aggressive in HIV-infected children. Herpes simplex may cause prolonged or recurrent ulcerations and varicella may disseminate to cause pneumonia.
A unique feature in pediatric HIV infection is the development of parotitis. This can be chronic, with slow progressive, painless growth, or it can be acute, xiated with rapid enlargement, fever, and pain. The etiology is unknown.
Pulmonary infection is a common and serious manifestation of HIV infection. The most commonly diagnosed infection is Pneumocystis carinii pneumonia (PCP), which can present acutely with respiratory distress or with a history of progressive cough and respiratory symptoms over days to weeks. Clinically, it may be difficult to distinguish PCP from more typical causes of childhood pneumonia. The chest X-ray typically shows a diffuse interstitial pneumonitis, although almost every pattern of infiltrate has been seen with PCP.
A second common pneumonitis is lymphoid interstitial pneumonitis (LIP); the cause is unknown. Children with LIP often have a longstanding history of pulmonary symptoms, particularly cough. They are usually not febrile or acutely dyspneic, and rarely have significant auscultatory findings. A concomitant infection can cause a child with pre-existing LIP to present acutely. LIP is most often seen in children with other lymphoproliferative manifestations of HIV such as lymphadenopathy and parotitis; these patients may have signs of chronic pulmonary disease such as clubbing. The chest X-ray shows a diffuse interstitial infiltrate similar to that seen with PCP, but in some longstanding cases there may be a diffuse nodular pattern with widening of the superior mediastinum and hilus. LIP is currently a diagnosis of exclusion.
In addition to PCP and UP, other routine and opportunistic infections must be considered in an HIV-infected child with respiratory distress. Bacterial pathogens are frequent. Another common pathogen is respiratory syncytial virus (RSV), an extremely common viral infection in young infants and children, which can cause giant cell pneumonia in the compromised host. Cytomegalovirus can be cultured from the lung in these patients, although it is not always clear that it is the primary pathogen. Other opportunistic pulmonary infections are also in the differential diagnosis, including atypical mycobacteria and fungi.
CNS disorders are a prominent part of the clinical spectrum of HIV infection in children. Encephalopathy, either static or progressive, is often noted. Manifestations often include acquired microcephaly, progressive motor dysfunction, loss of developmental milestones, ataxia, and extrapyramidal rigidity. Isolated seizures are unusual but may occur with a concomitant febrile illness. Focal neurologic signs are uncommon in pediatric AIDS and should suggest possible CNS lymphoma. Opportunistic infections, particularly cryptococcal meningitis, may be present in the child with CNS symptoms. However, in most series of children dying with HIV encephalopathy, opportunistic infection of the CNS is rare, and most signs and symptoms are secondary to HIV iniection o! the nervous system.
Gl illnesses, especially diarrhea, are a major problem for HIV-infected patients. Salmonella can be a persistent problem, particularly in patients with blood or mucus in the stool. Severe or prolonged diarrhea in pediatric AIDS patients also occurs with parasitic enteric pathogens, most notably Glardia lamblia, and cryptosporidium. In some instances, even after extensive evaluation, no specific etiology can be found to account for the diarrhea.
Use an aggressive diagnostic approach, because many of the acute illnesses are treatable. For example, a child with HIV infection who presents with fever is quite likely to have a bacterial infection; obtain a complete blood count (CBC), blood culture, urinalysis, and chest X-ray if there is no obvious source of fever on examination. Other imaging studies such as sinus films may be indicated. If the child has a history of neutropenia or is receiving azidothyrnidine (AZT), the absolute neutrophil count may be depressed, which would influence therapeutic decisions. The new onset of pulmonary symptoms requires a thorough evaluation. Although many of these patients may not have an easily treated form of pulmonary disease, early therapy is important. Because it is difficult to differentiate clinically the common forms of pneumonia in pediatric AIDS patients, hospitalization is often required. In such patients, the initial diagnostic tests include chest X-ray, WBC count, blood culture, and, in the appropriate epidemiologic setting, nasopharyngeal swabs for immunofluorescence or culture.
Weight loss and diarrhea may be acute or chronic and are often quite severe. In addition to routine bacterial culture, obtain stool for ova and parasites. Assess the patient's state of hydration clinically and measure serum electrolytes, blood urea nitrogen, and creatinine, since enormous fluid losses and profound electrolyte imbalances are sometimes present. CNS symptoms and physical signs will determine whether lumbar puncture or scanning is appropriate. If a spinal tap is performed, obtain more fluid than necessary to diagnose bacterial meningitis, because additional tests are often indicated, such as a culture for acid-fast organisms, viral culture, and cryptococcal antigen. If focal neurologic signs are present, arrange for a CT scan to evaluate for lymphoma or toxoplasmosis.
The treatment plan and the decision to hospitalize the patient must be made in conjunction with the family; many families want aggressive diagnostic and therapeutic plans, while others may prefer to keep medical intervention limited, with the goal of making the patient comfortable.
Consider hospitalizing HIV-infected patients with fever without\ a focus of infection, recent onset of pulmonary or CNS manifestations, or severe failure to thrive or diarrheal disease.
Patients who are not acutely ill and do not require hospitalization may require antibiotic therapy. If a focal infection is identified, such a sinusitis or otitis media, and there is no evidence of bacterernia, the patient can ordinarily be managed as an outpatient. However, a longer duration of therapy is required; for example.treat sinusitis for a minimum of 3 weeks.
In cases of possible bacterernia, the antimicrobials must be effective against the encapsulated organisms and the enteric gram-negative rods.
For any HIV-infected patient who does not require hospitalization, arrange for the necessary follow-up of the acute problem with the primary physician and make appropriate referrals for long-term management. Because of the chronic and complex nature of pediatric HIV infection, non-urgent problems are best handled in the calmer, more familiar outpatient office or clinic, not the ED.
Isolation techniques are based upon the mode of transmission of the disease.
Make a general conclusion on a theme of a class №1 and conducted practical work.
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