3: Common Childhood Illnesses/Disorders

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Part 3 Common Childhood Illnesses/Disorders

ACUTE RESPIRATORY DISTRESS SYNDROME

Description

Acute respiratory distress syndrome (ARDS) is a complex respiratory illness characterized by respiratory distress and hypoxemia that occur within 72 hours of a serious injury or surgery in a person with previously normal lungs. ARDS may occur as a result of clinical conditions and injuries such as sepsis, trauma, viral pneumonia, fat emboli, drug overdose, reperfusion injury after lung transplantation, smoke inhalation, and near-drowning.

Pathophysiology

The hallmark of ARDS is increased permeability of the alveolarcapillary membrane that results in pulmonary edema. During the acute phase of ARDS, the alveolocapillary membrane is damaged, with an increasing pulmonary capillary permeability and resulting interstitial edema. When fibrosis occurs, the child may demonstrate respiratory distress and the need for mechanical ventilation. The lungs become stiff as a result of surfactant inactivation, gas diffusion is impaired, and eventually bronchiolar mucosal swelling and congestive atelectasis occur. The net effect is decreased functional residual capacity, pulmonary hypertension, and increased intrapulmonary right-to-left shunting of pulmonary blood flow. Surfactant secretion is reduced, and the atelectasis and fluid-filled alveoli provide an excellent medium for bacterial growth. Hypoxemia is expressed as the partial pressure of oxygen (PaO₂) to fraction of inspired oxygen (FiO₂) ratio, or P/F ratio; the P/F ratio for ARDS is 200.

Clinical Signs and Symptoms

The child with ARDS may first demonstrate only symptoms caused by an injury or infection, but, as the condition deteriorates, hyperventilation, tachypnea, increasing respiratory effort, cyanosis, and decreasing oxygen saturation occur. At times the developing hypoxemia is not responsive to oxygen administration.

Diagnostic Evaluation

The criteria for diagnosis of ARDS in children are an acute antecedent illness or injury, acute respiratory distress or failure, no evidence of prior cardiopulmonary disease, and diffuse bilateral infiltrates evidenced on chest radiography.

Treatment

Treatment involves supportive measures, such as:

Maintenance of adequate oxygenation and pulmonary perfusion

Treatment of infection (or the precipitating cause)

Maintenance of adequate cardiac output and vascular volume, hydration, adequate nutritional support, comfort measures, prevention of complications, such as GI ulceration and aspiration, and psychologic support

Prone positioning may be used to improve oxygenation. The use of endotracheal intubation, positive end-expiratory pressure, and low tidal volume may be required to ensure maximum oxygen delivery by increasing functional residual capacity, reducing intrapulmonary shunting, and reducing pulmonary fluid.

Additional supportive strategies in the treatment of ARDS in children include the use of lung-protective ventilator strategies, permissive hypercapnia, inhaled nitric oxide, exogenous surfactant administration, high-frequency ventilation, partial liquid ventilation, and extracorporeal life support (extracorporeal membrane oxygenation, or ECMO).

Patient and Family Teaching

Information about child’s status

Communication techniques with intubated and mechanically ventilated child

Involvement in care of child during acute phase

Safety prevention: avoidance of conditions that may cause severe respiratory illness such as house fire; reduce exposure to noxious chemicals.

ADRENAL HYPERPLASIA, CONGENITAL

Description

Congenital adrenal hyperplasia (CAH) is a family of disorders caused by decreased enzyme activity required for cortisol production in the adrenal cortex. The most common defect is 21-hydroxylase deficiency, which constitutes more than 90% of all cases of CAH.

Pathophysiology

Interference in the biosynthesis of cortisol during fetal life results in an increased production of ACTH, which stimulates hyperplasia of the adrenal gland. Depending on the enzymatic defect, increased quantities of cortisol precursors and androgens are secreted. There are six major types of biochemical defects. The most common is partial or complete 21-hydroxylase deficiency. With partial deficiency, enough aldosterone is produced to preserve sodium, and adequate cortisol is produced to prevent signs of adrenocortical insufficiency.

Clinical Signs and Symptoms

Masculinization of external female genitalia causes the clitoris to enlarge so that it appears as a small phallus. Fusion of the labia produces a sac-like structure resembling the scrotum without testes. However, no abnormal changes occur in the internal sexual organs, although the vaginal orifice is usually closed by the fused labia.

In males, ambiguous genitalia should be considered in any male infant with hypospadias or micropenis and no palpable gonads, and a diagnostic evaluation for CAH should be contemplated. Males do not display genital abnormalities at birth.

Increased pigmentation of skin creases and genitalia caused by increased ACTH may be a subtle sign of adrenal insufficiency.

A salt-wasting crisis frequently occurs, usually within the first few weeks of life.

Infants fail to gain weight, and hyponatremia and hyperkalemia may be significant.

Untreated CAH results in early sexual maturation, with enlargement of the external sexual organs; development of axillary, pubic, and facial hair; deepening of the voice; acne; and marked increase in musculature.

Diagnostic Evaluation

Clinical diagnosis is initially based on congenital abnormalities that lead to difficulty in assigning gender to the newborn and on signs and symptoms of adrenal insufficiency or hypertension.

Evidence of increased 17-ketosteroid levels is found in most types of CAH.

In complete 21-hydroxylase deficiency, blood electrolytes demonstrate loss of sodium and chloride and elevation of potassium.

Chromosome typing for positive sex determination and to rule out any other genetic abnormality (e.g., Turner syndrome) is always done in any case of ambiguous genitalia.

Ultrasound to identify the absence or presence of female reproductive organs in a newborn or child with ambiguous genitalia

In older children bone age is advanced, and linear growth is increased.

Treatment

The initial medical objective is to confirm the diagnosis and assign a gender to the child, usually according to the genotype.

In both sexes, cortisone is administered to suppress the abnormally high secretion of ACTH.

Depending on the degree of masculinization in the female, reconstructive surgery may be required to reduce the size of the clitoris, separate the labia, and create a vaginal orifice.

Nursing Care Management

Early recognition of ambiguous genitalia in newborns is essential

If there is any question regarding assignment of gender, the parents need to be told immediately to prevent the embarrassing situation of informing family members of the child’s gender and then having to change the announcement.

Patient and Family Teaching

Because infants are especially prone to dehydration and salt-losing crises, parents need to be aware of signs of dehydration and the urgency of immediate medical intervention to stabilize the child’s condition.

Parents should have injectable hydrocortisone available and know how to prepare and administer the intramuscular injection. The parents should be advised that there is no physical harm in treating for suspected adrenal insufficiency that is not present, whereas the consequence of not treating acute adrenal insufficiency can be fatal.

ALLERGIC RHINITIS

Description

Allergic rhinitis affects many children and is associated with numerous airway disorders, including asthma, OME, and chronic sinusitis. Seasonal allergic rhinitis (or hay fever) usually follows a spring-fall pattern and is caused by tree, grass, and weed pollens. Seasonal allergic rhinitis usually does not develop until the individual has been sensitized by two or more pollen seasons. Peak incidence for allergic rhinitis is in the adolescent and postadolescent age groups, but younger children are also affected.

Pathophysiology

Allergic rhinitis requires two conditions: a familial predisposition to develop allergy and exposure of a sensitized person to the allergen. Inhalants in the form of microscopic airborne particles (e.g., pollens, mold, animal danders, and environmental dusts) enter the upper respiratory tract with inhalation and bind to submucosal mast cells in the respiratory tract epithelium. In the allergic child, symptoms are mediated by immunoglobulin E (IgE), which is produced by the child’s B lymphocytes. The IgE molecules on the cell surfaces trigger the rapid release of mast cell mediators (e.g., histamine, prostaglandins, and leukotrienes), as well as cell interactive compounds called cytokines. Histamine, a potent vasodilator, acts directly on local receptors to produce vasodilation, mucosal edema, and increased production of mucus. The cytokines summon cells to the area and are responsible for the slower late-phase allergic reaction of inflammation and destruction of the mucosal surface that progresses to chronic nasal obstruction. Repeated exposure of these sensitized membranes to specific aeroallergens results in clinical allergic disease.

Diagnostic Evaluation

Based on a thorough history and physical examination

Nasal smear to determine the number of eosinophils in the nasal secretions

Blood examination for total IgE and elevated eosinophils

Skin allergen tests

Radioallergosorbent tests (RAST): used to determine the level of specific IgE antibodies to specific allergens

Treatment

Avoidance of offending allergens (food, drugs, animal dander, chemicals, dust, pollen)

Medications: antihistamines; nasal corticosteroids; leukotriene modifier; immunotherapy

Patient and Family Teaching

Medication administration

Allergen avoidance

Symptom management

Skin testing

ANEMIA, IRON-DEFICIENCY

Description

Anemia caused by an inadequate supply of dietary iron is the most prevalent nutritional disorder in the United States and the most common mineral disturbance. Children 12 to 36 months of age are at risk for anemia as a result of cow’s milk being a major staple of many infants’ diet. Preterm infants are especially at risk because of their reduced fetal iron supply. Adolescents are also at risk because of their rapid growth rate combined with poor eating habits.

Pathophysiology

Iron-deficiency anemia can be caused by any number of factors that decrease the supply of iron, impair its absorption, increase the body’s need for iron, or affect the synthesis of Hgb.

Clinical Signs and Symptoms

Pallor, fatigue, irritability, loss of appetite, decreased physical activity

In severe cases, congestive heart failure may develop.

Diagnostic Evaluation

CBC, MCV, RDW, reticulocyte count

Transferrin saturation, FEP, ferritin

Treatment

In formula-fed infants the most convenient and best sources of supplemental iron are iron-fortified commercial formula and iron-fortified infant cereal.

Dietary addition of iron-rich foods is usually inadequate as the sole treatment of iron-deficiency anemia, because the iron is poorly absorbed and thus provides insufficient supplemental quantities of iron.

Oral iron supplements at a dose of 4-6mg/kg of elemental iron are prescribed for approximately 3 months. Ferrous sulfate, more readily absorbed than ferric iron, results in higher Hgb levels. Ascorbic acid (vitamin C) appears to facilitate absorption of iron and may be given as vitamin C–enriched foods and juices with the iron preparation.

If the Hgb level fails to rise after 1 month of oral therapy, it is important to assess for persistent bleeding, iron malabsorption, noncompliance, improper iron administration, or other causes for the anemia.

Nursing Care Management

An essential nursing responsibility is instructing parents in the administration of iron.

Oral iron should be given as prescribed in three divided doses between meals, when the presence of free hydrochloric acid is greatest, because more iron is absorbed in the acidic environment of the upper GI tract.

A citrus fruit or juice taken with the medication aids in absorption.

Patient and Family Teaching

A primary nursing objective is to prevent nutritional anemia through family education. Because breast milk is a poor iron source after 5 months of lactation, reinforce the importance of administering iron supplementation in the exclusively breast-fed infant by 6 months of age.

In the formula-fed infant, discuss with parents the importance of using iron-fortified formula and the introduction of solid foods at the appropriate age during the first year of life. Cereals are one of the first semisolid foods to be introduced into the infant’s diet at approximately 6 months of age.

Diet education of teenagers is especially difficult, especially because teenage girls are particularly prone to following weight-reduction diets. Emphasizing the effect of anemia on appearance (pallor) and energy level (difficulty maintaining popular activities) may be useful.

Discuss side-effects of iron therapy:

An adequate dosage of oral iron turns the stools a tarry green color.

Vomiting or diarrhea can occur with iron therapy. If the parents report these symptoms, the iron can be given with meals and the dosage reduced and then gradually increased until tolerated.

Liquid preparations of iron may temporarily stain the teeth. If possible, the medication should be taken through a straw or given through a syringe or medicine dropper placed toward the back of the mouth. Brushing the teeth after administration of the drug lessens the discoloration.

ANOREXIA NERVOSA

Description

Anorexia nervosa (AN) is an eating disorder characterized by a refusal to maintain a minimally normal body weight and by severe weight loss in the absence of obvious physical causes.

Pathophysiology

The disorder appears to be caused by a combination of genetic, neurochemical, psychodevelopmental, and sociocultural factors. The dominant aspects of AN are a relentless pursuit of thinness and a fear of fatness, usually preceded by a period of mood disturbances and behavior changes.

Diagnostic Evaluation

Diagnosis is made on the basis of criteria established by the American Psychiatric Association (see Box 17-16 in text book).

Treatment

Immediate medical care for person with life-threatening medical (fluid and electrolyte imbalance); or psychiatric disturbance such as suicide attempt

Restore a healthy weight.

Establish healthy eating patterns.

Psychotherapy to correct deficits and distortions in psychologic functioning

Resolve disturbed family interaction patterns.

Nursing Care Management

Monitor nutritional status.

Enforce healthy eating habits.

Help adolescent set limits and avoid destructive behaviors/habits.

Assist with treatment of life-threatening conditions such as electrolyte imbalance.

Reinforce behavioral contract and plan of care with adolescent.

Participate in individual and family therapy.

Patient and Family Teaching

Nutritional counseling

Behavioral modification techniques

Individual and family coping skills that are not disruptive to family functioning

Teach family how to support adolescent and how to help adolescent set realistic goals.

AORTIC STENOSIS

Description

Narrowing or stricture of the aortic valve, causing resistance to blood flow from the left ventricle, decreased cardiac output, left ventricular hypertrophy, and pulmonary vascular congestion. The prominent anatomic consequence of aortic stenosis (AS) is the hypertrophy of the left ventricular wall, which eventually leads to increased end-diastolic pressure resulting in pulmonary venous and pulmonary arterial hypertension. Left ventricular hypertrophy also interferes with coronary artery perfusion and may result in myocardial infarction or scarring of the papillary muscles of the left ventricle, which causes mitral insufficiency. Valvular stenosis, the most common type, is usually caused by malformed cusps that result in a bicuspid rather than tricuspid valve or fusion of the cusps. Subvalvular stenosis is a stricture caused by a fibrous ring below a normal valve; supravalvular stenosis occurs infrequently. Valvular AS is a serious defect for the following reasons: (1) the obstruction tends to be progressive; (2) sudden episodes of myocardial ischemia, or low cardiac output, can result in sudden death; and (3) surgical repair rarely results in a normal valve. This is one of the rare instances in which strenuous physical activity may be curtailed because of the cardiac condition.

Pathophysiology

A stricture in the aortic outflow tract causes resistance to ejection of blood from the left ventricle. The extra workload on the left ventricle causes hypertrophy. If left ventricular failure develops, left atrial pressure will increase; this causes increased pressure in the pulmonary veins, which results in pulmonary vascular congestion (pulmonary edema).

Newborns with critical AS demonstrate signs of decreased cardiac output with faint pulses, hypotension, tachycardia, and poor feeding (see Box 3-1, Common Signs and Symptoms of Congestive Heart Failure). Children show signs of exercise intolerance, chest pain, and dizziness when standing for a long period. There is a characteristic murmur that is low-pitched, harsh, and rasping, heard loudest at the base in the second intercostal space. Patients are at risk for bacterial endocarditis, coronary insufficiency, and ventricular dysfunction.

BOX 3-1 Common Signs and Symptoms of Congestive Heart Failure

Impaired Myocardial Function	Pulmonary Congestion
Tachycardia	Tachypnea
Sweating (inappropriate)	Dyspnea
Decreased urinary output	Retractions (infants)
Fatigue	Flaring nares
Weakness	Exercise intolerance
Restlessness	Orthopnea
Anorexia	Cough, hoarseness
Nausea	Cyanosis
Vomiting	Wheezing
Pale, cool extremities	Grunting
Weak peripheral pulses
Decreased blood pressure	SYSTEMIC VENOUS CONGESTION
Chest pain	Weight gain
Palpitations	Hepatomegaly
Gallop rhythm	Peripheral edema, especially periorbital
Cardiomegaly	Ascites
Duskiness	Neck vein distention (children)
Change in level of consciousness

Diagnostic Evaluation

See Table 3-1, Procedures for Cardiac Diagnosis; and Table 3-2, Current Interventional Cardiac Catheterization Procedures in Children.

TABLE 3-1 Procedures for Cardiac Diagnosis

PROCEDURE	DESCRIPTIVE
Chest radiograph (X-ray)	Provides information on heart size and pulmonary blood flow patterns
Electrocardiography (ECG)	Graphic measure of electrical activity of heart
Holter monitor	24-hour continuous ECG recording used to assess dysrhythmias
Echocardiography	Use of high-frequency sound waves obtained by a transducer to produce an image of cardiac structures
Transthoracic	Done with transducer on chest
M-mode	One-dimensional graphic view used to estimate ventricular size and function
Two-dimensional (2-D)	Real-time, cross-sectional views of heart used to identify cardiac structures and cardiac anatomy
Doppler	Identifies blood flow patterns and pressure gradients across structures
Fetal	Imaging fetal heart in utero
Transesophageal (TEE)	Transducer placed in esophagus behind heart to obtain images of posterior heart structures or in patients with poor images from chest approach
Cardiac catheterization	Imaging study using radiopaque catheter placed in a peripheral blood vessel and advanced into heart to measure pressures and oxygen levels in heart chambers and visualize heart structures and blood flow patterns
Hemodynamics	Measures pressures and oxygen saturations in heart chambers
Angiography	Use of contrast material to illuminate heart structures and blood flow patterns
Biopsy	Use of special catheter to remove tiny samples of heart muscle for microscopic evaluation; used in assessing infection, inflammation, or muscle dysfunction disorders; also to assess the level of rejection after heart transplant
Electrophysiology (EPS)	Special catheters with electrodes employed to record electrical activity from within heart; used to diagnose rhythm disturbances
Exercise stress test	Monitoring of heart rate, blood pressure, electrocardiogram (ECG), and oxygen consumption at rest and during progressive exercise on a treadmill or bicycle
Cardiac magnetic resonance imaging (MRI)	Noninvasive imaging technique; used in evaluation of cardiac and vascular anatomy of the heart (i.e., coarctation of the aorta, vascular rings), estimates of ventricular mass and volume; uses for MRI are expanding

TABLE 3-2 Current Interventional Cardiac Catheterization Procedures in Children

INTERVENTION	DIAGNOSIS
Balloon atrial septostomy: Use is well established in newborns; may also be done under echocardiographic guidance	Transposition of great arteries (BAS used as an intermediary step to improve cyanosis until surgery) Some complex single-ventricle defects

Balloon dilation: Treatment of choice

Valvular pulmonic stenosis

Branch pulmonary artery stenosis

Congenital valvular aortic stenosis

Rheumatic mitral stenosis

Recurrent coarctation of aorta

Further follow-up required in native coarctation of aorta in patients >7 mo

Congenital mitral stenosis

Coil occlusion: Accepted alternative to surgery

Patent ductus arteriosus (<4 mm)

Aortopulmonary collaterals

Transcatheter device closure: Several devices in clinical trials Atrial septal defect (ASD) Amplatzer septal occluder: Approved for ASD closure ASD Ventricular septal defect devices: In clinical trials Ventricular septal defects Stent placement

Pulmonary artery stenosis

Coarctation of the aorta in adolescents

Use to treat other lesions; investigational

Radiofrequency ablation Some tachydysrhythmias

Data from Allen HD, Beekman RH 3rd, Garson A Jr, and others: Pediatric therapeutic cardiac catheterization: AHA scientific statement, Circulation 97:609-625, 1998; updated from Rome J, Kreutzer J: Pediatric interventional catheterization: reasonable expectations and outcomes, Pediatr Clin North Am 51:1589-1610, 2004.

Aortic valvotomy is performed under inflow occlusion. It is used rarely because balloon dilation in the catheterization laboratory is the first-line procedure. Newborns with critical AS and small left-sided structures may undergo a Stage 1 Norwood procedure.

Procedure may involve incising a membrane if one exists or cutting the fibromuscular ring. If the obstruction results from narrowing of the left ventricular outflow tract and a small aortic valve annulus, a patch may be required to enlarge the entire left ventricular outflow tract and annulus and replace the aortic valve, an approach known as the Konno procedure.

Nursing Care Management

Manage Common Side Effects of Cardiac Defects

Prevent fatigue during feeding; offer small frequent feedings to infant’s or child’s tolerance.

Organize nursing care to allow child/infant uninterrupted rest.

Promote activities that do not cause fatigue.

Provide Support for the Child and Family

Communicate with the child and family in an appropriate style.

Provide the child and family with honest answers.

Provide emotional support.

Offer age-appropriate interventions.

Provide information on available resources for support for the child and family.

Patient and Family Teaching

Prepare the Child and Family for Diagnostic and Operative Procedures

Provide explanation of diagnostic tests and why each test is performed because many of them are invasive procedures.

Prepare the child prior to the invasive procedure. Remember discussion is dependent upon the child’s age and development.

Use simple words or pictures to describe procedures and answer all questions the child and family may have.

Postoperative wound care teaching as needed

Post-cardiac catheterization wound care teaching as needed

Assess and record results of teaching and family’s participation in care.

Educate the Child and Family

Assess child’s and family’s level of knowledge regarding aortic stenosis.

Assess child’s and family’s understanding of what they have heard about aortic stenosis.

Assess child’s and family’s understanding of the surgery and/or cardiac catheterization.

Teach the child and/or family at least four characteristics of congestive heart failure that may occur because of the aortic stenosis such as:

Fatigue after exertion

Fast heart rate

Fast breathing, shortness of breath, dyspnea

Decreased urinary output

Puffiness (edema)

Fussiness

Decreased appetite

Educate child and family about care such as medication preparation and administration.

Assess child’s and family’s access to appropriate pharmacy for any special preparation medications.

If the child is on anticoagulation therapy, educate the child and family about:

Anticoagulation therapy

Dietary restrictions

Laboratory testing required

The need for close medical follow-up

Signs and symptoms of complications from blood clots and bleeding

Educate child and family about when to notify their physician of any clinical changes.

Provide appropriate educational resources and review materials with them.

Clarify information presented by the health care team including appointment for follow-up visit.

Discuss SBE (subacute bacterial endocarditis) prophylaxis with the pediatric cardiologist.

APLASTIC ANEMIA

Description

Aplastic anemia (AA) refers to a condition in which the formed elements of the blood are simultaneously depressed. The peripheral blood smear demonstrates pancytopenia or the triad of profound anemia, leukopenia, and thrombocytopenia. Aplastic anemia can be primary (congenital, or present at birth) or secondary (acquired). The best-known congenital disorder of which aplastic anemia is an outstanding feature is Fanconi syndrome, a rare hereditary disorder characterized by pancytopenia, hypoplasia of the bone marrow, and patchy brown discoloration of the skin resulting from the deposit of melanin and associated with multiple congenital anomalies of the musculoskeletal and genitourinary systems. The syndrome appears to be inherited as an autosomal recessive trait with varying penetrance; therefore, affected siblings may demonstrate several different combinations of defects.

Pathophysiology

Most of the cases of AA are considered idiopathic where no cause is found. Several etiologic factors contribute to the development of acquired hypoplastic anemia:

Human parvovirus infection, hepatitis, or overwhelming infection

Irradiation

Immune disorders such as eosinophilic fascitis and hypoimmunoglobulinemia

Drugs such as certain chemotherapeutic agents, anticonvulsants, and antibiotics

Industrial and household chemicals, including benzene and its derivatives, which are found in petroleum products, dyes, paint remover, shellac, and lacquers

Infiltration and replacement of myeloid elements, such as in leukemia or the lymphomas

Clinical Signs and Symptoms

Onset of clinical symptoms of anemia, leukopenia, and decreased platelet count are usually insidious.

Diagnostic Evaluation

Definitive diagnosis is determined from bone marrow aspiration, which demonstrates the conversion of red bone marrow to yellow, fatty bone marrow.

Severe AA is defined as less than 25% bone marrow cellularity with at least two of the following findings: absolute granulocyte count <500 mm³, platelet count <20,000/mm³, and absolute reticulocyte count <40,000/mm³.

Moderate AA is defined as more than 25% bone marrow cellularity with the presence of mild or moderate cytopenias.

Treatment

Therapy is directed at restoring function to the marrow and involves two main approaches:

Immunosuppressive therapy to remove the presumed immunologic functions that prolong aplasia. Antilymphocyte globulin (ALG) or antithymocyte globulin (ATG) is the principal drug treatment used for aplastic anemia. Cyclosporine may also be used. ATG and cyclosporine suppress T cell–dependent autoimmune responses but do not cause bone marrow suppression.

Replacement of the bone marrow through transplantation. Bone marrow transplantation is the treatment of choice for severe aplastic anemia when a suitable donor exists. Hematopoietic stem cell transplantation should be considered early in the course of the disease if a compatible donor can be found.

Colony-stimulating factor (CSF), and granulocyte-macrophage colony-stimulating factor (GM-CSF) given parenterally, may be used to enhance bone marrow production.

Androgens also may be used with ATG to stimulate erythropoiesis if the AA is nonresponsive to initial therapies.

Nursing Care Management

The care of the child with aplastic anemia is similar to that of the child with leukemia (see pp. 243-244)—specifically, preparing the child and family for the diagnostic and therapeutic procedures, preventing complications from the severe pancytopenia, and emotionally supporting them in terms of a potentially fatal outcome.