ANAPHYLAXIS

Anaphylactic reactions are acute, life-threatening hyper­sensitivity reactions, provoked by variety of injected, inhaled or ingested foreign substances. Note that the term anaphylactoid reaction denotes clinically similar reactions to certain agents, e.g.

TABLE 8.6: Precipitating agents for anaphylaxis

• Drugs, e.g. penicillins, blood, equine sera, etc.

• Foods, e.g. sea-food, egg, nuts, additives, etc.

• Insect stings and venoms

• Biological contact agents, e.g. latex, wool, etc.

• Exercise-induced

• Idiopathic

Causes: Common precipitating agents for anaphylaxis are enumerated in Table 8.6, though the cause remains unidentified in many cases.

Pathogenesis: Anaphylactic reactions are type I hyper­sensitivity reactions, mediated by specific IgE antibodies, formed in response to previous sensitization. These antibodies are present on surface of basophils and mast cells and subsequent exposure to the same allergen leads to degranulation of mast cells and release of numerous chemical mediators.

Final effect of these mediators may manifest imme­diately with a few minutes (acute phase reaction) or after many hours (late phase reaction), with three main clinical components of anaphylaxis—acute bronchospasm, increased vascular permeability and increased secretory activity of mucous glands.

Clinically, these reactions usually begin within few minutes of exposure to offending allergen, presenting with sudden onset of:

• Dermatologic manifestations involving skin and mucus membranes, e.g. urticaria, pruritus, flushing, perioral tingling, red/itchy eyes, sneezing/rhinor rhea and extreme diaphoresis;

• Respiratory manifestations, e.g. wheezing, stridor and/ or respiratory distress;

• Cardiovascular manifestations, e.g. hypotension, bradycardia or shock and a general feeling of sinking or impending doom, with rapidly developing unconsciousness.

• Gastrointestinal manifestations in some cases with abdominal cramps, diarrhea and vomiting.

Many cases die rapidly due to airway obstruction or cardio-respiratory arrest, unless treated immediately.

Some patients after initial recovery develop recurrence (biphasic reaction) after 6-8 hours due to late-phase reactions.

D/D: While history of exposure to an offending agent and catastrophic clinical picture is characteristic, anaphylaxis needs to be differentiated from: (a) vasovagal attacks, (b) cardiac arrhythmia, (c) foreign body aspiration, (d) hypoglycemia, and (e) acute poisoning. Elevated IgE levels and eosinophilia differentiates anaphylaxis from anaphylactoid reactions.

Sudden development of clinical manifestations involving at least two of the three different systems-dermatological,

respiratory and cardiovascular system, is considered as strongly indicative of anaphylaxis.

Management: Anaphylaxis is a life-threatening emer­gency, which needs immediate resuscitative measures and subsequent hospitalization for at least 24 hours to watch for late-phase reactions. Immediate resuscitative measures include:

• Subcutaneous adrenaline is the cornerstone of management of anaphylaxis, given as 1:1000 aqueous preparation (0.1 ml/kg; max 0.5 ml) and repeated every 15-20 minutes till response. In superficial venom injections, e.g. insect stings, half of the SC dose (diluted in 2 ml saline) may be given locally at the site of injection.

All public vaccination sites are provided with anaphylaxis kit containing adrenaline, insulin/tubercu­lin syringe, 24-25 G needle and instructions about age-wise doses of adrenaline - 0.05 ml lt; 1 year, 0.1 ml from 1-6 years and 0.2 ml from 6-12 years, 0.3 ml from 12-18 years and 0.5 ml in adults.

• Place the child in supine position and assess the airway, breathing, circulation.

• Respiratory support with airway/oxygen/ventilatory support and tracheostomy, if needed.

• Cardiovascular support with IV fluids (normal saline 20 ml/kg bolus) and inotropes, e.g.

• Nebulized epinephrine (0.5 ml/kg) or nebulized salbutamol (0.15 ml/kg) in cases with stridor or wheeze respectively, which may be repeated after 10-15 minutes,

• Antihistaminics, e.g. diphenhydramine or chlor­pheniramine for next 24-48 hours, have no role in the management of acute attack but may prevent late reactions.

• Systemic steroids, e.g. IV hydrocortisone (5 mg/kg 6-hourly), although controversial in acute manage­ment, may help to decrease the duration and severity of manifestations.

• If a precipitating agent, e.g. drug is identified, a clear warning should be noted on medical records to prevent further episodes.

System-specific allergic disorders, e.g. asthma, allergic rhinitis and atopic dermatitis, etc. have been discussed in respective chapters.

BIBLIOGRAPHY

1. Bargir UA. 2019 Update on Primary Immunodeficiency Disorders by the International Union of Immunological Societies. Indian Pediatr. 2021;57:565.

2. Madkaikar M et al. Diagnostic Approach to Primary Immuno­deficiency Disorders. Indian Pediatrics, 2013;50:579.

3. Gupta N et al. Anaphylaxis. Standard treatment guidelines. Indian Academy of Pediatrics. 2022.