Anaphylactic (Allergic) Shock – This type of reaction is usually of a violent nature, often occurring with very little warning within a few seconds to minutes following administration of drugs such as vaccines, toxoids, immune globulins, antitoxins, diagnostic solution (tuberculin skin test), antibiotic (such as penicillin), pollen or other allergic extract, or after stinging by venomous insects.
Anaphylactic shock should be distinguished from a syncopal episode which is characterized by pallor, slow pulse, salivation, nausea, vomiting and sweating. These syncopal signs and symptoms respond to measures taken to improve circulation to the brain: lowering of the head and/or raising the feet. For an incipient episode, having the patient take a few deep breaths may help.
If someone has had an anaphylaxis reaction before, they have a higher risk of having another one, and should carry at least two doses of epinephrine with them at all times. You also have a higher risk if you have a family history of anaphylaxis or have asthma.
Allergen sensitisation is a process in which a normally harmless protein (allergen) leads to the production of a specific type of allergy antibody (IgE). IgE antibodies are produced by plasma cells (mature B cells) in response to exposure to the allergen. IgE attaches to tissue mast cells in the skin, gastrointestinal tract, and/or respiratory system and peripheral blood basophils. In the absence of further contact with the allergen, binding of IgE to mast cell receptors produces no symptoms.
Mechanisms of an allergic reaction
Subsequent exposure to the allergen with cross-linking of IgE antibodies can cause rapid mast cell activation in some individuals. This results in the release of histamine and other inflammatory mediators. Multiple inflammatory mediators cause increased vascular permeability, smooth muscle spasm, mucosal oedema and inflammation. This results in clinical effects such as urticaria, angioedema, bronchospasm and anaphylaxis.
The first signs of an anaphylactic reaction may look like typical allergy symptoms: a runny or stuffy nose, sneezing or a skin rash. But within about 30 minutes, more serious signs appear.
• Skin: hives, rash, swelling, flushing, itchiness, or the skin may appear blue.
• Swollen or itchy lips or tongue
• Swollen or itchy throat, hoarse voice, trouble swallowing, tightness in your throat
• Respiratory: shortness of breath or trouble breathing, rapid heartbeat, wheezing, pain with swallowing, coughing; pain, itching, or tightness in your chest
• Fainting, dizziness, confusion,
• Weakness, weak pulse, paleness
• Vomiting, diarrhea, or cramps
• Cardiac Arrest
Use an ABCDE approach for assessment. This approach, combined with knowledge of presenting symptoms/signs and implementation of diagnostic criteria, aids a prompt diagnosis. Once anaphylaxis has been recognised, you should also follow an ABCDE approach in management. For life threatening or severe reactions, you must do this together with the prompt administration of intramuscular adrenaline. A rapid decision is needed as to whether the surgical procedure is able to continue.
It is recognised that many healthcare providers may have limited resources and limited access to drugs and monitoring equipment. It is important to recognise that many reactions can be treated successfully with implementation of simple measures and the early administration of adrenaline alone.
Stop further administration of potential causative agents, administer supplementary oxygen and place the patient supine with legs raised. These are simple measures to implement. These can be instituted whilst extra help, equipment and adrenaline is obtained. If not already in place, obtain appropriate airway management and vascular access. Treat cardiac arrest using the standard resuscitation protocols.
Adrenaline is the most important drug for the treatment of an anaphylactic reaction. Although there are no randomised controlled trials, adrenaline is a logical treatment and there is consistent anecdotal evidence supporting its use to ease breathing difficulty and restore adequate cardiac output. As an alpha-receptor agonist, it reverses peripheral vasodilation and reduces oedema. Its beta-receptor activity dilates the bronchial airways, increases the force of myocardial contraction, and suppresses histamine and leukotriene release.
There are also beta-2 adrenergic receptors on mast cells that inhibit activation, and so early adrenaline attenuates the severity of IgE-mediated allergic reactions. Adrenaline seems to work best when given early after the onset of the reaction but it is not without risk, particularly when given intravenously. Adverse effects are extremely rare with correct doses injected intramuscularly (IM). Sometimes there has been uncertainty about whether complications (e.g., myocardial ischaemia) have been caused by the allergen itself or by the adrenaline given to treat it.
Administer 0.01 mL/kg (maximum 0.5 mL per injection) intramuscularly (IM) into an un-immunized limb. Injecting epinephrine close or into the same site as the immunization agent is contraindicated as it dilates the blood vessels and may speed absorption of the vaccine (agent suspected of causing the severe allergic reaction).
It is essential to maintain a clear airway and give oxygen. Early endotracheal intubation is advised if there is any suggestion of upper airway obstruction developing. A range of endotracheal tube sizes should be available to allow for any developing laryngeal oedema and intubation difficulty. Surgical cricothyroidotomy may be required if there is severe oedema or if mask ventilation is not possible.
Bronchospasm may be alleviated by IM adrenaline through its action on beta-2 adrenoreceptors. Treatment with a nebulised beta-2 agonist, such as salbutamol 2.5-5mg is useful, although this should not delay administration of adrenaline if it is required.
Obtain vascular access, if not already secured, and begin fluid resuscitation. Change to the IO route if IV access is difficult. Give 20 ml.kg-1 IV bolus of crystalloid (0.9% saline or balanced salt solutions) if the child is hypotensive. Give further fluids titrated to blood pressure, urine output and heart rate. Position the child head down if hypotension persists. This increases venous return, and is useful if IV access has yet to be achieved or if access to IV fluids is limited. If more than 40ml.kg-1 IV fluid is required, consider inotropic support and invasive ventilation.
Histamine (H1) antagonists such as chlorpheniramine (2.5-10mg IM or slow IV) are useful in minor allergic reactions but their speed of action means they are not appropriate as first line agents. Some guidelines omit them entirely as there is a lack of strong evidence for their use, their effect on outcomes, or in prevention of biphasic reactions.
Steroids, such as hydrocortisone (25-200mg IV depending on age), are often given IV in the treatment of anaphylaxis, but offer little benefit in the acute phase. Intravenous methylprednisolone (1mg.kg-1) has been used in less severe reactions, or where the oral route is still available, prednisolone 1mg.kg-1 PO. Steroids are thought to reduce the risk of biphasic reactions. Biphasic reactions can occur in up to 20% of cases, with most occurring in the first 6 hours. A period of close observation is recommended in a wellstaffed and monitored environment. They are more often seen in those patients who have delayed administration of adrenaline, or in those who require repeated doses, so a period of observation is required after stability is achieved.