Anaphylaxis
An open learning pack for registered nurses, health visitors and midwives
What is shock?
What are the clinical forms of shock?
Anaphlyactic - allergic
Anaphylactoid - non – allergic or pseudoallergic
Seems to be increasing in incidence
Food
Animals
Drugs
Vaccines
Seconds to delayed
over an hour to several hours
Other hypersensitivity reactions may
be delayed by 72 hours
Mass release of histamine from mast
cells
Profound peripheral vasodilation
Bronchoconstriction
Hypotension Loss of consciousness Decreased capillary refill Tachycardia
Flushed – red man or red neck syndrome
Pale Urticaria
Dyspnoea - bronchoconstriction and/or upper airway oedema
Stridor, wheeze, cyanosis Pulmonary oedema
Abdominal pain, vomiting and diarrhoea
Agitation and anxiety Rhinitis Conjunctivitis
A wide range of possible presentations Reactions vary in severity
Beta blockers may increase severity Rag doll syndrome in
children
History – recent and past Faint Panic attack
118 cases from 25 million vaccinations
1:2300 attendees at A and E
departments
1 per 3 500 - 15 000 of the population
per year
Prevent Lie flat Remove
or stop the cause
100% oxygen CPR if indicated Intramuscular
adrenalin – give early
IV fluid infusions Salbutamol Corticosteroids, take 4 – 6
hours to work
Antihistamines (H1 blockers) Psychological management
Admit Take
blood to diagnose 10 mls clotted, 45 – 60 mins after
reaction
IM adrenalin is life saving
Never give iv
except in an immediate life threatening situation slowly with 1/ 10 000 with
ECG
SC is too slow
0.5 mg im.
Repeated after 5 minutes if required
Some cases require several doses
6 - 11 years give 250 mcg ie 0.25 ml 1/1 000
2 - 5
years give 125 mcg ie
0,125 ml 1/1 000
< 2 years give 62 mcg in an increased dilution
As for adults doses may be repeated
after 5 mins if necessary
Other interventions
Give an im
or slow iv antihistamine
Give hydrocortisone to avert relapse
Give iv fluid
for continued hypotension - crystalloid 1 - 2 litres may be required
Nebulised salbutamol
Medalert
Anaphylaxis
Anaphylaxis is uncommon but when it does occur prompt
action can be life saving.
The nature of anaphylaxis
Anaphylaxis is an
extreme abnormal reaction to a drug or other substance introduced into the
body. Basically two forms of reaction
are recognised, firstly anaphylaxis and secondly anaphylactoid
or pseudoallergic reactions, (table 1). An anaphylatic reaction is an abnormal form of allergic
sensitivity. This involves an abnormal antigen - antibody reaction. This
article will examine the normal function of this reaction and go on to consider
the severe life threatening abnormal allergic reaction of anaphylaxis, (type 1 hypersensivity reaction).
The function of the normal antibody - antigen reaction
An antigen is any
substance which causes an immune response in the body. It is therefore antigens
which stimulate the body to produce antibodies. Usually the antigen is a
foreign protein that the body recognises as non-self. The outer coatings of
bacteria and viruses contain such foreign proteins. Antibodies are complex
proteins which the body produces in response to exposure to an antigen. They
are correctly termed immunoglobulins.
For example the test for HIV infection does not look for the presence of
the antigen, (ie. the virus) directly. The test detects the presence of the
specific antibody made in response to the presence of the virus, so an
individual is antibody positive or negative.
When an antigen
is introduced into the body, specific antibodies will bind to it. This will result
in many antibody particles being "clumped" together. This will reduce
the pathogenic activity of the antigen and allow them to be easily phagocytosed,(1). In HIV infection there is a deficiency of antibody
production which results in low levels of antibodies and consequent
immunodeficiency.
Pathophysiological processes involved in anaphylaxis
Fatal allergic
reactions have been known for at least 4500 years,(2) but the pathophysiology has only been worked out this
century. In the pseudoallergic reaction no antigen -
antibody reaction is involved. The differences between the two are listed in
table 1. However the clinical features and treatment of both reactions are the
same.
In both
conditions there is a sudden widespread degranulation of mast cells and
basophils,(3) (plate 1). These granules store histamine. In normal physiology
localised mast cell degranulation will play a role in the generation of a local inflammatory
response. In anaphylaxis many mast cells and basophils are activated by bioactive
mediators, principally complexes of antigen and IgE, (immunoglobulin E). As
these complexes are humeral, (in body fluids) they may cause degranulation in
mast cells all over the body, (4, 5).
The effect of
widespread degranulation is analogous to giving a bolus dose of this powerful
vasodilator and bronchoconstrictor, (Fig 1). The
arterial vasodilation reduces the peripheral resistance of the circulation
therefore blood pressure drops. In addition to this the capillaries become more
permeable so fluid leaks from the blood into the tissues, leading to
hypovolaemia and possible pulmonary oedema. The combination
of these factors produce anaphylatic shock.
The heart rate will usually increase to attempt to compensate for the
hypotension. The broncho constriction inhibits the
flow of air into and out of the alveoli, leading to distress and hypoxia.
Clinical features
Often the first
indication of a developing reaction is patient anxiety and unease. This has
been described as a feeling of "impending doom".(3) Other features may develop in a matter of seconds. The
severity of the reaction may vary considerably from skin irritation and a
feeling of unease to complete collapse. Indeed in young children the collapse
has been of such severity that the child becomes completely flaccid, so called
"rag doll" syndrome.
In addition to
the hypotension and bronchospasm already described angioedema may develop. This
may exert pressure on the upper airway, compounding the respiratory
embarrassment caused by the bronchospasm. These problems will lead to wheezing,
distress, stridor and cyanosis.
In contrast to
the pallor seen in other forms of shock such as hypovolaemic, anaphylaxis causes hypotension largely by
vasodilation. This means that peripheral capillaries fill up with blood, as a
result of which the patient usually become erythromatosed,
indeed the condition has been referred to as red man or red neck syndrome,(6). (table 5).
Sneezing and
other irritation of the respiratory tract may be a feature. In addition to redness,
intensely itchy urticarial wheals may develop. Facial and peripheral oedema may
also be noted. Gasterointestinal symptoms may present
including vomiting, abdominal pain and diarrhoea.
The principle differential diagnosis
Young children
rarely, if ever, faint after a medical procedure such as a vaccination, so any
case of collapse in children will be organic in nature. Adults however
frequently faint, and so this is the most likely cause of acute
unconsciousness. In a faint the patient regains consciousness very quickly when
lying flat and there is no redness or wheals on the skin, (table 2). A central
pulse is maintained during a faint or convulsion,(7) Central pulses should be palpated for five seconds as
there is often a bradycardia during a faint.
Presentation
Anaphylactic
reactions are more common in people with a history of allergy or previous reactions, there may also be a history of asthma. Gaining
information about an individuals allergies and any
previous abnormal reactions is therefore a vital part of a nursing assessment.
The reaction may
occur after exposure to a wide range of agents, the more common of which are
listed in table 3. However almost any agent may cause
anaphylaxis in idiosyncratically sensitive individuals and present without
warning. Topical agents such as povidone-iodine are also possible causes
of anaphylaxis,(8). Desensitising vaccines used to be a frequent cause, so these should now
only be used in special units with full resuscitation facilities.
Non - drug causes of anaphylaxis
Although in
hospital anaphylaxis is most common after parenteral administration of drugs,
it may also occur as a result of food allergy or insect stings (9). The classic foods causing this are
peanuts, other nuts, shell fish, bananas and eggs, (table 3). Every time the
individual ingests the food to which they are allergic the body produces more
antibodies, so any subsequent reaction will be more severe. Food allergies are
potentially life threatening if not correctly managed.(10)
Recently there have been several reports of anaphylaxis in response to exposure
to latex gloves during surgical procedures, (11,12,13).
Precautions and prevention
In individuals
with known severe allergies, or previous anaphylactic type reactions, patient
education is vital. Clearly the causative agent should be avoided. This
involves clear identification of causative agents for an individual so they may
avoid them. A study of 266 cases in the
If a reaction to
an insect sting or food occurs in an isolated area the patient`s
life is at risk. Individuals who have had previous anaphylactic reactions to
foods or stings should carry a dose of adrenalin for self administration in the
event of the onset of a reaction,(16). Such action could be life saving,
allowing time to seek professional advice. This involves the health care
professional understanding the condition and being able to communicate
essential knowledge to the individual and significant others such as parents.
This will also involve teaching correct injection technique.
Full
documentation is essential in any individuals with a history of allergy or hypersensivity reaction. Records should be kept in the patients medical and nursing notes and on drug prescription
sheets. Individuals should also carry "Med Alert" cards or bracelets
to cover any unforeseen eventualities.
Clinical interventions in anaphylaxis
This is an
emergency situation and prompt action is vital. Anaphylactyic
reactions usually present suddenly within seconds to minutes after exposure to
the antigenic substance, however "immediate" reactions delayed by up
to half an hour have been reported,(17). In the latest edition of
Immunisation Against Disease, (1996) it is reported that in "vaccines
which are administered subcutaneously or intramuscularly, the time of onset of
anaphylaxis is variable and onset may be delayed for up to 72 hours. Patients
should be advised to seek medical attention if they develop early symptoms such
as breathlessness, swelling and rash". This information has clear
implications for nursing observation of patients after administration of
vaccines or parenteral drugs for any immediate reaction. In addition the
implications for patient education about more delayed reactions are also self
evident.
The causative
agent should be identified and if possible discontinued,(18). This cannot be done after a bolus
dose of a vaccine, but will be possible if an infusion is the cause. If the
reaction is caused by an insect sting the area may be infiltrated with a small
dose, (0.1 - 0.2 ml of 1:1 000) of adrenaline as this will slow down the rate
of antigen absorption due to localised vasoconstriction.
The patient
should be nursed lying flat or left lateral if unconscious. The legs may be
elevated to maximise cerebral and myocardial perfusion. Help should be summoned and the patient
should never be left alone. If pulmonary oedema is suspected, the need for
cerebral perfusion should be balanced with the asphyxiating effect of this
oedema. Full support and reassurance should be given. If the patient loses
consciousness an airway should be inserted if available. If
available 100% oxygen should also be given via a mask. If there is no
cardiac output the situation may present as a cardiac arrest and then should be
treated as such. If facilities are available intravenous access should be
established and an infusion started. Colloids with large osmotic molecules will
help to compensate for the hypovolaemia caused by fluid lost to the tissues.
The role of adrenaline in management
It must be
stressed that the key to successful management is adrenaline. This is a potent
bronchodilator and vasoconstrictor, it is therefore
capable of reversing the principle effects of histamine. It should be given by
deep intramuscular injection, unless the patient has a strong central pulse and
his or her overall condition is good,(19). Benign allergic reactions should
usually not be treated with adrenaline,(20)
The dose and
route of adrenaline given should be appropriate to the severity of the
reaction, 0.2 - 0.5 mls of 1 in 1 000 given subcutaneously may be sufficient in
adults for milder reactions such as puritus and
urticaria,(4). The decision on the dose and route of adrenaline will depend on the practitioners assessment of how severe the reaction is. If
five to ten minutes after intramuscular injection of adrenaline there is no
improvement in the patients condition the dose should be repeated, up to a
maximum of three doses. Doctors may decide to give adrenaline 1:10 000 by
intravenous injection very slowly in severe reactions as an extreme emergency,
in this case the cardiac rhythm should be monitored. The usual appropriate
doses for different age groups are given in table 5. Nebulised adrenaline may
be given for bronchospasm, angio-oedema or laryngeal oedema.
As adrenaline may
irritate the myocardium the lower the dose given the better, providing the
given dose is sufficiently therapeutic. Inadvertent intravenous injection of a
bolus dose of adrenaline may well lead to ventricular fibrillation. The slight
risk of cardiac complications after intramuscualr
adrenaline will be reduced if 100 per cent oxygen is given to prevent
myocardial hypoxia.
Other drugs which may be prescribed
Medical help must
be summoned as quickly as possible. Chlorpheniramine,
(Piriton) 10 - 20 mg, (adult dose) may be given
intravenously by appropriately trained individuals. This antihistamine
counteracts some of the activity of the excess histamine. In mild cases Chlorpheniramine may be given orally. Hydrocortisone, 100 -
500 mg (adult dose) intravenously may be medically prescribed to prevent
further deterioration in more severely effected cases. Salbutamol
respiratory solution may also be given nebulized for
the direct relief of bronchospasm, (table 4).
All patients who
have had an anaphylactic reaction should be automatically admitted to hospital
for review by a physician. If drugs or vaccines were aetiologicaly
involved, the medical staff should report the reaction using the yellow card
scheme to the Committee on the Safety of Medicines.
Incidence of anaphylaxis
By way of
reassurance it should be noted that anaphylaxis is a comparatively rare
reaction. The incidence has been
reported to be as low as 3.2 cases per 100 000 per year,(21). With reference to the
Anaphylactic Pseudoallergic
Mast cell degranulation
caused by abnormal activity of Mast cell degranulation
the immune system, an antibody- occurs without immune
antigen reaction. system
involvement.
Dose independent, reactions Dose dependent, larger
may occur with very small doses doses cause a more
of antigen. severe reaction.
Occurs on subsequent exposure May occur as a
to the causative agent, the body hypersensitivity
must first be sensitised by the reaction after a first
production of antibodies. exposure.
Table 1. The
differences between an anaphylatic and a pseudoallergic hypersensitivity reaction,(the
management in both cases is the same).
Vaso-vagal
Full carotid pulse persists, but may be bradycardic
Respiration continues
No upper airway oedema
No bronchospasm
No itching
Pallor
Patient regains consciousness rapidly when lying down
Young children do not faint
Anaphylaxis
Usually sinus tachycardia
Hypotension
Possible apnoea, especially in children
Upper airway oedema, sneezing may occur
Bronchospasm, possible retrosternal
tightness, dyspnoea, may be an audible expiatory wheeze
Urticarial lesions, erythema
Patients does not revive when lying
down
Table 2, Differential diagnosis of a Vaso-vagal attack and anaphylaxis
* Antibiotics
* Nonsteroidal anti-inflammatories
* Blood
and blood products
* Colloidal
intravenous infusions
* Vaccines
* Insect
stings
* Morphine
and codeine based preparations
* Muscle
relaxants
* X
Ray
contrast mediums
* Latex,
natural rubber, (eg. in surgeons gloves)
* Some
foods, eg. shell fish, nuts, bananas, eggs, mangoes,
chocolate.
Table 3. Some of the agents which may cause an anaphylactic reaction.
Drug Route Adult dose
Adrenaline Intramuscular 0.5 of 1 in 1 000 or
5
- 10 mls of 1 in 10 000
Chlorpheniramine Intravenous 10-20 mg injection over 1 minute
Hydrocortisone Slow
intravenous 100
- 500 mg
injection
Salbutamol Inhalation 2.5
- 5 mls in 4
mls of normal saline
Table 4. Drugs used
in the treatment of anaphylaxis
Age Dose
of adrenalin
1:1000
(1 mg per ml)
Less than on year 0.05
ml
1 year 0.1
ml
2 years 0.2
ml
3 -4 years 0.3
ml
5 years 0.4
ml
6 -10 years 0.5
ml
Adults 0.5
- 1 ml
Table 5. Dosages of
adrenalin by usually deep intramuscular injection for different age groups,(7).
* Shock,
(acute hypotension)
* Collapse
* Tachycardia
and possible arrthymias such as extrasystoles
* Bronchospasm
* Anxiety,
agitation and distress
* Upper
airway oedema with possible larygeal spasm
* Sneezing
* Husky
voice
* Facial
oedema
*
* Itchy
urticarial wheals
* Gastrointestinal
symptoms
Table 6. Clinical
features which may present in an anaphylactic reaction.
References.
1. The Open University, (1989), Book 5 Immunology, OU. Course S325 Biochemistry and Cell
Biology, The OU Press,
2. Mathewson Kuhn M.A. (1990),
Anaphylaxis Versus Anaphylactoid
Reactions: Nursing Interventions, Critical Care Nurse, 10 (5): 121- 36, May
3. Brueton
MJ. Lortan JE. Morgan DJR. Sutters
CA. Management of Anaphylaxis, Hospital Update, 1991 May:386 - 398
4. Isselbacker KJ. Braunwald E. Wilson JD. (1994),
5. Wyngaarden JB. Smith LH Bennett JC. (1992), Textbook
of Medicine, (19th Ed.) Saunders,
6. Anonymous, (1990), Red Men Should
Go, The Lancet, 335(8696):1006-7 April
28th.
7. HMSO,
8. Waran KD. Munsick RA.
Anaphylaxis from povidone-iodine, Lancet. 345(8963):1506, 1995 Jun 10.
9. Youlten
L. (1982), Bites and Stings, Nursing, 2(6):166-8
10. Arkinstall WW. Fatal anaphylactic reactions to food in children, Canadian Medical Association Journal. 150(11):1758, 1994 Jun 1.
11. Barnett MP. Epidemiology, diagnosis, precautions,
and policies of intraoperative
anaphylaxis to latexn Journal of the
12. Steiner DJ. Schwager RG.
Epidemiology, diagnosis, precautions, and policies of intraoperative anaphylaxis to latex, Journal of the American
College of Surgeons. 180(6):754-61,
1995 Jun.
13. Mansell PI. Reckless JP. Lovell CR. Severe anaphylactic reaction to
latex rubber surgical gloves BMJ. 308(6923):246-7, 1994 Jan 22.
14. Kemp SF. Lockey RF. Wolf BL.
Lieberman P. Anaphylaxis.
A review of 266 cases,
Archives of Internal Medicine. 155(16):1749-54, 1995 Sep 11.
15. Kemp SF. Lockey RF.
Peanut anaphylaxis from food cross-contamination, JAMA. 275(21):1636-7, 1996 Jun 5.
16. Davies
H. Harris J. Kakoo A. Treatment of acute anaphylaxis. Patients should be
taught how to inject adrenaline BMJ. 312(7031):638, 1996 Mar 9.
17. Davies D.M. (Ed.), (1985), Textbook
of Abnormal reactions to Drugs, Oxford University Press,
18. Scadding GK. Treatment of acute anaphylaxis. Remove the patient from
contact with the allergen,
BMJ.
311(7017):1434, 1995 Nov 25.
19. HMSO,
20. Hourihane JO. Warner JO.
Treatment of acute anaphylaxis. Benign allergic
reactions should not be treated with adrenaline, BMJ. 311(7017):1434, 1995 Nov 25.
21. Srensen
H.T. Nielsen B. Nielson J. (1989), Anaphylactic Shock Occurring Outside
Hospital, Allergy, 44:288-90
22. Division of Allergic Diseases, Mayo Clinic,
Underreporting of anaphylaxis in a
community emergency room. Source
Journal of Allergy & Clinical Immunology. 95(2):637-8,
1995 Feb.
Answer all of the following questions.
Some of the information necessary to
answer these questions has already been given to you, others you will need to
discuss with colleagues, try to discuss the issues raised with medical and
pharmacy staff as well as other nurses and midwives.
What does the term shock mean?
Why is it important to observe a
patient for some time after giving a drug or vaccine?
How long after giving a drug will it
take for an anaphylactic reaction to manifest itself it is going to occur?
What are the three principle life
threatening features of an anaphylactic reaction?
What medications/vaccines used on your
area of practice are most likely to cause an
anaphylactic reaction?
What agents other than medications and
vaccines may lead to anaphylaxis, give as many
specific examples as you can.
What preventative information would
you give a boy of 10 who has a severe peanut allergy?
What information would you need to
give his parents?
How may a severe reaction be treated
by his parents if it were to occur at home or while out walking?
What is the role of histamine in the pathogenesis
of anaphylaxis?
How common/uncommon is anaphylaxis?
Are there any groups of patients who
are more at risk from anaphylaxis than others?
How will you recognise an anaphylactic
reaction?
How will you differentiate between an
anaphylactic reaction and a faint after giving an injection?
What action will you immediately take
if you suspect an anaphylactic reaction?
What is the procedure in your area of
practice to summon emergency medical help?
Where is the adrenaline stored in your
clinical area?
How would adrenaline be administered
in a case of a diagnosed severe anaphylactic reaction?
Is it important to keep a patient with
anaphylaxis well oxygenated, if so why?
Give the adrenaline doses for all age
groups of patients treated in your clinical area.
Why is adrenaline effective in terms
of its physiological actions, ie. what effect does
adrenaline have on vaso and bronchial tone?
What complications/side effects may
arise when adrenaline is given?
What other preparations/management
measures may medical staff prescribe in the management of anaphylaxis?
If you were outside hospital would you
automatically arrange for the admission of a person who had suffered an
anaphylactic reaction or could they go home as soon as they feel better?