anaphylaxis Flashcards
define anaphylaxis
Anaphylaxis is a severe, life-threatening, generalised or systemic
hypersensitivity reaction. It is characterised by rapidly developing,
life-threatening problems involving: the airway (pharyngeal or laryngeal
oedema) and/or breathing (bronchospasm with tachypnoea) and/or circulation
(hypotension and/or tachycardia). In most cases, there are associated skin
and mucosal changes
define anaphylactoid
a non-immunologic mechanism of anaphylaxis
outline the process of how anaphylaxis forms including the first exposure.
Prior exposure to the antigen/drug
IgE antibodies formed after exposure to molecule
IgE becomes attached to mast cells or leucocytes, expressed as cell surface receptors
Re-exposure causes mast cell and basophil degranulation and release of pharmacologically active substances such as histamine, prostaglandins, leukotrienes, platelet activating factor etc
how quickly does anaphylaxis occur and how long does it last?
Occurs within minutes and lasts 1-2 hours
during anaphylaxis, second exposure, pharmacologically active substances are released, what are these and what are their functions?
Histamine – vascular permeability and vasodilatation
Prostaglandin D – bronchoconstriction
Leukotrienes – bronchoconstriction and vascular permeability
PAF – bronchoconstriction and vascular permeability
symptoms of anaphylaxis.
Occurs within minutes and lasts 1-2 hours
Vasodilation
Increased vascular permeability
Bronchoconstriction
Urticaria
Angio-oedema
25-30% have GI symptoms
Drug anaphylaxis majority of deaths due to anaphylaxis
Insect venom most common cause followed by medications
1-20% have biphasic response
outline common inducers of anaphylaxis of all severities.
Commonest food triggers:
Peanuts
Tree nuts
Cow’s milk (children)
Commonest triggers are:
Antibiotics
Chemotherapy drugs
Commonest drug triggers in peri-operative setting:
Antibiotics
Neuromuscular blocking agents (NMBAs) Chlorhexidine
insect stings - 6.5% of hospital admissions coded as anaphylaxis
name the most common causes of FATAL anaphylaxis.
Commonest food triggers:
Peanut or tree nuts
Cow’s milk
Commonest drug triggers:
NMBAs
Antibiotics
Contrast media
Non-steroidal anti-inflammatory drugs
insect stings - 14% of anaphylaxis-related deaths
type 2 hypersensitivity reactions
- antibody dependant cytotoxicity
- Drug or metabolite combines with a protein
- Body treats it as foreign protein and forms antibodies (IgG, IgM)
- Antibodies combine with the antigen and complement activation damages the cells e.g. methyl-dopa-induced haemolytic anaemia, pemphigus
type 3 hypersensitivity
- immune complex mediated
- Antigen and antibody form large complexes and activate complement
- Small blood vessels are damaged or blocked
- Leucocytes attracted to the site of reaction release pharmacologically active substances leading to an inflammatory process
- Includes glomerulonephritis, vasculitis,
type 4 hypersensitivity
- lymphocyte mediated
- Antigen specific receptors develop on T-lymphocytes
- Subsequent admin, adminstration leads to local or tissue allergic reaction
- E.g. contact dermatitis
- E.g. Stevens Johnson syndrome (TEN)
how to assess if someone is having anaphylaxis initially.
- use the ABCDE approach
- airway, breathing, circulation, disability, exposure
disability - dizziness, decreased conscious level or loss of consciousness
exposure - flushed, itchy, urticaria, hives, angioedema
if no access to medicines what should you originally do if someone is undergoing anaphylaxis?
- remove trigger if possible eg stop IV
- lie patient flat (with or without legs elevated)
- a sitting position may make breathing easier
- if pregnant lie on left side
management of anaphylaxis.
Commence basic life support. ABC
Stop the drug if infusion
Adrenaline IM 500micrograms(300mcg epi-pen)
High flow oxygen
IV fluids – aggressive fluid resuscitation
If anaphylactic shock may need IV adrenaline with close monitoring
Antihistamines eg cetirizine not first line treatment but can be used for skin symptoms
Corticosteroids no longer recommended
what should you do if you have given the patient 2 appropriate doses of intramuscular adrenaline.
- give rapid IV fluid bolus
- start adrenaline infusion
what receptors does adrenaline act on and what does this cause?
Alpha-1 - smooth muscle contraction and increased vascular resistance
Alpha- 2 - smooth muscle contraction and inhibition of transmitter release
Beta-1- increases cardiac contraction and heart rate
Beta- 2 - decreases mediator release and increases bronchodilation
affects of adrenaline during anaphylaxis.
Vasoconstriction - increase in peripheral vascular resistance, increased BP and coronary perfusion via alpha1-adrenoceptors
Stimulation of Beta1-adrenoceptors positive ionotropic and chronotropic effects on the heart
Reduces oedema and bronchodilates via beta2-adrenoceptors
Attenuates further release of mediators from mast cells and basophils by increasing intracellular c-AMP and so reducing the release of inflammatory mediators
investigations for anaphylaxis
should not delay treatment
as for a medical emergency:
12-lead ECG
Chest x-ray
urea and electrolytes
blood gases
mast cell tryptase
risk factors for hypersensitivity
Medicine factors:
Protein or polysacharide based macro molecules
Host factors:
Females > Males – we don’t know why
EBV, HIV
Prev drug reactions
Uncontrolled asthma
Genetic factors:
Certain HLA groups
Acetylator status
clinical criteria for allergy
Does not correlate with pharmacological properties of the drug
No linear relation with dose (tiny dose can cause severe effects)
Reaction similar to those produced by other allergens
Induction period of primary exposure
Disappearance on cessation
Re-appears on re-exposure
Occurs in a minority of patients on the drug
