Anaphylaxis and allergy Flashcards
Definition
Acute, severe, life threatening allergic reaction in pre-sensitised individual leading to a systemic response caused by inflammatory mediator response by mast cells/basophils At least 2 organ systems involved->skin, upper/lower respiratory tract, CV, neurological, GI systemcs
Most frequent causative agents
Medicines Food ++ peanut tree nuts, cow milk, eggs, soy, shell fish, wheat Immunotherapy Insect stings Exercise, idiopathic, latex, tranfusion
When similar symptoms are due to non-immunological mechanisms
Anaphylactoid
Lifetime prevalence
0.5-2%
Respiratory responses
smooth muscle spasm in the respiratory and gastrointestinal (GI) tracts, vasodilation, increased vascular permeability, and stimulation of sensory nerve endings. Increased mucous secretion and increased bronchial smooth muscle tone, as well as airway edema
Cardiovascular response
-ve vascular tone +permeability
Pathogenesis
Allergen exposure->IgE produced= sensitisation->subsequent exposure->degranulation of mast cells releasing: Histamine, prostaglandin D2, leukotrienes, platelet-activating factor, tryptase, nitric oxide, and eosinophil and neutrophil chemotactic factors vascular permeability, vasodilation, and myocardial dysfunction hypotension and cardiovascular collapse, as up to 50% of intravascular volume can shift to the extravascular compartment in minutes. Altered smooth muscle tone results in bronchospasm and asthma in the respiratory tract, and may also lead to uterine cramps. Activation of the autonomic nervous system causes tachycardia, anxiety, and mucus hypersecretion. Increased platelet aggregation and subsequent recruitment of more immune cells complete the picture of the systemic inflammatory response.
Classification of immediate-type, life-threatening allergic/pseudoallergic
- IgE antibody mediated w/ systemic 2. IgE with local, life threatening laryngeal edema 3. Immunological, not IgE->anaphylotoxins C3a, C5a, MAB against lymphocytes 4. Munchausenas- real or factitious 5. Anaphylactoid: clinically indistinguishable from anaphylaxis, IgE not seen->radiocontrast, NSAID 6. Idiopathic
Features of idiopathic anaphylaxis
cause cannot be identified generalised frequent: >6 episodes per year, or ≥2 episodes within a 2-month period generalised infrequent: less often than generalised frequent angio-oedema (potentially life-threatening) frequent: >6 episodes per year or ≥2 episodes within a 2-month period angio-oedema (potentially life-threatening) infrequent: less often than angio-oedema frequent.
High risk
History of anaphylaxis Multiple allergies Poorly controlled asthma Pre-existing lung disease
Respiratory features
Respiratory/chest features (Most common in children) Tongue swelling Stridor Hoarse voice or change in character of the cry Subjective feeling of swelling or tightness/tingling in the throat Persistent cough Wheeze Dysphagia
Gastrointestinal features
NVD Pain
Mucocutaneous features
Generalised pruritus Urticaria/ intense erythema Conjunctival erythema and tearing Flushing Angioedema Neurological features Headache (usually throbbing) Dizziness Confusion Collapse with or without unconsciousness
Investigations
Anaphylaxis is a clinical diagnosis
Management
- ABCD call for help 2. Posture: treat the patient in supine position, or left lateral position for vomiting patient (or sitting at 45 degrees if breathing is difficult Legs should be elevated in the setting of hypotension. Do not stand. 3. Intra-muscular adrenaline 0.01ml/kg of 1/1000 (maximum 0.5ml), into lateral thigh which should be repeated after 5 minutes if patient not improving. 4. High flow Oxygen Do not use subcutaneous adrenaline, as absorption is less reliable than the intramuscular route. Do not use IV bolus adrenaline unless cardiac arrest is imminent. 5. An adrenaline infusion (0.05 - 1mcg/kg/min) if repeated doses of IM adrenaline are required. 6. Resuscitate boluses 20 ml/kg of 0.9% saline may be required for shock. 7. Nebulised adrenaline is not recommended as first-line therapy, but may be a useful adjunct to IM adrenaline if upper airway obstruction is present. 8. If airway oedema is not responding to parenteral and nebulised adrenaline, early intubation is indicated. 9. Corticosteroids, antihistamines and antileukotrienes have no proven immediate benefit on life threatening anaphylaxis. They may improve mild cutaneous symptoms. Other therapies to consider 10. Nebulised salbutamol is recommended if the patient has respiratory distress with wheezing or consider other anti asthma medications. 11. Antihistamines may be given for symptomatic relief of pruritus. Second generation antihistamines are preferred (promethazine can cause hypotension). 12. Corticosteroids may be considered at the discretion of the treating physician, especially for bronchospasm, although the limited evidence available does not support their use.
