Aaphylaxis; causes, treatment and managment


Anaphylaxis is a life-threatening, systemic allergic reaction caused

by IgE-mediated release of histamine and other vasoactive

mediators. Clinical features are wheeze, stridor, angioedema, urticaria

and a feeling of impending doom. Potential allergen triggers

should be ascertained. The most common are:

Foods (peanut, shellfish, eggs).


 Insect venom (bee and


Drugs (penicillin, anaesthetic agents).

The route of allergen exposure influences the features of the reaction;

e.g. an inhaled allergen leads to wheezing. Anaphylactoid reactions

result from non-IgE-mediated degranulation of mast cells by

drugs (opiates, aspirin), chemicals (radiocontrast media) or other

triggers (exercise, cold). The clinical presentations are indistinguishable,

and in the acute situation discriminating between them is


Physio Guideline


Measurement of acute and convalescent serum mast cell tryptase

concentrations may be useful to confirm the diagnosis. Specific IgE

tests may be preferable to skin prick tests when investigating

patients with a history of anaphylaxis.


Anaphylaxis is an acute medical emergency. The immediate management


Prevention of further allergen exposure (e.g. removal of bee sting).

Ensuring airway patency.

Prompt administration of adrenaline

(epinephrine; 0.3–0.5 mL 1 : 1000 IM, repeat if needed).


(e.g. chlorphenamine 10 mg IM).


(e.g. hydrocortisone 200 mg IV) to prevent late-phase symptoms.


Restoration of BP (lay the patient flat, give IV fluids).

Nebulised β2-agonists for wheeze.

Patients should be referred for specialist assessment. The aims

are to:

Identify the trigger factor.

 Educate the patient regarding avoidance

and management of subsequent episodes.

Establish whether

immunotherapy is indicated.

Patients and their carers should be prescribed and taught to use

self-injectable adrenaline (epinephrine) and should wear a MedicAlert

bracelet. If the trigger factor cannot be identified (~30%), recurrence

is common.

Respiratory failure, including ARDS

Respiratory failure is classified by ABGs as either:

Type 1 (hypoxia without hypercapnia, resulting from perfused but

under-ventilated lung units).

Type 2 (hypoxia with hypercapnia,

resulting from gross ventilation/perfusion mismatch or overall

alveolar hypoventilation).

The mechanisms and underlying causes are covered elsewhere

. Hypoxaemia should always be assessed with reference to

the inspired oxygen fraction; the lower the ratio of PaO2 to inspired

oxygen (FiO2), the more severe the disease.

Initial management of circulatory collapse

Correct hypoxaemia: oxygen therapy

Consider ventilation:

Intractable hypoxaemia Respiratory distress

Hypercapnia: PaCO2 > 6.7 kPa (50 mmHg) Impaired conscious level

Assess circulation:

Heart rate CVP

BP: direct arterial pressure Peripheral perfusion

Optimise volume status: fluid challenge(s):

CVP < 6 mmHg: 250 mL 0.9% saline or colloid

CVP > 6 mmHg or poor ventricular function suspected: 100 mL boluses

Consider pulmonary artery catheter or oesophageal Doppler

Optimise Hb concentration: 70–90 g/L; 100 g/L if ischaemic heart disease. Red

cells as required

Achieve target BP: use vasopressor/inotrope once hypovolaemia corrected

Achieve adequate CO and DO2: inotropic agent if fluid alone inadequate

Monitor trend in haemodynamics, ABGs, H+, base deficit, lactate

Actions of commonly used vasoactive drugs

Drug Vasoconstrictor Inotrope Chronotrope

Adrenaline (epinephrine) ++ ++ +

Noradrenaline (norepinephrine) ++++ + (+)

Dobutamine * ++++ ++

*In most patients dobutamine acts as a vasodilator but in some it causes vasoconstriction

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