ANAPHYLAXIS

Demographics: palpitationsNo gastrointestinal symptoms such as

Name: Catherine Mwansa nausea, vomiting, or diarrheaNo neurological deficits or
Age: 34 changes in consciousnessNo genitourinary complaints
Sex: Female Past Medical and Drug History: Ms. Mwansa denied any
Occupation: Teacher known history of allergies, chronic medical conditions,
Location: kalingalinga or current medication use.Social History: She reported
being a non-smoker with occasional alcohol
History of Presenting Complaints: consumption and no history of illicit drug use.
Pt presented to the emergency department with Furthermore, she had no recent travel history outside
sudden onset difficulty in breathing, swelling of the of Zambia.
face and lips, and generalized itching. She reported
experiencing similar symptoms after eating groundnuts
(peanuts) earlier in the day. Approximately 30 minutes
after consuming groundnuts at lunchtime, she
developed itching around her mouth followed by
swelling of her lips and face. Shortly afterward, she
experienced difficulty in breathing and felt light-
headed. She promptly sought medical attention at the
nearest healthcare facility.
Review of Systems:No history of chest pain or
Physical Examination: Upon examination, Ms. Mwansa appeared alert and oriented
but in moderate distress. Vital signs revealed a blood pressure of 105/68 mmHg,
heart rate of 110 bpm, respiratory rate of 28 breaths/min, and a temperature of
37°C. Her skin exhibited diffuse urticaria and angioedema of the lips and face.
Respiratory examination revealed audible wheezing, use of accessory muscles, and
diminished air entry bilaterally.
 Anaphylaxis is a severe, life-threatening, generalized or systemic
hypersensitivity reaction
 It is characterized by rapidly developing life-threatening airway
(pharyngeal or laryngeal) edema and/or breathing (bronchospasm
and tachypnea) and/or circulation (hypotension and tachycardia)
problems usually associated with skin and mucosal changes
 It is an acute, potentially fatal, multiorgan system reaction caused
by the release of chemical mediators from mast cells and basophils.
 Anaphylactic shock : a type of distributive shock that results from
anaphylaxis ( blood pressure drops so low that cells don’t get
enough oxygen )
 Anaphylactoid reaction is a reaction that is clinically similar to
anaphylaxis but mediated by direct nonimmune-mediated activation
of either mast cells or complement cascade
• Acute onset of an illness (minutes to several hours) with
involvement of the skin,
mucosal tissue AND at least 1 of the following:
• Respiratory compromise (eg, dyspnea, wheeze-bronchospasm,
stridor, hypoxemia)
• Reduced BP or associated symptoms of end-organ dysfunction
(eg, hypotonia
• [collapse], syncope, incontinence)

• It is a clinical diagnosis based on topical systemic

manifestations, often with a history of acute exposure to a
causative agent.
• It is a medical emergency that requires immediate recognition
and intervention.
REVIEW!
• TYPES OF HYPERSENSTIVITY
• A) Immediate hypersensitivity
• • Type 1 IgE – Mediated hypersensitivity
• • Type 2 Cytotoxic hypersensitivity
• • Type 3 immune complex – mediated
• hypersensitivity
• B)Delayed hypersensitivity
• • Type 4 hypersensitivity
Type I: IgE-mediated
Antigens bind to IgE on the surface of basophils and mast cells, leading
to the release of
inflammatory mediators. Examples include drug reactions, urticaria,
angioedema, and
Anaphylaxis, anaphylactic transfusion reactions.
Type II: Cytotoxic
Antigens bind to the cell surface, which attracts IgM and IgG antibodies
promoting cell
lysis via the complement system. One example is drug-induced
hemolytic anemia, hemolytic disease of the fetus & newborn.
Type III: Immune complex
Antigens bound to IgG forming an immune complex and are deposited
in the vessel wall, leading to an inflammatory reaction. Example is
serum sickness, SLE, PSGN.
Type IV: Delayed, cell-mediated
Previously sensitized T1 helper cells recognize an antigen and recruit
Types I and IV are the most common hypersensitivity
reactions seen in the ED.
In a type I hypersensitivity reaction, the body is exposed to a
certain allergen. Macrophages alert the body to this foreign
material, and the body produces allergen-specific IgE on the
surface of mast cells and basophils. When the body is re-exposed
to the allergen, the pre-existing IgE on mast cells and basophils
degranulates to release histamine, leukotrienes, prostaglandins,
tryptase, and other inflammatory mediators. Histamine is a
potent vasodilator that increases blood flow, vascular
permeability, cardiac contractility, and glandular secretion.
The other inflammatory mediators perpetuate this vascular
permeability and contribute to bronchoconstriction.
The inflammatory mediators released in severe anaphylaxis lead
to a mixed cardiogenic, hypovolemic, and distributive shock.
•PATHOPHYSIOLOGY
 IgE mediated hypersensitivity reaction to an antigen
 leads to profound histamine and serotonin release from basophil and mast cell
degranulation.
 Anaphylaxis (type I hypersensitivity reaction) or anaphylactoid reactions → degranulation of mast cells
→ massive histamine release → systemic vasodilation → increased capillary leakage → anaphylactic
shock

Biphasic reactions
 the recurrence of anaphylaxis symptoms soon after the initial episode
 occur about 5% of the time
 may occur >24 hours after the initial episode
 usually less severe than the initial episode
 possible risk factors include:
1. delayed administration of adrenaline
2. slow response to adrenaline
3. need for repeated doses of adrenaline
4. need for IV fluids
ETIOLOGY
Exposure to antigen:
 stings
 foods
 antibiotics
 contrast media
 thrombolytics
 NSAIDs
 suxamethonium
 non-depolarising neuromuscular blockers
Clinical features
The speed of onset and severity vary with the nature and amount of the
stimulus, but the onset is usually in minutes/ hours. A feeling of impending
death may be present. Patients on β- blockers or witha history of ischaemic
heart disease (IHD) or asthma may have especially severe features. Usually
two or more systems are involved:

• Respiratory Swelling of the lips, tongue, pharynx, and epiglottis may

lead to complete upper airway occlusion. Lower airway involvement
is similar to acute severe asthma— dyspnoea, wheeze, chest tightness,
hypoxia, and hypercapnia.
• Skin Pruritus, erythema, urticaria, and angio- oedema.
• Cardiovascular Peripheral vasodilatation and i vascular permeability
cause plasma leakage from the circulation, with d intravascular volume,
hypotension, and shock. Arrhythmias, ischaemic chest pain, and ECG
changes may be present.
• Gastrointestinal (GI) tract Nausea, vomiting, diarrhoea, abdominal
cramps.
Rapid onset (within minutes) of some
combination of:
 Angioedema
 Stridor
 Respiratory distress
 Bronchospasm
 Hypotension and cardiovascular collapse
 Abdominal cramps
 Diarrhoea
 Flushing or pallor
 Urticaria
 Coagulopathy
•INVESTIGATIONS
•Emergency tests
 anaphylaxis is primarily a clinical diagnosis but tests may help
longterm management
 histamine levels (rarely performed, peak at 10 minutes, back to
baseline at 1 hour)
 serum tryptase (see below)
•Serum tryptase
 released from secretory vesicles of mast cells
 take at 1, 6 and 24 hours
 serum separated and stored at 20 C
 normal: <1ng/mL
 non-specific and anaphylactoid reactions: 1-15ng/mL
 true anaphylaxis levels: >15ng/mL
•RAST testing
 radioallergosorbent test for antigen-specific IgE antibodies
•CAP testing
 an antigen coated capsule is exposed to the patients serum under laboratory conditions
 if serum contains antigen specific IgE a measurable colour change is produced
 superceded RAST testing
 available for testing pencillin, sux and latex allergy – sensitivity low -> thus negative result
requires skin testing
•Skin or intradermal testing
 skin testing has been shown to be diagnostic for anaphylaxis (but not for anaphylactoid
reactions)
 should take place 4-6 weeks post event to allow regeneration of IgE
 antihistamines should not have been given within the last 5 days
 use skin prick testing first
 test all drugs given before the event
 use a saline as a negative control
 use histamine solution as a positive control
 weal >2mm wider than saline = positive
 repeat positive test with a 1:10 dilution to reduce the chance of a false positive
 once positive drug detected -> test other drugs in same class
 if history is strong, but skin prick test negative -> test intradermally with diluted drugs
•
•MANAGEMENT
•Address potential life threats
 Stop trigger
 Call for help
 Position supine (head down)
 O2 (FiO2 1.0 if possible)
 Exclude alternatives
Pulse present
 Adrenaline 0.5mg IM ( beta adrenergic agonist – causes an increase in cardiac output &
HR, decrease in pvr, increase in vascular permeability and vasoconstriction, bronchial
smooth muscle relaxation)
 IV access
 Fluid boluses if SBP <90mmHg
 Promethazine 25-50mg IV ( anti histamine)
 Hydrocortisone 250mg IV ( corticosteroid – anti inflammatory)
 Persistant hypotension/bronchospasm -> repeat Adrenaline 0.5mg IM after 5 minutes; if
still persists after 5 minutes start adrenaline infusion
 Pulse absent
 CPR
 Raise legs
 2 large IVs
 2 L IVF
 Increasing Adrenaline (adult – 1-4mg) (children – 10-
100mcg/kg)
 H1 and H2 antagonists
 Extended CPR
Persisting hypotension
 Ranitidine (H2 antagonism)
 Adrenaline/Noradrenaline infusion
 Invasive monitoring
 Colloid
Persistent bronchospasm
 As per asthmatic emergencies
Persisting angioedema
 Nebulise adrenaline (1mg)
 ETT
 Cricothyroidotomy
 Tracheostomy
Seek and treat underlying causes and complications
DISPOSITION
 observe minimum 6 hours in most cases (according to expert
consensus guidelines)
Admit if:
 severe anaphylaxis
 uncontrolled asthma
 slow response to adrenaline
 need for bolus fluids
 need for a second dose of adrenaline
Prior to discharge ensure:
 provide appropriate discharge instructions (e.g. written
action plan)
 teach use of adrenaline auto-injector
 provide prescriptions and ensure that the patient is able to fill
them
 ensure that the patient can access to emergency medical
services (e.g. phone, not too remote)
 arrange follow up (GP, allergist, report reaction to Med Safe,
medic alert bracelet)
 appropriate documentation (record allery in clinical notes)