Chronic anemia can be primary or secondary.

Primary chronic anemia

Primary chronic anemias are the true chronic anemias, in which anemia (defined as a hemoglobin level more than 2 standard deviations below the mean reference value for age) is part of the basic disease process. The basic disease process is hematologic (eg, sickle cell disease, HS), and the degree of anemia varies markedly from etiology to etiology and from patient to patient, even with the same etiology. (See Etiology and Workup.)

Secondary chronic anemia

Secondary chronic anemias are chronic anemias that may provide a diagnostic clue to an underlying pathology. They are the consequence of a nonhematologic problem (eg, chronic blood loss, chronic renal failure, osteomyelitis, inflammatory bowel disease, tuberculosis).

Etiology

Chronic anemia is classified into the following 3 primary categories:

• Decreased red cell production
• Increased red cell destruction (hemolysis)
• Blood loss

Clinical Presentation

Patients with chronic anemia are usually asymptomatic, even with remarkably low levels of hemoglobin. Symptoms more often relate to the underlying cause.

Hemoglobin levels as low as 5-6 g/dL are well tolerated in most patients, and patients do not require transfusion. Parents, however, frequently note that patients become much more active following a transfusion.

Inquire carefully regarding any evidence of blood loss (eg, hemoptysis, hematochezia, melina, hematuria, menorrhagia). In endemic areas, a history of papulovesicular skin lesions on the feet may suggest a diagnosis of hookworm infestation.

Age is always an important consideration. Nutritional iron deficiency is seen in older infants and toddlers (aged 6 mo to 3 y), whereas iron deficiency due to blood loss occurs in menstruating girls. The deficiency can be surprisingly severe, but transfusion is indicated only in the rare circumstance of impending high-output cardiac failure.

The patient’s sex must always be considered in hemolytic anemias. Severe G-6-PD deficiency may be seen as a chronic nonspherocytic anemia, usually in males.

Dietary history is important with regard to the amount and source of milk ingested by infants and toddlers and to their risk of chronic iron deficiency (24 oz of milk/d or more is a clear risk factor for nutritional iron deficiency in infants and young children).

Chronic hemolysis with extramedullary hematopoiesis, such as in ?-thalassemia major or sickle cell anemia, may result in frontal bossing and prominent cheeks.

Pallor may be difficult to appreciate unless carefully sought. Pallor of the conjunctivae, nail beds, palm creases, or gums may be recognized. Parents and friends usually do not notice any difference, because the problem is chronic.

Scleral icterus is common in chronic hemolytic anemia. The icterus waxes and wanes.

Diagnosis

To evaluate anemia, obtain initial laboratory tests, including a complete blood count (CBC), a reticulocyte count, and a review of the peripheral smear. Imaging studies can play a role in the diagnosis of underlying disease, while bone marrow aspiration and biopsy can be used to identify the presence of tumor cells and determine cellular morphology.

Management

Chronic anemia merits prompt, if not immediate, attention.

Patients with chronic anemias rarely need inpatient care, even during the diagnostic process.

Treatment options include:

• Transfusion
• Splenectomy
• Prevention Of Anemia

Chronic anemia due to intrinsic RBC abnormalities such as hemoglobinopathies, unstable hemoglobins, red cell membrane abnormalities, and red cell enzyme abnormalities do not warrant specific medications.

Nutritional anemia can be treated with supplements of deficient factors.

Recombinant erythropoietin has been useful in managing anemia related to chronic renal failure, rheumatoid arthritis, AIDS

Pathophysiology

The infectious agent in roseola infantum/exanthem subitum was demonstrated to be present in blood by inoculating healthy infants with serum from ill infants, a procedure considered very dangerous by today’s standards.

Clinical Presentation

Human herpesvirus 6 (HHV-6) is the single most common cause of hospital visits in infants with fever.

Roseola is characterized by an initial febrile phase of 3-5 days, with temperatures reaching 40°C.

With the fever, some children exhibit bilateral periorbital edema in the prodrome.

At or near the period of defervescence, a maculopapular rash is observed on the infant’s trunk and neck; however, this rash is found in the minority of patients (10%).

Children can contract primary human herpesvirus 6 without manifesting a rash.

Human herpesvirus 6 can be isolated from the blood for the first 5 days and later is found intermittently or persistently in saliva, stool, and, rarely, urine.

Physical Examination

High-grade fever higher than 39.5°C (103°F) persists for 3-5 days and then resolves abruptly.

Rash appears after 12-24 hours of resolution of fever. In many incidents of human herpesvirus 6, rash appears during defervescence or within a few hours.

Rash of roseola is erythematous, nonpruritic, mildly elevated, and consists of rosepink papules (roseola meaning pink-colored rash). The rash blanches on pressure and mainly is distributed on the trunk, arms, and neck.

The rash fades in 1-2 days.

Most children are playful despite high-grade fever; however, anorexia, irritability, and listlessness may be the presenting signs.

Laboratory studies

Laboratory diagnosis is rarely required in patients who are immunocompetent because of the self-limiting nature of primary human herpesvirus 6 (HHV-6) infection.

Leukopenia with lymphocytosis may suggest the diagnosis.

Transaminase elevations, cholestasis, and thrombocytopenia were noted.

Obtain serology. Four-fold increase in human herpesvirus 6 immunoglobulin G (IgG) antibodies in serum suggests active human herpesvirus 6 infection (primary or reactivated).

Management

Provide supportive therapy for patients with symptomatic human herpesvirus 6 (HHV-6) infection.

Ensure adequate fluid balance.

Administer acetaminophen or ibuprofen to patients with high-grade fever, patients who are uncomfortable, or patients who have a previous history of febrile seizures.

Pathophysiology

Diaper rash affects the areas within the confines of the diaper. Increased wetness in the diaper area makes the skin more susceptible to damage by physical, chemical, and enzymatic mechanisms. Wet skin increases the penetration of irritant substances. Superhydration urease enzyme found in the stratum corneum liberates ammonia from cutaneous bacteria. Urease has a mild irritant effect on nonintact skin. Lipases and proteases in feces mix with urine on nonintact skin and cause an alkaline surface pH, adding to the irritation. (Feces in breastfed infants have a lower pH, and breastfed infants are less susceptible to diaper dermatitis.) The bile salts in the stools enhance the activity of fecal enzymes, adding to the effect.

Age

Diaper dermatitis commonly affects infants, with peak incidence occurring when the individual is aged 9-12 months. One study determined that at any given time, diaper dermatitis is prevalent in 7-35% of the infant population.

Diaper dermatitis can affect persons of any age who wear diapers, in particular, elderly people.

Physical Examination

If candidiasis is suspected or proven by potassium hydroxide (KOH) preparation or culture, an antifungal agent effective against yeast is indicated.

The safest OTC emollient available for newborns is pure white petrolatum ointment, which acts by trapping water beneath the epidermis.

Prevention

Prevention of diaper dermatitis can be summarized with the acronym ABCDE (air, barrier, cleansing, diaper, and education).