First Aid Management of Anaphylaxis & Anaphylactic Shock

Article 2


Management of Anaphylaxis &
Anaphylactic Shock


Lim Ju Boo

Regional Staff Officer for Training
St John Ambulance Malaysia

Anaphylactic shock, is a shock resulting from a very severe allergic reaction when the body is challenged with an antigen in which the body had previously being sensitized (e.g. intake of certain foods like peanuts, beef, prawns, or contact with certain plants, latex, horse serum, an insect bite, venom, antivenin, antibiotics, especially penicillin and antitetanus injections, etc.). However, I must admit that food taken orally rarely result in anaphylactic shock, except for allergic reactions to those who are sensitive. A severe hypersensitive state (syn. Serum sickness) is called anaphylaxis. It is the result of an antigen-antibody reaction when the body had previously been challenged by an antigen. Initially there may be no reaction. Severe reactions occur on second and subsequent exposures when antibodies (chiefly the immunoglobulins called IgE) begin to build up to trigger off wide spread histamine release by mast cells. Severe allergic reactions, short of anaphylactic shock, may also occur if; say a baby takes an egg or cow’s milk, or foods for which he is sensitive.

No pre-exposure:

A baby may not have been previously exposed to eggs or cow’s protein, but his mother was, and the specific antibodies (IgE) from the maternal blood had already entered his foetal circulation during intra-uterine life. Similarly, a patient developing anaphylactic shock from a single, first-time penicillin injection may have already been sensitized previously by moulds (Penicillium notatum, P. chrysogenumin) in the food and air even in exceedingly minute amounts (1). Anaphylaxis is normally characterized by extensive angiooedema (a very severe form of urticaria and swelling) to the laryngeal region, and there may be bronchial spasm. This may lead to respiratory and circulatory collapse. Death can occur within minutes when the body is challenged with a serum, venom or any allergen for which the person is highly sensitive to. The victim must be transported to a hospital immediately where adrenaline, steroids, antihistamine drugs, and oxygen may be administered.

First line of management:

There may be no first-aid for this condition, except to help the victim to breathe better, treat for shock and prepare for resuscitation if necessary. However as it involves bronchospasm, before cardiopulmonary collapse set in, it may be helpful if enquiries are made from bystanders who may be milling around, to find out if any of them is an asthmatic, and who may happen to carry a salbutamol (a bronchodilator) inhaler. Interesting questions we would ask here are: (i) Would one or two puff from such an inhaler borrowed from an asthmatic who may happen to be nearby, be of help to ease or reverse the bronchospasm while waiting for an ambulance to arrive or when the situation is getting very critical, and there is going to be a delay in transporting the patient? (ii) Can a first-aider borrow someone’s inhaler in an emergency when acute bronchospasms and death becomes inevitable? Is it allowed or ethical? (iii) Would such interim measure be helpful?

Alternative approach:

For that matter, even a common cough syrup - diphenhydramine hydrocloride (Benadryl) is also known to do the trick of counteracting excessive and extensive histamine release. In a hospital setting, diphenhydramine HCl (not the syrup) is given i.v. (intravenously) at a dose of 20 mg slowly, or 1-2 mg/kg up to 50 mg i.m (intramuscularly) over 3 mintues (2, 3, 4, 5). The equivalent dose is just 2 teaspoonful of the syrup per kilogram of body weight. Again the question we will have to ask is whether or not a remedy as simple as a cough syrup can save a life in such a crisis, albeit the medication in the form of a syrup taken orally is very mild, as it is not as rapidly absorbed and fast-acting as it would have been, if given parenterally, say via vascular access (intravenously). You may think that this rationale is correct, but I do not know the answer myself. Unless a study is done, I don’t think anyone can answer for certain. We may think otherwise, but sometimes unexpected results suddenly show up in clinical research. Somebody must carry out a study.

The golden hour:

Like in AMI, the first hour determines the chances of survival. In first-aid of asthma, or shock nothing much can be offered other than sitting the victim up or in a comfortable position to ease breathing. If there is shock, treat for shock (Trendelenburg position), and prepare to resuscitate if necessary, before sending the victim to a hospital. But what should first reponders / first-aiders do in an extreme crisis, when life or death is just minutes away, and transport is going to be delayed, or an ambulance being caught in a traffic jam on the way to a hospital? Should emergency medication be given by a first-aider if he is properly trained? These are questions people should be asking? I know that in the United States, Emergency Medical Technician-Basic (someone whose training is even less than that of a paramedics) are allowed to give even epinephrine (adrenaline) injections via an auto-injector to an anaphylactic victim, whereas paramedics are trained for even invasive procedures like insertion of endotracheal tubes, initiation of IV lines, administration of medications, interpretation of electrocardiograms, and cardiac defibrillations.

So are paramedics in Australia, France, and some other countries trained for this (8). I read that when Princess Diana was injured in the Paris car crash, ambulance crew called to the scene, had to stop the ambulance on the way to the hospital so that the ambulance crew could administer intracardiac adrenaline to her, although this procedure is now debatable, and no more recommended by the United Kingdom Resuscitation Council. Shouldn’t first-aiders/first responders, paramedics, ambulance crew etc. in this country be similarly trained up to that standard as well?

Alternative first aid medicine:

Interestingly, in one form of alternative medicine (reflexology), the modality of treatment is to massage certain pressure zones on the soles of both feet. This seems to elicit a response by sending pulses to the brain, which in turn stimulates the sympathetic autonomic nervous system* (see foot-note for explanation) to force the bronchi to relax, simultaneously sending another set of impulses to the adrenal glands (lies superior to the kidneys) to excite the cortex (outer layer) of this gland to release all the corticosteroidal hormones, and also the medulla (inner layer) of the adrenal gland to discharge the much needed adrenaline and noradrenaline into the blood. Noradrenaline is also produced by the sympathetic ganglia other than from the medulla. These natural hormones produced by the body are exactly the same drugs (other than antihistamines) a doctor would have injected to counteract the anaphylaxis. I know of at least two cases where patients recovered (at least for bronchial asthma) uneventfully through this procedure without any further intervention. This drug-free approach seems very interesting. However a larger population study would be needed for statistical analysis on this harmless modality if conventional first-aid becomes ineffective in certain situations.

Coffee as a bronchodilator:

Let us now move on to consider another very safe and common bronchodilator. And that’s just plain black coffee. Numerous clinical studies and I shall quote just two (6, 7), have shown that coffee has the same therapeutic value as aminophylline, a bronchodilating agent. Aminophylline is given at a dose of 250-350 mg i.v. over 15 minutes to keep the bronchioles patent in asthmatic patients (3). This dose is equivalent to 600 mg of caffeine which is found in two cups of very strong black coffee (no milk please. Cow’s milk protein can trigger off an allergic reaction, and makes the problem worse). Coffee contains these two drugs – aminophylline and theophylline, already present naturally in it. Both these agents are used as powerful bronchodialators in prolonged and severe asthma (status asthmaticus). Even if the aminophylline and theophylline are removed from coffee, the caffeine in the coffee itself will metabolically breakdown into these two natural drugs and make them available to the body.

Alternatives with similar mode of action:

Consider these mechanisms as some of the possibilities in first-aid for bronchospasm and angiooedema as features of anaphylaxis? I do not know the answers with certainty myself, but I am thinking of them as possibilities in the light of our scientific knowledge, and the work done by others (3,6,7). Again, questions we must seriously ask are: Can some of these harmless naturally occurring substances which show similar and promising pharmacological actions as the more powerful drugs, be used in the interim before medical intervention with more powerful and faster acting agents becomes accessible to the victim? Can they be given in the first place? Should they be given? Will they be effective? Of course one must remember not to feed anything through the mouth, not even a teaspoonful of water (except wetting the lips with water) if the patient is unconscious or unable to swallow. Once in the hospital, all medication or fluid may have to be given parenterally (non-oral route) via vascular access. For the moment the priority for the first-aider is merely to secure the airway, ensure breathing, and circulation, and transport the victim as early as possible to a hospital. Good luck. Hope you wont meet such a casualty. It can be very eventful.

Foot-note:

By the way, for those not familiar with the meaning of autonomic nervous system, very briefly, the autonomic nervous system is part of the central nervous system, and is made up of ganglia and fibres. It is divided into two major components – the sympathetic and the parasympathetic nervous systems. The functions of both systems are to control involuntary activities involving the smooth muscles, such as those responsible for respiration, heart beat, digestion, pupil size, etc. The sympathetic and parasympathetic nervous systems work in opposite action to one another. One stimulates, and the other inhibits the action.

Physiology of the 10th cranial nerve:

For example, the sympathetic nerve accelerates the heart beat, while the parasympathetic slows it down. The 10th cranial nerve is the vagus nerve, and is a parasympathetic nerve that controls and slows down the heart-rate. The nerve that accelerates the heart is called the accelerator or augmentor sympathetic nerve. If the vagus nerve is stimulated, it will slow down the heart rate to the extent of inducing a cardiac arrest (similar to giving excessive potassium). But if the stimulus is continuously applied, the heart will escape this vagal restraint, and commence to beat again (‘vagal escape of the heart’), with the first few ventricular contractions being exceptionally forceful. I must say nature is very kind to us to ensure we continue to survive.

Vagal escape:

If the vagus nerve is cut, or temporary paralyzed by a full dose of atropine (a drug with parasympatholytic action), the heart rate will be doubled (150 –180 beats per minute). Just for information sake, the vagus nerve is not there just to control the heart. After it emerges from the medulla oblongata (part of the brain stem), this longest cranial nerve starts to supply branches to the larynx, pharynx, trachea, heart, lungs, and most of the digestive system, and controls all of them.


References:


1. Yadav, M., Formerly, Professor of Immunology, University of Malaya, currently Consultant Immunologist and Allergist. Penicillin and Anaphylaxis. A Personal Communication. Nov. 1998.

2. Feng, P.H., Fock, K.M., Eng, Philip. Handbook of Acute Medicine (5th edition, 1992), Pages 76-78. APAC Publishers, Singapore.

3. Robinson, R., Stott, Robin. Medical Emergencies, Diagnosis and Management (6th edition, 1994), 345-346. CBS Publishers & Distributors, Delhi, India

4. Bochner B. et al. (1991). Anaphylaxis. N. Engl. J. Med. 324:1785.

5. Brueton M. et al. (1991). Management of anaphylaxis. Hospital Update May, page 386.

6. Becker, A.B., et al. The Bronchodilator Effects and Pharmacokinetics of Caffeine in Asthma.” New Engl. J. Med. (March 22, 1984). 310 (12): 743-746.

7. Gong. H., Jr., et al. Bronchodilator Effects of Caffeine in Coffee. A Dose-Response Study of Asthmatic Subjects.” Chest (March, 1986), 89(3): 335-342.

8. Brady Emergency Care, Grant, H.D, et al. (7th edition, 1995). Prentice-Hall International (UK) Ltd. London.