• Anaphylaxis is a severe, life-threatening, generalised or systemic hypersensitivity reaction
  • It is characterised 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
  • a patient can have anaphylaxis without any urticaria or mucosal signs
  • in the patient with known allergies, anaphylaxis may present as isolated hypotension
  • early recognition and treatment is important — delay in adrenaline adminstration is associated with increased mortality and increased rates of biphasic reactions


Multiple definitions exist —  the definition of anaphylaxis below is that of the National Institute of Allergy and Infectious Disease and the Food Allergy and Anaphylaxis Network.

  • Anaphylaxis is highly likely when any 1 of the following 3 criteria are fulfilled:

1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (eg, generalized hives, pruritus or flushing, swollen lips-tongue-uvula) AND at least 1 of the following:

  • Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)
  • Reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia [collapse], syncope, incontinence)

2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours):

  • Involvement of the skin-mucosal tissue (eg, generalized hives, itch-flush, swollen lips-tongue-uvula)
  • Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)
  • Reduced BP or associated symptoms (eg, hypotonia [collapse], syncope, incontinence); persistent gastrointestinal symptoms (eg, crampy abdominal pain, vomiting)

3. Reduced BP after exposure to known allergen for that patient (minutes to several hours):

  • Infants and children: low systolic BP (age specific) or greater than 30% decrease in systolic BP
  • Adults: systolic BP of less than 90 mm Hg or greater than 30% decrease from that person’s baseline


  • IgE mediated hypersensitivity reaction to an antigen
  • leads to profound histamine and serotonin release from basophil and mast cell degranulation.

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


Exposure to antigen:

  • stings
  • foods
  • antibiotics
  • contrast media
  • thrombolytics
  • NSAIDs
  • suxamethonium
  • non-depolarising neuromuscular blockers

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


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


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
  • IV access
  • Fluid boluses if SBP <90mmHg
  • Promethazine 25-50mg IV
  • Hydrocortisone 250mg IV
  • 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

Persistant bronchospasm

  • As per asthmatic emergencies

Persisting angioedema

  • Nebulised adrenaline (1mg)
  • ETT
  • Cricothyroidotomy
  • Tracheostomy

Seek and treat underlying causes and complications


  • 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)

References and Links


Journal articles

  • Bjornsson HM, Graffeo CS. Improving diagnostic accuracy of anaphylaxis in the acute care setting. West J Emerg Med. 2010 Dec;11(5):456-61. PubMed PMID: 21293765; PubMed Central PMCID: PMC3027438.
  • Brown SG. The pathophysiology of shock in anaphylaxis. Immunol Allergy Clin North Am. 2007 May;27(2):165-75, v. Review. PubMed PMID: 17493496.
  • Brown SG, Mullins RJ, Gold MS. Anaphylaxis: diagnosis and management. Med J Aust. 2006 Sep 4;185(5):283-9. Review. Erratum in: Med J Aust. 2006 Oct 2;185(7):400. Dosage error in article text. PubMed PMID: 16948628. [Free Full Text]
  • El-Shanawany T, Williams PE, Jolles S. Clinical immunology review series: an approach to the patient with anaphylaxis. Clin Exp Immunol. 2008 Jul;153(1):1-9. doi: 10.1111/j.1365-2249.2008.03694.x. Review. PubMed PMID: 18577027; PubMed Central PMCID: PMC2432091.
  • Kirkbright SJ, Brown SG. Anaphylaxis–recognition and management. Aust Fam Physician. 2012 Jun;41(6):366-70. PubMed PMID: 22675674. [Free Full Text]
  • Peavy RD, Metcalfe DD. Understanding the mechanisms of anaphylaxis. Curr Opin Allergy Clin Immunol. 2008 Aug;8(4):310-5. doi: 10.1097/ACI.0b013e3283036a90. Review. PubMed PMID: 18596587; PubMed Central PMCID: PMC2683407.
  • Nel L, Eren E. Peri-operative anaphylaxis. Br J Clin Pharmacol. 2011 May;71(5):647-58. doi: 10.1111/j.1365-2125.2011.03913.x. Review. PubMed PMID: 21235622; PubMed Central PMCID: PMC3093071.
  • Wölbing F, Fischer J, Köberle M, Kaesler S, Biedermann T. About the role and underlying mechanisms of cofactors in anaphylaxis. Allergy. 2013 Aug 2. doi: 10.1111/all.12193. [Epub ahead of print] PubMed PMID: 23909934. [Free Full Text]

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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