In 1991, the Centers for Disease Control and Prevention (CDC) recommended and the AAP endorsed universal screening between ages 9 and 12 months and then again at age 2 years. They revised these guidelines in 1998, because in certain geographic areas, the incidence of abnormal BLLs was so low that it did not justify the cost. The CDC felt that targeted screenings would be more appropriate than universal screenings. The AAP endorsed and justified this measure to reduce unnecessary testing of children unlikely to be at risk.

The new guidelines appear complex and difficult to interpret and implement. In communities where the prevalence of elevated BLL (>10 mcg/dL) is unknown and where older housing predominates (more than 27% built before 1950), universal screening is still recommended. Targeted screening based on the answers to a questionnaire (Display 48-1) is recommended for locales where less than 12% of children have BLLs greater than 10 mcg/dL or where less than 27% of the homes were built before 1950. The burden for determining which communities will have targeted or universal screening falls to local and state public health officials (AAP, 1998). It is not surprising that this apparent backslide in policy has raised controversy, particularly among public health officials (Needleman, 1998; Silbergeld, 1997).

Patient education is recommended as part of anticipatory guidance for all. The AAP in its 1998 policy statement identifies risk factors and prevention strategies that are listed in Table 48-1. Management of elevated BLLs identified during screening, as recommended by the AAP, including education and abatement, is outlined in Table 48-2.

The 1995 AAP policy statement provides an excellent review of the classic chelation modalities, dimercaprol (BAL in oil) and calcium disodium EDTA. Parenteral administration for each is required. Penicillamine is also discussed as an oral chelator.

Most clinicians who treat lead poisoning now use succimer (an oral analog of dimercaprol). As an oral agent, it may be used on an outpatient basis but only after environmental safety is guaranteed. There is no evidence that with BLLs between 25 and 45 mcg/dL, chelation avoids or reverses neurotoxicity (Berlin, 1997); however, if elevated levels persist in this range, despite all efforts at abatement, succimer may be indicated after consultation with an expert. Succimer is definitely indicated for children with BLLs greater than 45 mcg/dL who have no symptoms of encephalopathy. Hospitalization
is usually recommended, initially to monitor for side effects and then either to abate the current housing or to find new safe housing. The dose is 30 mg/kg/d for 5 days followed by 20 mg/kg/d for 14 days. Some children report GI discomfort and malaise. There have been case reports of reversible neutropenia and anemia; therefore, hematologic surveillance is recommended during therapy (AAP, 1995).

For cases of encephalopathy manifested by changes in the level of consciousness, headache, or vomiting or those with BLLs greater than 70 mcg/dL, parenteral chelation combining BAL and EDTA is advised. Only professionals experienced in treating lead toxicity should undertake this type of treatment.

The bridging of two adjacent IgE antibodies by an antigen leads to a release of preformed mediators of allergy, resulting in the early phase of the type 1 reaction and, in severe cases, anaphylaxis.

The exact incidence of anaphylaxis in children is unknown; however, data suggest that the incidence of anaphylaxis may be 0.25% in patients receiving allergy immunotherapy. Anaphylaxis to Hymenoptera occurs in about 1% to 2% of the general population, and fatalities (mostly in adults) from Hymenoptera stings total approximately 25 to 50 per year in the United States. Fatal reactions to penicillin also have been reported but are extremely rare and occur mostly due to parenteral administration at a rate of 0.002%. Anaphylaxis is much less likely if penicillin is administered orally. The incidence
of fatal anaphylaxis appears to be twice as high in patients with asthma. Patients on beta-blockers also may be at high risk for anaphylaxis (Lang, 1995).

Risk factors for anaphylaxis include the following:

Quick recognition of clinical symptoms listed in Table 48-3 is key to establishing a diagnosis of anaphylaxis. Key features include rapid onset of generalized itching, urticaria, angioedema, flush, erythema, headache, sneezing, rhinorrhea, wheezing, difficulty swallowing, abdominal cramping, diarrhea, sensation of impending doom, respiratory arrest, and sometimes cardiovascular collapse. The presentation varies, and not all organ systems are involved in all patients. Nonetheless, in this potentially life-threatening situation, symptoms can start within seconds, reaching a peak severity from 5 to 30 minutes after exposure to the offending agent. Late-phase reaction also may occur 6 to 12 hours later, with symptoms lasting up to as much as 24 hours despite treatment. Most children have cutaneous symptoms, which may progress to involve the respiratory system and a feeling of anxiety. Only rarely, however, do symptoms progress to respiratory failure or cardiovascular collapse.

The diagnosis is based on obtaining a history of exposure to an offending agent or recognition of the classic signs and symptoms. The presence of cutaneous symptoms and signs (ie, pruritus, urticaria, angioedema) makes the diagnosis more obvious.

Anaphylaxis can be confused with vasovagal syncope. Distinguishing features are that vasovagal reactions occur during stressful conditions, such as venipuncture, vaccinations, and allergy skin tests. Patients appear pale and sweaty and may have bradycardia. Unlike with anaphylaxis, patients with vasovagal episodes maintain normal blood pressure and have no pruritus, urticaria, angioedema, or bronchospasm. They also recover spontaneously within minutes.

Laboratory tests are generally not necessary to establish a diagnosis of anaphylaxis; however, tryptase levels are elevated in most cases. Providers may draw a level if diagnosis of anaphylaxis is in doubt. The window in which tryptase levels may accurately reflect anaphylaxis is about 2 hours after onset of symptoms (Schwart et al., 1989). After the event, if the etiology is in doubt, allergy skin testing may be indicated if a clinician suspects an ingestant (food), Hymenoptera sting, or inhalant as the culprit.

Prompt recognition and treatment of anaphylaxis are important, because anaphylaxis can be life threatening. The reader is referred to the algorithm in Figure 48-1, which describes the treatment of an acute allergic reaction in the office or clinic setting. Epinephrine is the drug of choice in anaphylaxis. It reduces mediator release and may reverse the physiologic effects of many mediators. Because most providers in private practice are not experienced in advanced life support, which may be needed in management of anaphylaxis, they must know when to call for help for patients who fail to respond to the administration of epinephrine and antihistamines. Providers can encounter anaphylaxis at any time; therefore, mock drills practicing management of anaphylaxis may be helpful. An emergency cart accessible to all personnel also is essential. All health care providers should maintain basic cardiopulmonary resuscitation certification. Display 48-2 presents the basic supplies and equipment recommended for management of anaphylaxis in an office setting.

Most children report a painful sting, although they are unable to identify the insect that stung them. In the United States, the most common culprits are insects from the hornet family, with yellow jackets being most common, followed by other hornets, wasps, and finally honeybees. The various presentations consist of local and systemic reactions. At the least, there is usually redness, pain, and some degree of swelling at the site of the sting, due to irritation from the venom. Allergic reactions to Hymenoptera are sometimes confused with large local reactions, which are raised, red, painful, and at times itchy at the site of the sting. The differential point is that these reactions are limited to the bite site, and no systemic signs of generalized pruritus, urticaria, or airway difficulty are present. Local reactions do not involve the IgE antibody. Evidence has shown that about 50% of individuals with history of a systemic reaction give a history of progressively increasing large local reactions before occurrence of the first systemic reaction. Some individuals with large local reactions may have higher than normal IgE antibodies against the class of stinging insect responsible for the sting. The symptoms of more systemic reactions and anaphylaxis to a Hymenoptera sting are the same as for other causes, and the reader is referred to Table 48-3.

The history of a sting immediately preceding a local, systemic, or anaphylactic reaction establishes the diagnosis. As recurrent allergic reactions to Hymenoptera insects can be life threatening, the provider needs to identify the stinging insect responsible. To do so, a consultation with an allergist for appropriate skin testing for Hymenoptera may be necessary.

The exact incidence of drug allergy in children is unknown; however, about 5% to 15% of the general population will give a history of an adverse drug reaction as a result of penicillin. A controlled study suggests an actual incidence of 3.2%. Allergic reactions to second- or third-generation cephalosporins are rare (1%–3%). Cross-reactivity with patients who are allergic to penicillin is about 2%. The vast majority of parents confuse side effects and idiosyncratic reactions with true allergic reactions.

A meticulous history is most important and must include a detailed drug history. What medications was the child taking at the time of the reaction? Was the reaction urticarial? Was the rash pruritic? Were there signs of anaphylaxis? Unfortunately, in children, the history may not be reliable. Many parents or children do not remember the name of the antibiotic or type of reaction. Because the actual incidence of drug allergy is usually lower than what parents relate, labeling a patient allergic to drugs (especially the beta lactams) may lead to use of alternate, less effective, more toxic, more broad spectrum, and commonly more expensive drugs. Hence, a proper diagnosis of drug allergy is most important.

In true drug allergies, typical symptoms, such as itching, sneezing, and wheezing, will be present. Urticaria and angioedema are seen frequently. Classic anaphylaxis is rare but is obviously the most serious manifestation.

Symptoms of true drug allergy may include the following:

Common nonallergic symptoms that many parents falsely perceive to be allergic include the following:

The provider can narrow down the possibility of drug allergy by reviewing a detailed and careful history. If suspicion for true allergy is low, such as a nonpruritic, nonurticarial rash after amoxicillin, then he or she can give an oral challenge in the office and observe the patient carefully for an hour. (The office should be equipped and personnel trained to handle anaphylaxis.)

In situations in which suspicion is high and the suspected drug is indeed the treatment of choice, then the provider should consider consultation with an allergist. He or she should consider skin testing for drug allergy in these patients. Skin tests, however, are hindered by the fact that, for most drugs, appropriate antigens are not available. Even for penicillin allergy, all necessary testing reagents (especially the minor determinants of penicillin allergy) are not yet commercially available, making the task of proper diagnosis difficult. Physicians experienced with these procedures, such as allergists, should perform skin testing and graded oral challenges.

Providers can use the following steps when diagnosing drug allergy:

Acute reactions are treated based on symptoms. Mild pruritic reactions are best treated with antihistamines. Bronchodilators may be necessary for wheezing. Anaphylaxis will require adrenaline, as discussed in the module on anaphylaxis. Once the diagnosis is established, avoidance is advised.

Common drug allergy problems encountered by pro-viders are discussed below.