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Anaphylaxis, Pediatric


Basics


Description


  • Anaphylaxis is a serious, life-threatening, systemic allergic reaction that is rapid in onset, and is a result of mast cell and basophil activation and degranulation.
  • Skin and mucosal symptoms such as flushing, itching, urticaria, or angioedema are present in 80-90% of patients with anaphylaxis. Yet, absence of skin findings does not exclude anaphylaxis.
  • In fatal anaphylaxis, initial signs and symptoms may include respiratory distress without urticaria resulting in delayed diagnosis and treatment.

Epidemiology


  • 0.05-2% lifetime prevalence
  • Rate of occurrence appears to be increasing.
  • Estimated to be fatal in 0.7-2% of cases

Risk Factors


Genetics
There are few studies of genetic factors in human anaphylaxis; however, individuals with a previous history of anaphylaxis or a history of atopy are at increased risk for future anaphylaxis episodes.  

Pathophysiology


  • In anaphylaxis, mast cells and basophils are activated via an IgE-mediated (most common) or non-IgE-mediated mechanism releasing preformed and newly generated mediators of inflammation.
    • Mediators include histamine, tryptase, proteoglycans, leukotrienes, prostaglandins, platelet-activating factor, and cytokines.
    • Local or systemic effects can include increased vascular permeability, vasodilation, smooth muscle contraction, complement activation, and coagulation.
  • IgE-mediated anaphylaxis occurs when IgE is synthesized in response to allergen exposure (sensitization) and becomes fixed to high-affinity IgE receptors located on the surface of mast cells and basophils. Subsequent allergen exposure results in receptor-bound IgE aggregation and cell activation.
  • Non-IgE-mediated anaphylaxis generally results from nonimmune stimulation of mast cells or basophils. Rarely, IgG and complement can be implicated.

Etiology


  • IgE-mediated:
    • Foods (peanut, tree nuts, fish, shellfish, milk, egg, wheat, soy)
    • Medications (antibiotics, especially, β-lactams, NSAIDs, biologic products)
    • Venoms (usually from stinging insects including fire ants)
    • Latex (direct exposure to natural rubber or ingestion of cross-reacting foods)
    • Other (vaccines, occupational allergens, and rarely inhaled allergens)
  • Non-IgE-mediated:
    • Radiocontrast media (can also trigger IgE-dependent anaphylaxis)
    • Medications (opiates, NSAIDs, dextrans, vancomycin, polymyxin B)
    • Physical stimuli (exercise, cold, heat, sunlight/UV radiation)
    • Ethanol

Diagnosis


Anaphylaxis is a clinical diagnosis that is considered highly likely when any one of the following three criteria is met:  
  • Acute onset of illness (minutes to hours) with involvement of skin, mucosa, or both and at least one of the following: (a) respiratory compromise or (b) reduced blood pressure or associated symptoms of organ dysfunction.
  • Two or more of the following occurring acutely (minutes to hours) after exposure to a likely allergen: (a) involvement of skin-mucosal tissue (b) respiratory compromise (dyspnea, wheezing, stridor, hypoxemia), (c) reduced blood pressure or associated symptoms of organ dysfunction, (d) persistent gastrointestinal symptoms (abdominal cramping, vomiting).
  • Reduced systolic blood pressure acutely (minutes to hours) after exposure to known allergen for that patient. Defined by age-specific normals or >30% decrease from patient's baseline

History


  • A detailed history of exposures and events in minutes to hours prior to onset should be obtained after treatment is initiated.
  • Any previous history of anaphylaxis?
    • Can help direct history and patient education, especially if epinephrine was indicated but not given or if a known allergen was not recognized
  • Food triggers
    • Most common: peanut, tree nuts, fish, shellfish, milk, egg, wheat, soy, sesame, additives (spices, colorants, contaminants)
    • Foods need to be ingested for a reaction to occur, but rarely anaphylaxis can be caused by inhalation of aerosolized vapors from cooking or processing (fish and shellfish).
    • Gastrointestinal symptoms tend to be more prominent than in other etiologies.
  • Medication triggers
    • Specifically inquire about NSAIDs, supplements, and herbal treatments.
    • β-Blockers and ACE inhibitors can increase severity and/or make treatment of anaphylaxis more difficult.
  • Insect stings
    • If possible, attempt to identify the insect (honeybees leave stinger at sting site).
    • All patients should be referred to an allergist, as immunotherapy is effective in preventing 98% of future anaphylactic reactions.
  • Natural rubber latex
    • Latex-allergic patients can develop anaphylaxis after ingestion of cross-reactive foods including banana, kiwi, papaya, avocado, potato, and tomato.

Alert
For patients with anaphylaxis who are taking β-blockers or ACE inhibitors and have persistent hypotension and bradycardia despite epinephrine, consider giving glucagon.  

Physical Exam


  • Skin and mucosa
    • Flushing, itching, conjunctival erythema, urticaria, angioedema
  • Respiratory
    • Upper airway: nasal itching, congestion, rhinorrhea, sneezing, dysphonia, hoarseness, stridor, drooling (can be a sign of angioedema or obstruction)
    • Lower airway: tachypnea, cough, wheezing/bronchospasm, decreased peak expiratory flow
    • Cyanosis, respiratory arrest
  • Cardiovascular system
    • Tachycardia or bradycardia (less common), hypotension, arrhythmias, shock, urinary or fecal incontinence, cardiac arrest
  • Gastrointestinal
    • Abdominal pain/cramping, vomiting, diarrhea, dysphagia
  • Central nervous system
    • Patients may appear uneasy or describe a sense of impending doom.
    • Altered mental status, confusion, tunnel vision

Diagnostic Tests & Interpretation


Anaphylaxis is a clinical diagnosis; however, certain tests can aid in confirming the diagnosis. Treatment of anaphylaxis should be initiated immediately if a patient presents with a clinical picture that is consistent with anaphylaxis.  
Lab
  • Serum total tryptase
    • Elevated 15 minutes to 3 hours after onset of anaphylaxis
    • Elevated in patients with anaphylaxis due to injected medications, insect stings, and when hypotension is present
    • Can be normal in anaphylaxis due to foods or in those who are normotensive
    • Normal serum tryptase does not rule out anaphylaxis.
    • Laboratory test that is routinely used in practice
  • Plasma histamine
    • Elevated if measured 15-60 minutes after onset of anaphylaxis due to its short half-life
    • Blood sample requires special handling.
    • Normal level does not rule out anaphylaxis.
  • Urine histamine and N-methylhistamine
    • 24-hour urine histamine and N-methylhistamine (metabolite) can be elevated in the context of anaphylaxis.

Imaging
Chest radiograph: may be useful to rule out foreign body aspiration, or congenital malformations of the respiratory or gastrointestinal tract  

Differential Diagnosis


  • Allergic/atopic
    • Acute urticaria
    • Acute asthma
    • Pollen-food syndrome
  • Cardiovascular
    • Myocardial infarction
    • Pulmonary embolus
  • Genetic/metabolic
    • Hereditary or acquired angioedema
  • Infectious
    • Septic shock
  • Neoplastic
    • Mastocytosis/clonal mast cell disorders
    • Carcinoid
    • Basophilic leukemia
    • Pheochromocytoma
  • Neurologic
    • Syncope
    • Seizure
  • Nonorganic disease
    • Panic attack
    • Vocal cord dysfunction
    • Munchausen syndrome
  • Other:
    • Foreign body aspiration
    • Scombroidosis (ingestion of fish containing high levels of histamine)
    • Red Man syndrome

Treatment


Medication


First Line
  • IM epinephrine 1:1,000 (1 mg/mL) solution
    • 0.01 mg/kg, maximum of 0.3 mg (child) or 0.5 mg (adult), repeated q5-15min as needed (most respond to 1 or 2 doses)
    • Many deaths from anaphylaxis are associated with delayed administration of epinephrine.

Second Line
  • Diphenhydramine IV or PO (or equivalent H1-antihistamine)
    • 1 mg/kg, maximum of 50 mg, q4-6h
  • Albuterol 2.5 mg/3 mL solution
    • Nebulized and inhaled via face mask
  • Ranitidine IV
    • 1 mg/kg, maximum 50 mg
  • Methylprednisolone IV (or equivalent glucocorticoid)
    • 1-2 mg/kg, maximum of 60 mg (may be continued PO once daily for 1- to 3-day course)
    • Thought to prevent biphasic or protracted anaphylaxis, but unlikely to provide benefit in initial minutes of anaphylaxis

Additional Therapies


General Measures
  • Maintain airway:
    • Supplemental oxygen
    • Bag mask or intubation if necessary
  • Maintain circulation:
    • Place patient supine and elevate lower extremities if possible.
    • Volume resuscitation with 0.9% saline
    • IV vasopressors may be necessary in patients with refractory hypotension or shock.

Ongoing Care


Follow-up Recommendations


Most patients who are diagnosed with anaphylaxis will benefit from a referral to an allergist/immunologist for further evaluation, recommendations, and management.  
Patient Monitoring
Biphasic anaphylaxis, in which symptoms recur within 1-72 hours (usually 8-10 hours) after resolution of initial symptoms, occurs in up to 23% of adults and up to 11% of children with anaphylaxis.  
  • A prescription for autoinjectable epinephrine should be provided on discharge in any patient diagnosed with anaphylaxis.
  • A 1- to 3-day course of oral steroids may prevent or limit biphasic or protracted anaphylaxis.
  • Medical monitoring after return to baseline should be individualized and depend on degree of symptoms and other risk factors.
    • Patients with moderate respiratory compromise should be monitored for a minimum of 4 hours or longer if indicated (especially young patients or patients with comorbidities).

Patient Education


All patients should be instructed on allergen avoidance measures and provided with a written personalized emergency plan detailing appropriate management of future anaphylactic episodes.  

Prognosis


Good with trigger identification and avoidance  

Complications


  • Laryngeal edema and airway obstruction
  • Pulmonary edema, pulmonary hemorrhage, and pneumothorax
  • Myocardial ischemia and infarction
  • End-organ ischemia and damage
  • Death secondary to airway obstruction (asphyxiation) and/or shock

Additional Reading


  • Greenberger  PA, Rotskoff  BD, Lifschultz  B. Fatal anaphylaxis: postmortem findings and associated comorbid diseases. Ann Allergy Asthma Immunol.  2007;98(3):252-257.  [View Abstract]
  • Simons  FE. Anaphylaxis. J Allergy Clin Immunol.  2010;125(2)(Suppl 2):S161-S181.  [View Abstract]
  • Simons  FE, Ardusso  LR, Bil ²  MB, et al. World Allergy Organization guidelines for the assessment and management of anaphylaxis. World Allergy Organ J.  2011;4(2):13-37.  [View Abstract]
  • Webb  LM, Lieberman  P. Anaphylaxis: a review of 601 cases. Ann Allergy Asthma Immunol.  2006;97(1):39-43.  [View Abstract]

Codes


ICD09


  • 995.0 Other anaphylactic reaction
  • 995.60 Anaphylactic reaction due to unspecified food
  • 989.5 Toxic effect of venom

ICD10


  • T78.2XXA Anaphylactic shock, unspecified, initial encounter
  • T78.00XA Anaphylactic reaction due to unspecified food, init encntr
  • T63.891A Toxic effect of contact with other venomous animals, accidental (unintentional), initial encounter
  • T88.6XXA Anaphylactic reaction due to adverse effect of correct drug or medicament properly administered, initial encounter

SNOMED


  • 39579001 Anaphylaxis (disorder)
  • 91941002 Food anaphylaxis (disorder)
  • 241930003 Venom-induced anaphylaxis (disorder)
  • 241937000 Drug-induced anaphylaxis (disorder)

FAQ


  • Q: Can a patient have an anaphylactic reaction on first exposure to an allergen?
  • A: In IgE-mediated anaphylaxis, a patient must have been previously exposed to the offending allergen for sensitization to occur with a subsequent exposure potentially resulting in anaphylaxis. Remember, however, that the absence of a previous exposure on history does not exclude an allergen as causal because sensitization may have previously occurred unknowingly (through skin contact, in breast milk, in utero). Non-IgE-mediated anaphylaxis can occur on first exposure to the offending allergen.
  • Q: Should patients with a history of anaphylaxis carry more than one autoinjectable epinephrine device?
  • A: Yes, up to 20% of patients with anaphylaxis are reported to require a second dose of epinephrine either because of ongoing symptoms or because of biphasic anaphylaxis.
  • Q: Can a patient develop anaphylaxis to an allergen that they have tolerated previously?
  • A: Yes, this often occurs with medications or foods (particularly peanut, tree nuts, fish, and shellfish) especially if there is a long period of time between exposures.
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