11.1 Food Allergy, Anaphylaxis & Emergency Planning

Allergy and immunology is clinical category #3 by exam volume on the PNCB CPNP-PC outline; otolaryngology is #4. This section is the allergy slice that kills children when the first drug is wrong: food allergy and anaphylaxis. Domain II wants IgE-mediated disease separated from non-IgE gut syndromes. Domain III wants an epinephrine-first emergency plan, autoinjector teaching, and a written action plan — not an antihistamine-first delay.

Exam trap — oral antihistamine is not first-line anaphylaxis care. Diphenhydramine, a second-generation H1 blocker, or a corticosteroid does not reverse airway edema, shock, or bronchospasm. Intramuscular epinephrine in the anterolateral thigh is first. Antihistamines may later reduce itch and hives. They never replace epinephrine.

IgE-mediated versus non-IgE food disease

IgE-mediated food allergy is a rapid, reproducible reaction after a specific food: urticaria, angioedema, vomiting, cough, wheeze, stridor, hypotension, or a combination. Onset is usually minutes to 2 hours. Skin-prick testing and food-specific IgE can support a matching history; they do not diagnose allergy by themselves. A positive test without a clinical reaction is sensitization. The oral food challenge, performed where anaphylaxis can be treated, remains the confirmation step when history and tests disagree.

Non-IgE disease is delayed and gut-predominant. Serum IgE and skin tests are typically negative and should not be used as a grocery-list fishing expedition.

FPIAP is the breastfed or formula-fed young infant with bloody stools who is otherwise well. The usual trial is maternal dietary cow's-milk elimination (add soy restriction if milk restriction fails) or a switch to an extensively hydrolyzed formula. Amino-acid formula is for hydrolysate failure or poor growth. Most infants outgrow FPIAP in the first year. Do not label this infant "milk anaphylaxis" and do not order a 30-food IgE panel.

Acute FPIES is a different emergency: repetitive vomiting, limpness, and pallor 1–4 hours after milk, soy, rice, or oat. Shock can occur. Management is hemodynamic support (saline boluses; ondansetron in acute care). Epinephrine is used if the picture overlaps anaphylaxis or the child is hypotensive and the mechanism is unclear — FPIES itself is not an IgE mast-cell event. Chronic FPIES from ongoing exposure presents as diarrhea, poor weight gain, and irritability. Diagnosis is clinical.

Clinic vignette. A thriving 8-week-old has flecks of blood in the stool and a normal abdominal exam. This is FPIAP until proven otherwise — not an autoinjector and not a diagnosis of IgE milk allergy.

The common pediatric food allergens

Counsel the foods that actually cause most U.S. pediatric reactions.

Sesame is increasingly recognized and is labeled under U.S. law. A "nut-free" classroom is not automatically sesame-free. Do not diagnose celiac disease as wheat anaphylaxis, and do not treat IgE wheat allergy with a celiac "trace gluten" lecture.

Avoid unselected food-IgE panels in chronic abdominal pain, isolated allergic rhinitis, or a well child. False-positive tests create needless elimination diets, growth failure, and family fear.

Early peanut introduction (NIAID / LEAP)

The LEAP trial showed that high-risk infants who ate peanut regularly developed less peanut allergy than infants who avoided peanut. NIAID's addendum guideline translated that into primary-care timing. Complementary feeding starts when the infant is developmentally ready; peanut is not delayed as a prevention strategy.

Whole peanuts and thick spoonfuls of peanut butter are choking hazards. Mix a small amount of peanut butter into puree, or use dissolvable peanut puffs. Once peanut is tolerated, keep it in the diet regularly; a one-time taste is not the LEAP protocol.

Prevention trap: delaying peanut, egg, or milk in a low-risk infant to "prevent allergy" is outdated and is the opposite of current peanut-prevention evidence.

Anaphylaxis: epinephrine first, then the plan

Anaphylaxis is a serious systemic allergic reaction that is rapid in onset and may cause death. In children it is often food-triggered. Recognize skin plus respiratory, skin plus cardiovascular, or hypotension after a known allergen even without hives. Isolated hives without other systems is urticaria, not automatically anaphylaxis — but do not withhold epinephrine if you are clinically unsure and the child is progressing.

First drug, first site, first next step

1. Epinephrine IM into the anterolateral thigh (vastus lateralis), through clothing if needed.
2. Use the autoinjector the family has, or 0.01 mg/kg of 1 mg/mL (1:1000) epinephrine IM. Usual pediatric community max is 0.3 mg per dose (some acute-care protocols allow 0.5 mg in adolescents).
3. Typical autoinjector teaching: 0.15 mg for most young children in the 15–30 kg range (0.1 mg devices exist for smaller infants); 0.3 mg at ≥30 kg. Teach the device the family actually carries and match current product labeling for weight.
4. Call EMS. Observation belongs where biphasic reaction and airway compromise can be treated — not in the family car while waiting to see if an antihistamine works.
5. A second IM dose may be given after 5–15 minutes if symptoms persist or worsen. Prescribe two devices.
6. Position: recumbent with legs raised if hypotensive; sitting forward if in respiratory distress; do not make a hypotensive child stand or walk.

Not first-line: oral or IM antihistamines, albuterol as monotherapy, systemic corticosteroids as the opening move, subcutaneous epinephrine, or waiting for IV access. Albuterol may help bronchospasm after epinephrine. Steroids are adjuncts and do not abort the acute reaction. H1 antihistamines treat urticaria, not shock.

Autoinjector teaching is a primary-care skill, not an optional handout. Demonstrate the trainer. Name the thigh — not the buttock and not a clothed deltoid as the preferred community site. Teach a second adult. Check expiration dates at well visits. Document a written allergy and anaphylaxis emergency action plan (FARE or equivalent) for home and school, and support a Section 504 plan when food is in the classroom. Children with food anaphylaxis and asthma need extra respect: most food-allergy fatalities involve delayed epinephrine and underlying asthma.

Biphasic reaction is a second wave of anaphylaxis after apparent resolution, without re-exposure, classically hours later (often taught in a 1–8 hour window, sometimes longer). That is why EMS and ED observation exist. It is not a reason to skip the first epinephrine dose; it is a reason not to discharge from the parking lot.

When the CPNP-PC refers to allergy

Refer rather than serial-guessing elimination diets:

• Any anaphylaxis
• IgE-mediated peanut, tree-nut, fish, shellfish, or multiple-food allergy
• High-risk infant (severe eczema and/or egg allergy) needing supervised peanut introduction or testing
• FPIES
• Need for oral food challenge or discussion of oral immunotherapy
• Food allergy plus uncontrolled asthma or repeated community epinephrine use
• Diagnostic uncertainty after a reaction that might have been viral urticaria, not food

Primary care still owns prevention counseling, the first epinephrine prescription after a community reaction, device teaching, the action plan, growth on elimination diets, and not ordering junk panels.

Exam traps

1. Oral antihistamine as first-line anaphylaxis treatment.
2. Treating FPIAP as IgE milk anaphylaxis, or treating FPIES as a problem that skin testing will diagnose.
3. Delaying peanut in a general-population infant until age 1 "to prevent allergy."
4. Sending a high-risk infant (severe eczema or egg allergy) home to try peanut with no testing or referral thought.
5. Diagnosing food allergy from a positive IgE panel without a matching history.
6. Letting the family "watch at home" after community epinephrine.

IgE versus non-IgE, introduce peanut on time, epinephrine in the thigh first, then EMS, two autoinjectors, and a written plan. That is food allergy on this exam.