Anaphylaxis; the term comes from the Greek words ανα ana (against) and φύλαξις phylaxis (protection), indicating that something has gone wrong with the protective mechanism of the body. Instead of protecting the body, in anaphylaxis, overactivity of one component of the immune system may actually cause death.
You would remember that IgE-bound mast cells containing histamine are found in the respiratory and gastrointestinal system; mainly as a protection against foreign particles and organisms. When exposed to these foreign particles, the release of histamine causes local increased blood flow, better inflammatory response and on the whole, the foreign particle is rapidly brought under control.
But in anaphylaxis, the abnormal overactivity, or a Type I hypersensitivity reaction causes excessive amounts of histamine to be released; totally inappropriate and out-of-proportion to the initial trigger, which can be very small (eg. single bee sting, small quantities of specific foods, or even some drugs in small test quantities). This histamine, in large amounts, causes all the effects of anaphylactic shock ie profound hypotension due to the widespread vasodilatation, severe ventilatory compromise due to the severe bronchospasm and mucosal oedema, and severe shock from the combination of the above.
Early treatment is vital, and is targeted at reversing the adverse effects of histamine. Interestingly, Adrenaline is the physiological antagonist of histamine ie they do not compete for the same receptors, but their effects are diagrammatically opposite. Histamine, vasodilatation, bronchocontricton. Adrenaline, vasoconstriction, bronchodilatation. Seems quite simple, give la Adrenaline.
But woaaahhhh hold on there bro. Adrenaline, in the wrong hands, can kill the patient. Adrenaline, given too much and too fast, increases the risk of stroke, myocardial infarction and especially life-threatening cardiac arrhythmias. So, it is not something to be taken lightly, nor administered without some serious consideration. For years, these has been an on-going argument within the medical fraternity about how adrenaline was to be given, whether subcutaneously, intra-muscularly or intra-venously. I think recent research have still failed to come up with strong evidence either way, so existing recommendations must stand.
The preferred way of administering Adrenaline in patients with life-threatening anaphylactic shock is to give intramuscular adrenaline (dose undiluted) according to the table shown below. In an adult, use 0.5 mg or 0.5 mls undiluted adrenaline, via a 20 - 22 G needle long enough to reach the muscle layer of the thigh. This can be repeated after 5 mins if the response is inadequate. This is done after the initial steps are taken, as shown below.

IV adrenaline should only be used by experienced doctors, or when profound shock occurs. Here 1 mg Adrenaline is diluted to 10 mls and given at 0.5 mls titrated doses with full cardiac monitoring. If the patient is in cardiac arrest, use the full 1 mg dose of Adrenaline, as in the guidelines.
It is also important to include the adjuvants ie the anti-histamines (which do not act against histamine already released) and the steroids (which reduce the entire inflammatory response both acutely and in the later phases).
Interestingly, all this is a return to what we had known for ages, that pre-packed adrenaline in syringes (Epi-Pen) administered intra-muscular early in anaphylaxis works well and is relatively safe. Funny that we had to argue so much over what our patients had been trying to tell us, all these years.



