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Anaphylaxis prehospital emergency: management

Anaphylaxis prehospital emergency: management

You have assessed the patient and found them to be an acute allergic reaction.  Worse, they have systemic signs and symptoms that have increased the provisional working diagnosis to be anaphylaxis.  A management plan has to be produced and implemented quickly.  In some respects, the management will be measured according to the presenting problems.  At the centre of all presentations though there will be a common and essential core.

Where bronchospasm is encountered, it can be treated with nebulised salbutamol and oxygen. Beta two agonists can have effect on the lower airway bronchospasm but not much else in the anaphylactic process so must not be considered a substitute for or delay the administration of adrenaline1. Just as with any other patient in respiratory distress, severe and breathing failure would be better managed with high concentration oxygen supported by some form of non invasive ventilation support as necessary.

Upper airway oedema can respond to nebulised adrenaline.  Adrenaline can cause local vasoconstriction and reduce the fluid shift that is occurring.  Adrenaline via any route would be an important part of management of any respiratory difficulty in anaphylaxis and should be considered the front line of all therapy.  The most severe cases might even require intubation though this could likely be difficult.  If it was necessary, nebulised adrenaline would also manage bronchospasm as well.

It must be remembered always that nebulised adrenaline is no substitute for intramuscular adrenaline.  If it is administered it must be as well as intramuscular therapy.

The other cause of respiratory difficulty in anaphylaxis is pulmonary oedema. Not all pulmonary oedema is the same.  Though the most common, not all is caused by cardiac failure.  The mechanism in anaphylaxis isn’t one of hydrostatic pressure change as it is with left ventricular failure.  Rather, it results from increased capillary permeability.  Hence, attempts to increase preload such as using autoinfusion, if tolerated, wouldn’t likely have the life threatening consequences it might in the cardiac setting.

Similarly, offloading preload with nitrates would be of less help.  Lower than normal blood pressure is likely to be already a problem, given the vasodilation and fluid shifting.  Don’t worsen it with treatments that provide similar actions.  Typical pulmonary oedema management for cardiac cause is not appropriate here.  Forget the nitrates and diuretics.  What is appropriate is normal anaphylaxis management, high flow oxygen and supporting ventilation if needed and urgent adrenaline therapy.

Most anaphylaxis will present rather quickly.  They may have great breathing difficulty or none at all.  They may have adequate perfusion or challenged by an un-recordable blood pressure.  They may have gastrointestinal complaints of nausea, vomiting or diarrhoea or none at all.

Diagnosis might be relatively certain.  Alternately it may be very unclear.  If there is doubt, the default diagnosis should be anaphylaxis if that is a real option.  Following appropriate positioning, oxygen therapy, beta2 agonist perhaps if indicated, assisted ventilation where respiratory failure is encountered, anaphylaxis is best managed with adrenaline.

The need for oxygen administration has become far less simple with it out of favour for such acute illness as stroke and acute coronary syndrome without clear need provided by pulse oximetry.  The time honoured maxim that ‘the good gas’ can do no harm no longer exists.  However, for many critical illness oxygen is still indicated in the first instance.  In anaphylaxis there are a number of problems with oxygenation.

Firstly, any respiratory distress can adversely impact on ventilation and oxygenation.  Supplemental oxygen can assist with maintaining oxygenation whilst the problems are corrected.  Secondly, any peripheral vasodilation can impair circulation.  Blood that should move quickly through the peripheral circulation will move slowly.  This stagnation of blood allows more time for oxygen to be removed than normal.  To correct this, the circulation needs to be restored of course but some temporary additional oxygen therapy can help increase diffusion from the alveoli back into the blood.  So oxygen therapy is a very important part of anaphylaxis management.

Basic care is always important and should precede more advanced options.  The position to place the patient on the bed, chair or floor is often underappreciated.  If it is ignored out of uncertainty this in itself allows an option to occur.

The patient in anaphylaxis is best positioned lying supine with their feet slightly elevated.  With significant vasodilation going on a lot of blood will be redistributed from the central circulation to the extremities.  This will make it very easy to excessively reduce venous return and impair cardiac output.

The patient in respiratory distress may not be comfortable laid supine.  Worse, they may not tolerate it and struggle to change position.  Where this is so they should be allowed to sit upright.  This allows use of accessory muscles to assist maximum expansion of the lungs during breathing.  If the patient has major vascular collapse it is likely that they may not have sufficient consciousness for this so will lay flat.

In any and all cases, the anaphylactic patient should not have their position suddenly changed from supine to upright or worse, to standing.  Any such position change can suddenly reduce venous return precipitating life threatening reduction in cardiac output and collapse1.

Adrenaline is almost perfectly suited to managing anaphylaxis.  In larger doses, its most significant effect is its alpha effects.  The vasoconstriction returns pooled blood into the central circulation and reduces capillary permeability so reducing swelling.  It also increases cardiac output directly with its beta (1) inotropic effect.  Its beta (2) action causes bronchodilation.  Finally, it helps stabilise the immune system cells (MAST cells) that are behind all of this in the first place.

Normally adrenaline is considered ‘advanced life support’.  It can be administered by almost any route:  Nebulised, endotracheal, intramuscular, subcutaneous, intravenous, and intraosseous.

Managing anaphylaxis is considered more a first aid option.  It is readily available for use by patients themselves or by first responders, carers and family members.  They are commonly found amongst scout and school first aid kits with users trained in anaphylaxis recognition and injector use.

Many anaphylaxis sufferers have their own medication.  The most dramatic of these is the self injection adrenaline devices such as the Epipen™.  This is a prepared syringe shaped like a pen.  It quickly and easily delivers a bolus of adrenaline, usually 300 micrograms for adults and 150 micrograms for children.

Consider for a moment where the patient you are treating administers their own Epipen™ and the symptoms resolve.  This is not an uncommon occurrence and is quite the intention of self administration.  The cause of the anaphylaxis will likely be appreciated fully and the treatment provided usually very appropriate and indeed consistent with that which a medical practitioner or even paramedics would provide.

Despite the temptation, all suspected anaphylaxis patients require transport to hospital.  The duration of the activity of the allergen is uncertain.  The adrenaline duration on the other hand will be short.  It is not uncommon for patient deterioration after such treatments in what is called biphasic anaphylaxis where the original episode returns sometimes as bad as the initial episode.  This has been noted more commonly where the initial management is either delayed or inadequate.  So all anaphylactic patients should be transferred to a medical facility for supervision regardless of treatment and recovery.  It is standard recommendation for a number of hours of observation for such patients with paediatric admission typical1,2.

Overwhelmingly for most anaphylaxis, intramuscular is the most appropriate.  Not too fast acting, not too dramatic.  Some references prefer subcutaneous which is even slower and less problematic though this is not well supported any longer.

Intramuscular adrenaline has one great bonus to add even at the moment of injection.  Though normally thought of as a potent alpha vasoconstrictor, one of the actions of adrenaline is to cause vasodilation of skeletal muscle.  This is part of the ‘fight or flight response’ and you need good leg muscles to take flight.

This has implications for the administration of adrenaline.  Injection into a large skeletal muscle will not only access the blood supply, the drug will in fact help itself to improve that access.  As it dilates blood vessels in the muscle that it is injected into, it will improve its own uptake.  This is why all users of autoinjectors are taught to inject into thigh muscles.  Medical responders should follow this lead.

Adrenaline is quite potent and can have significant side effects, particularly ventricular irritability and the ability to cause hypertension.  It is particularly dose and route sensitive and arrhythmias.  More commonly the patient may note the increase in myocardial contractility and sometimes heart rate with the feeling of palpitations.  In such cases they can be reassured that this is a sign the drug is being taken up and is active.  This symptom can be used to good effect to reassure the patient.  They can also be reminded that it is a transient feeling.  Make sure of course that the problem is not one of a more disturbing arrhythmia or cardiovascular problem though before dismissing this patient symptom.

Intramuscular adrenaline is well suited for the initial management of anaphylaxis.  Provided the patient has a clinical need for adrenaline, that is an anaphylactic presentation, there is no great likelihood of problems with correct dose treatment.

The intravenous route is saved for only the most severe cases and only after initial intramuscular therapy has proven to be inadequate.  By this route, the drug uptake and the alpha effects will be more rapid and noticeable.  Hence the patient in extremis and presenting with severe vascular collapse, profound hypotension (extremely poorly perfused) would be the only recipient.

Even severe respiratory distress should respond well to the intramuscular route.   Intravenous adrenaline is intended for severe vascular collapse.  No matter how severe the respiratory distress, intramuscular adrenaline remains appropriate unless there is profound vascular collapse.  This is important to remember as the sings of respiratory distress are far more visible than vascular collapse and may create a greater sense of urgency in the prehospital responder.

All anaphylaxis or potential anaphylaxis patients who do not respond to initial therapy should be taken by intensive care paramedics.  This acknowledges the seriousness of presentation and the instability of condition.  Those patients who should be transported by intensive care paramedics include:

  • The patient who has had a severe previous episode, even if looking well now
  • Any patient with any combination of signs and symptoms that can be considered as anaphylaxis and is not responding to initial therapy

Intravenous fluids may also have a role in the management of anaphylaxis.  Adrenaline is the best option for managing hypotension but when hypotension persists, so does fluid loss from capillaries.  In the persistent hypotension setting, hypotension should be managed with fluids as well as adrenaline therapy1.

Steroids, including hydrocortisone and dexamethasone, can certainly be considered as a part of the management of anaphylaxis.  Steroids help to suppress the activities of the immune system and reduce the inflammatory processes.  They can be effective for those cases involving bronchospasm or where there is a history of asthma.  They are not immediately effective as is adrenaline and so are not first line options for anaphylaxis.  The evidence for the use of steroids in the management of anaphylaxis is mixed and not strong1,4. That considered, the earlier administered, the earlier the action and benefit.

Histamines have no clear role in the management of anaphylaxis and can possibly distract some people from treating with adrenaline.  They form no part of the front line and so don’t typically appear in pre-hospital guidelines.

Jeff Kenneally www.prehemt.com

References

  1. Estelle R. Simons, Ledit R. F. Ardusso, M. Beatrice Bilò, Yehia M. El-Gamal, Dennis K. Ledford, Johannes Ring, Mario Sanchez-Borges, Gian Enrico Senna, Aziz Sheikh, and Bernard Y. Thong, for the World Allergy OrganizationWorld Allergy Organization Guidelines for the Assessment and Management of Anaphylaxis WAO Journal 2011; 4:13–37
  2. Anne K. Elli Biphasic Anaphylaxis: A Review of the Incidence, Characteristics and  Predictors The Open Allergy Journal, 2010, 3, 24-2
  3. D A Andreae, M H Andreae Should antihistamines be used to treat anaphylaxis? BMJ 2009;339:b2489
  4. ChooKJL, Simons FER, SheikhA. Glucocorticoids for the treatment of anaphylaxis. Cochrane Database of Systematic Reviews 2010, Issue 3. Art. No.: CD007596.
  5. F Estelle, R Simmons. Anaphylaxis: Recent advances in assessment and treatment. J Allergy Clin Immunol 2009;124:625-636
  6. Cicardi M, Zanichelli A. Allergy, Asthma & Clinical Immunology 2010, 6:14

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